Welcome To www.LupusMCTD.com
March 28, 2024, 08:50:44 am *
Welcome, Guest. Please login or register.

Login with username, password and session length
 
   Home   Forum Help Search Calendar Login Register  
Pages: 1   Go Down
  Print  
Author Topic: Renal (Kidneys)  (Read 30951 times)
0 Members and 1 Guest are viewing this topic.
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« on: April 30, 2006, 10:27:29 pm »

Background:
 lupus nephritis one of the most serious manifestations of systemic lupus erythematosus (SLE), usually arises within 5 years of diagnosis; however, renal failure rarely occurs before American College of Rheumatology classification criteria are met.
Histological evidence of lupus nephritis is present in most patients with SLE, even if they do not have clinical manifestations of renal disease. The symptoms are generally related to hypertension, proteinuria, and renal failure. With the advent of more aggressive immunosuppressive and supportive therapy, renal and patient survival rates are improving.

Pathophysiology:
 Autoimmunity plays a major role in the pathogenesis of lupus nephritis. The immunologic mechanisms include production of autoantibodies directed against nuclear elements. These autoantibodies form pathogenic immune complexes. In the kidneys, deposition of these immune deposits initiates an inflammatory response by activating the complement cascade and recruiting inflammatory cells that can subsequently be observed on biopsy specimens.

Frequency:

In the US: The prevalence of SLE is 1 case in 2000 in the general population. Because of the difficulty in diagnosis and a probable underestimation of SLE cases, researchers suggest that the prevalence may be closer to 1 case in 500-1000 population.
Histologically, the kidneys are affected to some degree in most patients with SLE. Estimates of the prevalence of clinical renal involvement in persons with SLE range from 30-90% in published studies. The true prevalence of clinical lupus nephritis is probably around 50%.

Mortality/Morbidity:
•   Over the last 4 decades, changes in the treatment of lupus nephritis and general medical care have greatly improved both renal and overall survival. During the 1950s, the 5-year survival rate for patients with lupus nephritis was close to 0%. Recently, with the addition of immunosuppressive agents such as intravenous pulse cyclophosphamide to therapy, the 5- and 10-year survival rates are documented as high as 85% and 73%, respectively.

•   Morbidity is related to the renal disease itself, as well as to treatment-related complications and comorbidities, including cardiovascular disease and thrombotic events. Progressive renal failure leads to anemia, uremia, and electrolyte and acid-based abnormalities. Hypertension may lead to an increased risk of coronary artery disease and stroke. Nephrotic syndrome may lead to edema, ascites, and hyperlipidemia, which add to the risk of coronary artery disease and the potential for thrombosis.

•   Therapy with corticosteroids, cyclophosphamide, and other immunosuppressive agents leads to increased risk of infection. Long-term corticosteroid therapy may lead to osteoporosis, avascular necrosis, diabetes mellitus, and hypertension, among other complications. Cyclophosphamide therapy may cause cytopenias, hemorrhagic cystitis, infertility, and an increased risk of malignancy.
Race: SLE is more common in black people and Hispanic people than in white people. Black people and Asian people may have a higher prevalence of more severe lupus nephritis than other ethnic groups.
Sex: Lupus nephritis is more common in females because the overall prevalence of SLE is higher in females (ie, female-to-male ratio of 9:1); however, males with SLE have an increased prevalence of clinical renal disease with a worse prognosis.
Age: Most patients develop lupus nephritis early in their disease course. SLE is more common among women in the third decade of life, and lupus nephritis occurs in patients aged 20-40 years.

 


    CLINICAL    Section 3 of 11       

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography


History:
•   General
o   Patients with active lupus nephritis often have other symptoms of active SLE, including fatigue, fever, rash, arthritis, serositis, or CNS disease. These are more common with focal proliferative and diffuse proliferative lupus nephritis.
o   Occasionally, patients are asymptomatic; yet, during regular follow-up, laboratory abnormalities such as elevated serum creatinine levels, low albumin levels, or urinary protein or sediment suggest active lupus nephritis. This is more typical of mesangial or membranous lupus nephritis.
•   Nephritis
o   Symptoms related to active nephritis may include peripheral edema secondary to hypertension or hypoalbuminemia. Extreme peripheral edema is more common in persons with diffuse proliferative or membranous lupus nephritis because these renal lesions are commonly associated with heavy proteinuria.
o   Other symptoms directly related to hypertension that are commonly associated with diffuse proliferative lupus nephritis include headache, dizziness, visual disturbances, and signs of cardiac decompensation.
Physical:
•   Focal proliferative and diffuse proliferative lupus nephritis: The physical examination may reveal evidence of generalized active SLE with the presence of a rash, oral or nasal ulcers, synovitis, or serositis. Signs of active nephritis are also common.
•   Active lupus nephritis: Patients have hypertension, peripheral edema, and, occasionally, cardiac decompensation.
•   Membranous lupus nephritis: Signs of an isolated nephrotic syndrome are common. These include peripheral edema, ascites, and pleural and pericardial effusions without hypertension.
Causes:
•   Genetic factors
o   As with many autoimmune disorders, evidence suggests that genetic predisposition plays an important role in the development of both SLE and lupus nephritis. Multiple genes, many of which are not yet identified, mediate this genetic predisposition. Environmental factors are probably important as a trigger for development.
o   SLE is more common in first-degree relatives of SLE patients. Concordance rates are higher with monozygotic twins than dizygotic twins, supporting an important role for genetics in the development of SLE. However, the concordance rate in monozygotic twins is not 100%, suggesting that environmental factors play a role in disease expression.
•   HLA class II genes
o   HLA-DR2 and HLA-DR3 are associated with SLE.
o   HLA-DR4 is associated with a lower prevalence of SLE and appears to be protective.
•   Complement genes
o   C1Q, C1R, and C1S deficiencies are associated with SLE, lupus nephritis, and production of anti–double-stranded DNA (anti-dsDNA).
o   C2 and C4 deficiencies are associated with SLE or lupuslike syndrome.
o   C4A and C4B (possibly) gene deletions are associated with SLE.
•   FcR genes
o   These mediate the binding of immunoglobulin G (IgG) and IgG-containing immune complexes to cells such as macrophages and other mononuclear phagocytes.
o   FcRIIa binds to IgG2 and is encoded by 2 codominant alleles, which are H131 (or high affinity) and R131 (or low affinity). The low-affinity phenotype (homozygous for R131 allele; 131R/R) is associated with lupus nephritis among the black population.
o   FcRIIIa binds to IgG1 and is encoded by 2 codominant alleles, which are V158 (or high affinity) and F158 (or low affinity). The low-affinity phenotype (homozygous for F158 allele; 158F/F) is associated with SLE.
•   Cytokine genes: Certain polymorphisms of the IL10 gene (high producers) and possibly the IL1RN and TNFA genes (low producers) are associated with SLE.
•   Apoptosis genes: Defects of several apoptosis genes are associated with lupuslike syndromes in mice and, rarely, SLE in humans, including CD95 (Fas) and CD178 (FasL).
•   Immunologic factors
o   The initial autoantibody response appears to be directed against the nucleosome, which arises from apoptotic cells. Patients with SLE have poor clearance mechanisms for the cellular debris. Other autoantibodies develop by a process of epitope spreading, including anti-dsDNA antibodies. These autoantibodies develop over time, in an orderly fashion, months to years before the onset of clinical SLE. Lupus nephritis is associated with the production of nephritogenic autoantibodies, which have certain characteristics, as follows:
   Antigen specificity directed against nucleosome or dsDNA: Some anti-dsDNA antibodies cross-react with the glomerular basement membrane.
   Higher-affinity autoantibodies may form intravascular immune complexes, which are deposited in glomeruli.
   Cationic autoantibodies have higher affinity for the anionic glomerular basement membrane.
   Autoantibodies of certain isotypes (IgG1 and IgG3) readily activate complement.
o   Immune complexes form intravascularly and are deposited in glomeruli. Alternatively, autoantibodies may bind to antigens already located in the glomerular basement membrane, forming immune complexes in situ. Immune complexes promote an inflammatory response by activating complement and attracting inflammatory cells, including lymphocytes, macrophages, and neutrophils. The histologic type of lupus nephritis that develops depends on a number of factors, including the antigen specificity and other properties of the autoantibodies, and the type of inflammatory response that is determined by other host factors. In more severe forms of lupus nephritis, proliferation of endothelial, mesangial, and epithelial cells and the production of matrix proteins lead to fibrosis.

Lab Studies:
•   General
o   Evaluating renal function in patients with SLE to detect any renal involvement early is important because early detection and treatment can significantly improve renal outcome.
o   The laboratory tests to evaluate renal function include the following:
   Blood urea nitrogen testing
   Serum creatinine level
   Urinalysis (to check for protein, RBCs, and cellular casts)
   Creatinine clearance
   Twenty-four–hour urinary protein excretion (spot urine for creatinine and protein)
•   Tests of SLE disease activity
o   Disease activity can be evaluated with anti-dsDNA, complement determinations (C3, C4, and CH50), and erythrocyte sedimentation rate (ESR) or C-reactive protein. The C-reactive protein level is generally not elevated in patients with SLE, even with active disease, unless the patient has significant arthritis or infection.
o   Generally, an elevated ESR and anti-dsDNA and low C3 and C4 levels are associated with active nephritis, especially focal proliferative and diffuse proliferative lupus nephritis.
o   Clinically relevant lupus nephritis is associated with a 30% decrease in creatinine clearance, proteinuria of greater than 1000 mg/d, and renal biopsy findings indicating active lupus nephritis.
Procedures:
•   Renal biopsy
o   Renal biopsy should be considered for any patient with SLE who has clinical or laboratory evidence of active nephritis, especially with the first episode of nephritis.
o   Renal biopsy may be useful in patients with recurrent episodes of nephritis, depending on the clinical circumstances. By revealing the histologic pattern and stage of disease (activity and chronicity), renal biopsy is useful in determining prognosis and treatment.
o   Findings from a thorough clinical and laboratory evaluation can be used to predict the histologic type of lupus nephritis in approximately 70-80% of patients; however, this is not accurate enough considering the toxicity of some of the treatment protocols. A good general rule is to perform a renal biopsy if the findings will potentially alter patient management. If a particular patient has other manifestations of SLE (eg, severe CNS or hematologic involvement) and will be treated with cyclophosphamide, a biopsy may not be necessary but still should be considered because it may help predict renal outcome.
o   Sampling error can occur during a renal biopsy. Thus, the results of the biopsy should always be evaluated for consistency with the clinical and laboratory presentation of the patient.
o   Considerable variability exists in the experience of pathologists in reading lupus nephritis biopsy specimens. Studies have suggested that the most consistent readers are in larger medical centers with substantial SLE patient populations.
Staging:
•   Pathologic classification
o   A classification scheme has been developed by the World Health Organization (WHO) and is based on light microscopy, immunofluorescence, and electron microscopy findings from renal biopsy specimens. See Table 1.
o   In addition to the pathologic classification, activity and chronicity indices are scored pathologically and are predictive of the renal prognosis (progression of renal disease). See Table 2.
o   The activity index reflects the state of active inflammation observed at biopsy, which may be reversible with medical therapy.
o   The chronicity index reflects the amount of fibrosis and scarring, which are unlikely to respond to therapy. Renal lesions with a high activity index are more likely to respond to aggressive therapy, whereas renal lesions with high chronicity are not.
Table 1. World Health Organization Classification of Lupus Nephritis (Modified)
Class I
Normal   Renal biopsy findings from light, immunofluorescence, and electron microscopy indicate an essentially normal kidney. No clinical evidence of renal disease is present.
Class II
Mesangial glomerulonephritis (see Image 1)

Class IIa
No or mild mesangial proliferation

Class IIb
Moderate mesangial proliferation   Light microscopy    Class IIa: Mesangial hypercellularity is not present or is mild.
Class IIb: Definite glomerular mesangial hypercellularity that is confined to the centrilobular areas away from the vascular pole and no influx of leukocytes, necrosis, or sclerosis are present.
   Immunofluorescence    Immune deposits are confined to the mesangium.
   Electron microscopy    Immune deposits are confined to the mesangium.
   Clinical manifestations    These patients have mild renal disease such as asymptomatic hematuria or proteinuria that usually does not warrant specific therapy.
Class III
Focal segmental proliferative glomerulonephritis (see Images 2-3)

Class IIIa
With active necrotizing lesions

Class IIIb
With active and sclerosing lesions

Class IIIc
With sclerosing lesions   Light microscopy   Proliferative inflammatory glomerular lesions with variable amounts of leukocyte infiltration, mesangial and endothelial cell proliferation, necrosis, and sclerosis are present. A portion (segmental) of less than 50% of all glomeruli are involved.
   Immunofluorescence   Diffuse mesangial and irregular capillary wall immune deposits are present.
   Electron microscopy   Subendothelial and mesangial immune deposits are present.
   Clinical manifestations   Many patients present with active generalized SLE and mild-to-moderate renal disease with hematuria and moderate proteinuria. A significant minority show worsening renal function and may progress to class IV lupus nephritis.
Class IV
Diffuse proliferative glomerulonephritis (see Images 4-6)

Class IVa
Without segmental lesions

Class IVb
With active necrotizing lesions

Class IVc
With active and sclerosing lesions

Class IVd
With active sclerosing lesions   Light microscopy   Proliferative inflammatory glomerular lesions with endothelial cell proliferation result in the loss of capillary space, leukocyte infiltration, variable amounts of necrosis, crescent formation, and sclerosis. Hyaline deposits are present in the capillary wall (“wire loops”) or vessel (“hyaline thrombi”). More than 50% of glomeruli are diffusely involved.
   Immunofluorescence   Irregular immune deposits are present in the mesangium and capillary walls.
   Electron microscopy   Large subendothelial and mesangial immune deposits and, occasionally, subepithelial and intramembranous deposits, may be found.
   Clinical manifestations   These patients usually present with clinical evidence of renal disease, including hypertension, edema, active urinary sediment, worsening renal function, and nephrotic range proteinuria.
Class V
Diffuse membranous glomerulonephritis (see Images 7-8)

Class Va
Pure membranous glomerulonephritis
Class Vb
Associated with mesangial hypercellularity   Light microscopy   Diffuse thickening of glomerular basement membrane occurs, without inflammatory infiltrate. With special staining, including silver and trichrome, one may see subepithelial deposits and surrounding basement membrane spikes. Membranous lesions are associated with proliferative lesions, either focal or diffuse (membranoproliferative glomerulonephritis).
   Immunofluorescence   Diffuse capillary wall and frequently mesangial immune deposits are present.
   Electron microscopy   Subepithelial and intramembranous immune deposits are present. Subendothelial deposits are present only in association with a proliferative component.
   Clinical manifestations   These patients have clinical and laboratory features of nephrotic syndrome, usually without manifestations of active SLE.
Class VI
(see Image 9)
Sclerosing glomerulonephritis   Light microscopy   This is characterized by advanced glomerular sclerosis, interstitial fibrosis, and tubular atrophy, all morphological manifestations of irreversible renal injury. Proliferative glomerular lesions are remnants or are absent.
   Clinical manifestations   These patients usually have significant renal insufficiency or end-stage renal disease and are unlikely to respond to medical therapy.
 
Table 2. Pathologic Features Used to Determine Activity and Chronicity Indices
    Activity Index   Chronicity Index
Glomerular features   Endocapillary proliferation
Leukocyte infiltration
Subendothelial hyaline deposits
Fibrinoid necrosis/karyorrhexis
Cellular crescents   Glomerular sclerosis
Fibrous crescents
Tubulointerstitial features   Interstitial inflammation   Tubular atrophy
Interstitial fibrosis
o   These indices serve as a prognostic tool and general guide to therapy. Signs of activity justify aggressive medical therapy because such therapy may arrest or reverse the pathologic changes. Signs of chronicity suggest irreversibility, and aggressive therapy is less likely to affect the outcome. The activity and chronicity indices are evaluated at a single point in time, and renal lesions may transform from one class to another either spontaneously or as a result of treatment.
    TREATMENT    Section 6 of 11       

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography


Medical Care:
•   General
o   The principal goal of therapy is to normalize renal function or, at least, to prevent the progressive loss of renal function. Therapy differs depending on the pathologic lesion.
o   Strongly consider performing a renal biopsy in patients who present with lupus nephritis.
o   Assess activity and chronicity indices.
o   Treat extrarenal manifestations and other variables that may affect the kidneys.
•   Medications
o   Use corticosteroids if the patient has clinically significant renal disease. Use immunosuppressive agents, in particular cyclophosphamide, azathioprine, or mycophenolate mofetil, if the patient has aggressive proliferative renal lesions because they improve the renal outcome. They can also be used if the patient has an inadequate response or excessive sensitivity to corticosteroids.
o   Treat hypertension aggressively. Consider ACE inhibitors if the patient has significant proteinuria, unless significant renal insufficiency is present.
o   Restrict fat intake for hyperlipidemia secondary to nephrotic syndrome.
o   Restrict protein intake if renal function is significantly impaired.
o   Administer calcium supplementation to prevent osteoporosis if the patient is on long-term corticosteroid therapy, and consider adding a bisphosphonate.
o   Avoid drugs that affect renal function, including nonsteroidal anti-inflammatory drugs, especially in patients with elevated creatinine levels.
o   Patients should avoid pregnancy if they have active lupus nephritis because it may worsen their renal disease.
o   Patients with end-stage renal disease, sclerosis, and a high chronicity index based on renal biopsy findings are unlikely to respond to aggressive therapy. In these cases, focus therapy on extrarenal manifestations of SLE and on possible kidney transplantation.
•   Therapies for renal biopsy–specific pathologic lesions
o   Class I lesions require no specific therapy.
o   For class II lesions, treatment of extrarenal manifestations may be the only therapy required. If proteinuria is greater than 1000 mg/d, elevated anti-dsDNA is present, and low complement levels are present, the patient could have a proliferative component not sampled in the biopsy specimen. Consider prednisone in low-to-moderate doses (ie, 20-40 mg/d) for 1-3 months, with subsequent taper.
o   With class III and IV lesions, patients are at high risk of progressing to end-stage renal disease and require aggressive therapy.
   Administer prednisone 1 mg/kg/d for at least 4 weeks, depending on clinical response. Then, taper it gradually to a daily maintenance dose of 5-10 mg/d for approximately 2 years. In acutely ill patients, intravenous methylprednisolone for 3 days may be used to initiate corticosteroid therapy.
   Use immunosuppressive drugs in addition to corticosteroids in patients who do not respond to corticosteroids alone, who have unacceptable toxicity to corticosteroids, who have worsening renal function, who have severe proliferative lesions, or who have evidence of sclerosis on renal biopsy specimens. Both cyclophosphamide and azathioprine are effective for proliferative lupus nephritis, although cyclophosphamide apparently is more effective in preventing progression to end-stage renal disease. Mycophenolate mofetil has been shown to be effective in treating these patients and may be used sequentially after a 6-month course of intravenous cyclophosphamide.
   Administer intravenous cyclophosphamide monthly for 6 months and every 2-3 months thereafter, depending on clinical response. The usual duration of therapy is 2-2.5 years. Reduce the dose if the creatinine clearance is less than 30 mL/min. Adjust the dose depending on the hematologic response.
   Azathioprine can also be used as a second-line agent, with dose adjustments depending on hematologic response.
   Mycophenolate mofetil may be useful if the patient does not respond to or cannot tolerate cyclophosphamide and azathioprine.
o   For class V lesions, patients are generally treated with prednisone for 1-3 months, followed by tapering for 1-2 years if a response occurs or, if no response occurs, by discontinuation. Immunosuppressive drugs are generally not used unless worsening renal function or a proliferative component is present on renal biopsy samples. Some clinical evidence indicates that azathioprine, cyclophosphamide, chlorambucil, and cyclosporine are effective in reducing proteinuria. Mycophenolate mofetil may also be effective.
•   End-stage renal disease
o   Patients with end-stage renal disease need dialysis and are good candidates for kidney transplantation.
o   Patients with end-stage renal disease secondary to SLE represent 1.5% of all patients on dialysis in the United States. The survival rate on dialysis is fair (ie, 5-y survival rate of 60-70%) and is comparable to patients on dialysis who do not have SLE.
o   Hemodialysis is preferred over peritoneal dialysis because several studies have documented higher anti-dsDNA levels, more thrombocytopenia, and higher steroid requirements in patients with SLE and end-stage renal disease who are on peritoneal dialysis. Hemodialysis also has anti-inflammatory effects with decreased T-helper lymphocyte levels. SLE is generally quiescent in patients on hemodialysis, although flares, including rash, arthritis, serositis, fever, and leukopenia, may occur and require specific treatment.
Surgical Care:
•   Patients with SLE account for 3% of all renal transplantations in the United States.
•   Ensure that the patient does not have active SLE disease at the time of transplantation.
•   A 3-month period of dialysis is usually prudent to ensure that spontaneous renal recovery does not occur.
•   Substantial evidence shows that patients with SLE fare worse than patients without SLE in terms of graft survival. Living-related allografts show better outcomes than cadaveric allografts.
•   In patients with SLE, reasons for a more severe outcome after transplantation include recurrent lupus nephritis and concomitant antiphospholipid antibody syndrome resulting in allograft loss.
Consultations:
•   Nephrologist (for renal biopsy or, if desired, for help in management of renal disease)
•   Pathologist (for renal biopsy): Substantial variation exists in the experience of pathologists in reading lupus nephritis biopsy specimens. The most consistent readers are usually found in larger academic centers with substantial populations of patients with SLE.
Diet: Alter the diet according to the presence of hypertension, hyperlipidemia, and renal insufficiency.


Corticosteroids are used in all patients with clinically significant renal disease. Immunosuppressive agents, particularly cyclophosphamide and azathioprine, are used in patients with aggressive renal lesions because they improve the renal outcome. They may also be used in patients with inadequate response or excessive toxicity to corticosteroids.
Drug Category: Corticosteroids -- Very useful in controlling acute inflammatory manifestations of SLE. Corticosteroids alone may be adequate to treat milder forms of lupus nephritis with a lower risk of progressive renal dysfunction, such as mesangial lupus nephritis, early focal proliferative lupus nephritis, or membranous lupus nephritis.
Oral corticosteroids can be used in most patients. If concern over adequate absorption exists (eg, bowel edema in nephrotic patient), intravenous methylprednisolone can be used.
Drug Name   Prednisone (Deltasone) -- Commonly used to treat inflammatory manifestations of SLE. Treatment of clinically significant lupus nephritis should include moderate-to-high initial doses.
Adult Dose   40-60 mg/d PO; taper as clinical condition improves
Pediatric Dose   0.5-1 mg/kg/d PO qd; taper as clinical condition improves
Contraindications   No absolute contraindications; severe bacterial, viral, or fungal infection; active peptic ulcer disease; diabetes mellitus
Interactions   May cause water and salt retention, exacerbating hypertension and increasing requirement for antihypertensive drugs in hypertensive patients; may aggravate hyperglycemia, increasing requirement for hypoglycemic agents in patients with diabetes; metabolism may be increased by drugs that induce hepatic microsomal enzymes, including phenytoin, phenobarbital, carbamazepine, and rifampin, thus increasing corticosteroid requirements
Pregnancy   B - Usually safe but benefits must outweigh the risks.
Precautions   Toxicities include weight gain, dyspepsia, mood changes, infection, peptic ulcer disease, hypertension, diabetes mellitus, osteoporosis, avascular necrosis, cataracts, glaucoma, myopathy, and skin changes; growth retardation in children; abrupt discontinuation may result in adrenal crisis
Drug Name   Methylprednisolone, oral (Medrol) -- Used in a similar manner to prednisone but has less mineralocorticoid effects and should be considered in patients with edema.
Adult Dose   40-60 mg/d PO, taper as clinical condition improves
Pediatric Dose   0.5-1 mg/kg/d PO qd, taper as clinical condition improves
Contraindications   No absolute contraindications; severe bacterial, viral, or fungal infection; active peptic ulcer disease; diabetes mellitus
Interactions   May cause water and salt retention, exacerbating hypertension and increasing requirement for antihypertensive drugs in hypertensive patients (less likely to do this than prednisone); may aggravate hyperglycemia, increasing requirement for hypoglycemic agents in patients with diabetes; metabolism may be increased by drugs that induce hepatic microsomal enzymes, including phenytoin, phenobarbital, carbamazepine, and rifampin, thus increasing corticosteroid requirements
Pregnancy   B - Usually safe but benefits must outweigh the risks.
Precautions   Toxicities include weight gain, dyspepsia, mood changes, infection, peptic ulcer disease, hypertension, diabetes mellitus, osteoporosis, avascular necrosis, cataracts, glaucoma, myopathy, and skin changes; growth retardation in children; abrupt discontinuation may result in adrenal crisis
Drug Name   Methylprednisolone, intravenous (Solu-Medrol) -- For treatment of severe active lupus nephritis, especially in inpatient settings.
Adult Dose   30 mg/kg/d IV for 3 d
Pediatric Dose   Administer as in adults
Contraindications   Severe bacterial, viral, or fungal infection; active peptic ulcer disease; diabetes mellitus
Interactions   May cause water and salt retention, exacerbating hypertension and increasing requirement for antihypertensive drugs in hypertensive patients (less likely to do this than prednisone); may aggravate hyperglycemia, increasing requirement for hypoglycemic agents in patients with diabetes; metabolism may be increased by drugs that induce hepatic microsomal enzymes, including phenytoin, phenobarbital, carbamazepine, and rifampin, thus increasing corticosteroid requirements
Pregnancy   C - Safety for use during pregnancy has not been established.
Precautions   Toxicities include edema, electrolyte imbalances, hyperglycemia, infections, and convulsions
Drug Category: Immunosuppressives -- In particular, cyclophosphamide and azathioprine are used in patients with aggressive renal lesions (eg, focal proliferative lupus nephritis, diffuse proliferative lupus nephritis) because they improve renal outcome. Can also be used in patients with inadequate response or excessive toxicity to corticosteroids. In some studies, mycophenolate mofetil has been shown to be effective for treatment of lupus nephritis.
Drug Name   Cyclophosphamide (Cytoxan) -- Indicated for treatment of most patients with focal proliferative lupus nephritis or diffuse proliferative nephritis. Although it has significant toxicity, has been shown to prevent progression of nephritis and improve renal outcome.
Adult Dose   500-1000 mg/m2 IV qmo; adjust dose depending on clinical response, hematologic response, and toxicity; after 6 mo, administer q2-3mo for 2-2.5 y; usually administered with antiemetic agents and may be administered with mesna
Pediatric Dose   Administer as in adults
Contraindications   Documented hypersensitivity; infection; severely depressed bone marrow function; severe cytopenias
Interactions   Long-term high-dose phenobarbital therapy may increase metabolism to its active metabolite, increasing toxicity; inhibits cholinesterase activity for up to 10 d after an intravenous dose, which can potentiate effects of succinylcholine chloride
Pregnancy   D - Unsafe in pregnancy
Precautions   Toxicities include nausea and vomiting, leukopenia, thrombocytopenia, anemia, infection, alopecia, hemorrhagic cystitis, infertility, teratogenicity, and risk of malignancy
Drug Name   Azathioprine (Imuran) -- Useful in moderate-to-severe lupus nephritis. Although it improves renal outcome, does not appear to be as effective as cyclophosphamide, although it is less toxic.
Adult Dose   2-3 mg/kg/d PO single or divided dose
Initial: 1 mg/kg/d; increase depending on clinical and hematologic response and toxicity
Pediatric Dose   2-3 mg/kg/d PO single or divided dose
Initial: 1 mg/kg/d; increase depending on clinical and hematologic response and toxicity
Contraindications   Documented hypersensitivity; active infection (relative); severe cytopenias (relative)
Interactions   When administered with allopurinol, decrease dose by 65-75% because azathioprine is metabolized by xanthine oxidase; may cause anemia or severe leukopenia in combination with ACE inhibitors; may reduce anticoagulant effect of warfarin
Pregnancy   B - Usually safe but benefits must outweigh the risks.
Precautions   Nausea and vomiting, leukopenia, thrombocytopenia, anemia, infection, and abnormal liver function test results may occur
Drug Name   Mycophenolate mofetil (CellCept) -- Has been shown useful in mild-to-moderate lupus nephritis in several recent studies. Has generally been well tolerated, and, in these studies has been as effective (possibly more effective) than more traditional therapies including cyclophosphamide and azathioprine, with less toxicity.
Adult Dose   1000 mg PO bid; starting dose is 500 mg/d PO and titrated up to 1000 mg PO bid over 2 mo as tolerated; may increase to 3000 mg/d in occasional patients; doses >2000 mg/d should be avoided in patients with significant renal impairment
Pediatric Dose   600 mg/m2 PO bid; titrate up to maximum of 1000 mg PO bid over 2 mo
Contraindications   Documented hypersensitivity; active infection (relative); severe cytopenias (relative)
Interactions   Antacids containing magnesium and aluminum may reduce absorption when administered simultaneously; live attenuated vaccines should be avoided during therapy
Pregnancy   C - Safety for use during pregnancy has not been established.
Precautions   Nausea, vomiting and other GI symptoms may occur; anemia and leukopenia are not uncommon; patients may be at risk for opportunistic infections, most likely viral; occasionally, abnormal LFT results may occur
    FOLLOW-UP    Section 8 of 11       

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography


Further Outpatient Care:
•   Follow-up visits
o   Schedule the patient for close follow-up after the initiation of therapy, especially those with focal proliferative, diffuse proliferative, or membranous glomerulonephritis, to monitor therapy response and treatment-related toxicities.
o   With the initiation of high-dose corticosteroids, cyclophosphamide, azathioprine, or mycophenolate mofetil, arrange for the patient to visit a physician at least every month.
•   Follow-up testing
o   Use the ESR, anti-dsDNA, and C3 and C4 to monitor SLE disease activity.
o   Cyclophosphamide therapy requires regular laboratory monitoring, including CBC count and urinalysis.
o   Azathioprine therapy requires regular monitoring of CBC count and less frequent monitoring of liver function test results.
•   Determine renal function, urinalysis results, and albumin levels monthly, and determine creatinine clearance and 24-hour urinary protein excretion every 3 months. After the initiation of therapy and as the patient's condition stabilizes, monitoring may be less frequent.
•   Exercise vigilance with flares of lupus nephritis, even in patients who are stable for many months or years.
Complications:
•   Disease-related complications may be secondary to hypertension and nephrotic syndrome and include the following:
o   Cardiovascular complications
o   Stroke
o   Hyperlipidemia
o   Hypercoagulability with thrombosis
•   Treatment-related complications include the following:
o   Infections
o   Cytopenias
o   Bladder toxicity
o   Infertility
o   Premature gonadal failure
o   Osteoporosis
o   Avascular necrosis
o   Premature atherosclerosis
o   Small increased risk of malignancy
Prognosis:
•   Poor prognostic indicators
o   Delay in treatment of more than 5 months from onset of nephritis
o   Young age at onset of nephritis
o   Male sex
o   Black racial background
o   Hypertension
o   Nephrotic syndrome
o   Elevated creatinine level (>3 mg/dL) at presentation
o   Persistently elevated anti-dsDNA and low C3 and C4 levels
o   Renal biopsy findings showing diffuse proliferative glomerulonephritis or high chronicity index
•   Excellent prognosis: Mesangial lupus nephritis (WHO class II) has an excellent prognosis.
•   Good prognosis: Focal proliferative lupus nephritis (WHO class III) has a good prognosis, with only a minority of patients developing progressive renal failure.
•   Fair prognosis
o   Diffuse proliferative lupus nephritis (WHO class IV) has a fair prognosis, with a significant number of patients developing progressive renal failure.
o   Membranous lupus nephritis (WHO class V) has a fair prognosis, with a significant number of patients developing progressive renal deterioration over time.
•   Poor prognosis: Sclerosing lupus nephritis (WHO class VI) has a poor prognosis.
Patient Education:
•   Educate the patient about the serious nature of lupus nephritis, various therapies, and potential toxicities of treatment.
•   The patient must understand signs of medication-related toxicities, such as infection and bladder toxicity, so that an immediate evaluation can be initiated.
•   These patients must also understand the risks for atherosclerotic and thrombotic events, even in young women, and that any signs or symptoms suggesting such an event warrant an immediate evaluation.
•   For excellent patient education resources, visit eMedicine's Diabetes Center, Blood and Lymphatic System Center, and Arthritis Center. Also, see eMedicine's patient education articles Chronic Kidney Disease and Lupus (Systemic Lupus Erythematosus).
    MISCELLANEOUS    Section 9 of 11       

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography


Medical/Legal Pitfalls:
•   Before instituting therapy for lupus nephritis, performing a renal biopsy is generally recommended to confirm the diagnosis and to determine the type of histology as a guide to appropriate therapy. The risk of renal biopsy must be clearly explained. If the patient refuses renal biopsy, the patient must understand how this can limit diagnostic accuracy.
•   Because the therapy for lupus nephritis has significant potential for toxicity, the potential adverse effects of corticosteroids and immunosuppressive agents must be discussed. The risks of withholding therapy must also be discussed.
Special Concerns:
•   Pediatric lupus nephritis
o   Renal manifestations are more common in pediatric SLE patients than in adults. Renal biopsy findings associated with pediatric lupus nephritis show a higher rate of focal proliferative and diffuse proliferative glomerulonephritis compared with findings associated with adult lupus nephritis, and the prevalence of progression to renal failure is increased. Renal involvement occurs in two thirds of children and adolescents with SLE. With the advent of immunosuppressive therapy, survival rates have improved; however, this improvement has occurred at the expense of long-term morbidity and complications of therapy, with profound consequences.
o   In the treatment of patients with pediatric lupus nephritis, a balance should exist between early therapy to control the disease and long-term follow-up to minimize the adverse effects of therapy and the disease complications. Poor prognostic features include a renal biopsy specimen showing diffuse proliferative glomerulonephritis, persistent hypertension, persistent elevated anti-dsDNA, and hypocomplementemia.
•   Pregnancy and lupus nephritis
o   Patients should avoid pregnancy because it may aggravate renal disease, especially in the presence of active lupus nephritis, nephrotic syndrome, severe hypertension, or serum creatinine levels elevated to more than 2 mg/dL.
o   Patients with lupus nephritis have a 50-60% chance of renal flare during pregnancy if they conceive during active disease.
o   Patients with well-controlled SLE who conceive after a 3- to 6-month period of remission have a 7-10% chance of renal flare.
o   Pregnant patients with lupus nephritis are prone to preeclampsia. Preexisting hypertension and antiphospholipid antibody syndrome are the 2 most common predisposing factors to preeclampsia.
o   Severe flares during pregnancy may cause acute renal failure and maternal and fetal death. Closely monitor pregnant patients with SLE, aggressively treat exacerbations, and carefully avoid administering teratogenic drugs.

**In Memory Of Valerie Anne Hudak AOL Message Board Member
http://www.lupusmctd.com/index.php?topic=530.0
The above link will take you to her obit & link to her Lagacy Guestbook online
If you wish to make a donation in the memory of Valarie those donations may be made to the American Lupus Foundation, 2000 L Street NW Suite 710, Washington, D.C. 20036.

[attachment deleted by admin]
« Last Edit: May 17, 2006, 05:16:36 pm by Kathy » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #1 on: May 29, 2006, 02:44:31 pm »

 Study Suggests Association of anti-C1q Antibody May Affect Lupus Flares and Risk of Kidney Disease

Researchers studied blood samples of 68 lupus patients to determine the frequency of different kinds of autoantibodies and their relationship to lupus disease activity. Autoantibodies are immune proteins which can be overly active in lupus patients and are associated with increased inflammation.

Three autoantibodies were measured in this study: anti-alpha-enolase, anti-C1q, and anti-doublestrandedDNA.  Anti-a-enolase, anti-C1q, and anti-dsDNA antibodies were found in 21%, 62%, and 63% of the lupus patients, respectively.  A relationship was found between anti-C1q and anti-dsDNA antibodies. 

Anti-C1q antibodies were correlated with disease activity which was measured with an ECLAM score (European Consensus Lupus Activity Measurement). They also seemed to be associated with low white blood cell counts, levels of inflammatory proteins (complement proteins), and active kidney disease.  These findings suggest there might be an association of anti-C1q antibodies with lupus flares and with active kidney disease. 

Anti-dsDNA antibodies also were higher in patients with kidney disease. This finding is not new so the association of anti-dsDNA antibodies and kidney disease was expected.

Anti-a-enolase antibodies did not seem to be associated with the other two antibodies or any of the other measurements.  It is still unclear whether those antibodies might be useful to measure for any reason or have any clinical significance.




ABSTRACT:

ABSTRACT. Objective. To evaluate the prevalence and clinico-serological correlations of anti-enolase, anti-C1q, and anti-dsDNA antibodies in patients with systemic lupus erythematosus (SLE).

Methods. Sixty-eight sera randomly obtained from SLE patients were examined. Anti-a-enolase antibodies were detected by immunoblot on recombinant protein; anti-C1q and anti-dsDNA antibodies were detected using an ELISA.

Results. Anti-a-enolase, anti-C1q, and anti-dsDNA antibodies were positive in 21%, 62%, and 63% of patients, respectively. A correlation was found between anti-dsDNA and anti-C1q antibodies, while anti-enolase antibodies did not correlate with the other 2 specificities. Anti-a-enolase antibodies were not correlated with any of the clinical and serological variables examined. Anti-C1q antibodies were correlated with ECLAM score, leukopenia, complement levels, and active renal involvement. Anti-dsDNA antibodies correlated with arthritis, leukopenia, complement levels, and the presence of renal involvement, independent of activity. In patients with active renal disease anti-dsDNA antibodies were correlated with a poor renal outcome, occurring after a mean period of 24 months.

Conclusion. These data suggest the association of anti-C1q antibodies with disease flares and active renal disease in SLE. The observed association of anti-dsDNA antibodies and renal disease was expected. Further analysis is required to fully assess the clinical significance of anti-a-enolase antibodies. (J Rheumatol 2006;33:695–7)




www.LupusMCTD.com





Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #2 on: June 02, 2006, 08:56:36 am »

The two medical terms for the kidney disease that occurs in systemic lupus erythematosus are lupus nephritis or lupus glomerulonephritis. It is estimated that about one-third of people with lupus will develop nephritis that requires medical evaluation and treatment. Lupus nephritis is an important and potentially serious symptom of lupus.

Clinical Course Of Lupus Nephritis
There are very few signs or symptoms of lupus nephritis.

It does not cause pain in the abdomen or back.
However, when protein leaks from the kidneys, it is eliminated from the body in the urine
Foamy, frothy urine and getting up to urinate during the night can suggest excessive protein loss.
The loss of protein in the urine from lupus nephritis may then lead to fluid retention with weight gain and swelling (edema). This is often the first symptom noticed of lupus nephritis.


The edema generally appears as puffiness in the feet, ankles and legs.

This swelling will be absent in the morning, but will gradually worsen as the person walks about during the day.
The clinical path of lupus nephritis is highly variable.

1) Often the signs of lupus nephritis are seen only in urine studies.

In many people, the urine abnormalities are very mild and may be present during one examination and absent the next.

This form of lupus nephritis is rather common and generally does not require any special medical evaluation or treatment.

2) In some people, though, abnormal findings in the urine studies may persist or even worsen over time.

People with this type of lupus nephritis are at risk for loss of kidney function.

These individuals will need additional studies to assess the extent of their lupus nephritis and to determine the best treatment for controlling the disease.
It is important to recognize that not all kidney problems in people with lupus are due to lupus nephritis.

Infections of the urinary tract, with burning on urination, are quite common in people with lupus and require antibiotic treatment.

Also, signs or symptoms of kidney disease that can be confused with lupus nephritis may be caused by some medications used in lupus treatment.

These problems usually go away when the medications are discontinued. Two medications that can cause fluid retention or loss of kidney function are:
-Salicylate compounds (e.g., aspirin)
- non-steroidal anti-inflammatory drugs (NSAIDs)


Studies To Evaluate Lupus Nephritis
There are a number of studies that can be done to test for kidney disease in a person with lupus:

1) Urinalysis

A urinalysis is by far the simplest and most commonly used study to test for lupus nephritis. In this test, a urine sample is examined for the presence of protein and blood cells which are not normally found in the urine.

The blood cells that may collect in the kidney to form and be excreted in the urine are called casts. Casts are seen when the urine is examined under the microscope.

The presence of protein in the urine is called proteinuria.

The presence of red blood cells in the urine is called hematuria

The presence of white blood cells in the urine is called leukocyturia.

The presence of any of these in the urine suggest the possibility of lupus nephritis and generally indicate the need for further studies.
 
2) Blood work

The main function of the kidney is to remove waste products and excess fluids from the body. Blood studies can be done to measure whether the kidney is doing this job properly.


Two studies that are done to indicate whether waste products are being adequately removed by the kidney and not building up in the blood:
-the blood urea nitrogen (BUN) study
-the serum creatinine study.


Losing protein in the urine may lead to lower levels of protein in the blood. This is measured by:
- the serum albumin study.


Imbalances of salt and water in the blood are detected by chemistry studies such as:
- the serum sodium study
- the potassium study
- the bicarbonate study.


Blood tests may also be done to detect immune system abnormalities that are commonly seen with lupus nephritis. Two commonly used blood tests are:
- the serum complement test, which measures the levels of proteins in the blood that typically are low in lupus nephritis, and
- the antibodies to DNA test which measures these antibodies that   typically are high in lupus nephritis.

3) 24-Hour urine collection
Studies of the urine collected by the patient over a 24-hour period determine whether the kidneys are working properly.
These studies measure the kidneys' ability to filter waste products:
-the creatinine clearance test
-the exact amount of protein lost in the urine over a 24-hour period.

4) Imaging studies
There are two ways to examine size and shape of the kidneys, which must be done before
a kidney biopsy to help guide the physician doing the biopsy:
an intravenous pyelogram (IVP) involves an injection of dye that collects in the kidneys. An x-ray of the abdomen is then taken which shows the outline of the kidneys.

a sonogram uses soundwaves transmitted through the body to show the shape and size of the surfaces of the kidney.
5) Kidney biopsy
If urine or blood studies suggest lupus nephritis, a kidney biopsy may be performed. The biopsy is done to:

confirm the diagnosis of lupus nephritis
to determine the extent and severity of kidney disease.
A kidney biopsy is done in a hospital by inserting a narrow needle through the skin of the back and removing a small piece of the kidney. (On rare occasions, a kidney biopsy may need to be done surgically in the operating room.)

The specimen of kidney tissue is then examined under a microscope to determine how much inflammation or permanent damage (scarring) is present. These findings classify the type of lupus nephritis by using a scoring system devised by the World Health Organization (WHO) (see Table 1). Knowing the type of lupus nephritis helps to determine the seriousness of the nephritis and the best approach to treatment.



World Health Organization (WHO) Classification System for Lupus Nephritis

The World Health Organization has established a classification system for types of lupus nephritis, which are described in the table below.



Table 1. World Health Organization (WHO)
Classification System for Lupus Nephritis

Class Designation Comment
I Normal No evidence of lupus nephritis on the kidney biopsy.
II Mesangial Nephritis Most mild form of lupus nephritis; typically responds completely to treatment with corticosteroids.
 
III  Focal Proliferative Nephritis Very early stage of more advanced lupus nephritis;
typically treated with high doses of corticosteroids, with excellent outcome.

IV
Diffuse Proliferative Nephritis
 Advanced stage of lupus nephritis with definite risk of loss of kidney function; typically treated with high doses of corticosteriods combined with immunosuppressive drugs.
 
V Lupus Membranous Nephropathy
Generally associated with excessive protein loss and edema; typically treated with high doses of corticosteroids, with or without immunosuppressive drugs.
 


Treatment And Therapy
Treatment for lupus nephritis must be individualized to the needs of the specific person. All of the following must be taken into consideration:
the amount of edema (swelling)
urine abnormalities
amount of protein in the urine
reduction of kidney function
findings of the kidney biopsy.
-Diuretic agents may be used to help eliminate excess fluid.
-Anti-hypertensive drugs can control increased blood pressure.
-Anticoagulation drugs are used in case of complications arising from blood clots.
-Changes in the diet can be made to control the intake of salt, proteins, and calories.
There are two major forms of drug therapy used for lupus nephritis: corticosteroids to control inflammation, and cytotoxic or immunosuppressive drugs to suppress the activity of the immune system.

Corticosteroids
Corticosteroids have been used to manage lupus nephritis for nearly forty years. Still, there are many unanswered questions as to exactly how they work and how they may be most effectively used.


High doses of corticosteroids, or even corticosteroids given for extended periods of time, may cause a number of side effects (some side effects can be lessened by a low calorie and low salt diet):
- increased appetite
- fluid retention with weight gain
- puffy face
- easy bruising
- moodiness
- loss of mineral from the bones
- cataracts
- thinning hair
- an increased risk of infection and diabetes.

High doses of corticosteroids (taken orally or intravenously) are given until the lupus nephritis improves.
The dose of corticosteroids is then slowly reduced under close watch of a physician to make certain that the nephritis doesn't worsen.
Cytotoxic or immunosuppressive drugs
These are generally regarded as standard treatment for people with serious lupus nephritis. These drugs block the function of the immune system, which in turn prevents further damage to the kidneys.

The most commonly used is cyclophosphamide (Cytoxan).

Immunosuppressives that are used less frequently include: azathioprine (Imuran), chlorambucil (Leukeran), and cyclosporine (Sandimmune or Neoral).
The application of these drugs typically varies according to classification:


Corticosteroids (such as prednisone, prednisolone and methylprednisolone, or Medrol) are considered necessary in the initial treatment in virtually all forms of lupus nephritis.

Corticosteroids are the only type of drug required for those with Class II (mesangial nephritis).
A combination of corticosteroids and immunosuppressives are used to treat most people with Class III (focal proliferative nephritis), Class IV (diffuse proliferative nephritis) or advanced Class V (membranous nephropathy).
 

Several promising experimental therapies for lupus nephritis are currently being studied. These include:
newer immunosuppressive drugs like cyclosporine and mycophenolate mofetil (CellCept)
the removal of antibodies associated with lupus nephritis by selective plasmapheresis

the administration of biologic agents that suppress the immune system.



Kidney Failure
Despite the prescribed treatment, some people with lupus nephritis do have progressive loss of kidney function. In the case of complete failure of both kidneys, dialysis, and eventually kidney transplantation will be required.

Dialysis can be done in two ways:


Hemodialysis passes the blood through a dialysis machine and filters it directly.


Peritoneal dialysis places fluid in the abdominal cavity and subsequently removes it.
Kidney transplantation has been very successful in people who have had kidney failure from lupus nephritis. Usually they are kept on artificial dialysis until there is little or no evidence of active lupus before the transplantation procedure is performed. Afterwards, immunosuppressive drugs will be used to prevent rejection of the transplanted kidney.




Conclusion
Over the past several decades, there have been major advances in the understanding of what causes lupus nephritis and, in particular, improvements in treatment. Today, more than 80 percent of people with lupus nephritis will live a normal life span.
 
« Last Edit: June 02, 2006, 08:59:21 am by Kathy » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #3 on: June 02, 2006, 09:03:41 am »

Nephritic Syndrome
 
 
 Nephritic syndrome is a disorder of glomeruli characterized by tissue swelling (edema), high blood pressure, and the presence of red blood cells in the urine.

Nephritic syndrome can develop suddenly or over a short time period (acute nephritic syndrome) or develop and progress slowly (chronic nephritic syndrome). In 1% of children and 10% of adults, the acute nephritic syndrome evolves into rapidly progressive glomerulonephritis, in which most of the glomeruli are destroyed, resulting in kidney failure.

Causes

Acute nephritic syndrome most often results from infection by streptococcus, a type of bacteria. Acute nephritic syndrome after a streptococcal infection (post-streptococcal glomerulonephritis) typically develops following a throat or skin infection in children between the ages of 2 and 14. Infections by other types of bacteria, such as staphylococcus and pneumococcus, viral infections such as chickenpox, and parasitic infections such as malaria can also result in acute nephritic syndrome. Membranoproliferative glomerulonephritis, IgA nephropathy, Henoch-Schönlein purpura, systemic lupus erythematosus, mixed cryoglobulinemia, Goodpasture's syndrome, and Wegener's granulomatosis are all noninfectious causes of acute nephritic syndrome. Acute nephritic syndrome that develops into rapidly progressive glomerulonephritis most often results from conditions that involve an abnormal immune reaction.

The cause of chronic nephritic syndrome cannot be identified in many people. Often, chronic nephritic syndrome seems to result from one of the same conditions that causes acute nephritic syndrome.

Symptoms

About half of the people with acute nephritic syndrome have no symptoms. If symptoms do occur, the first to appear are fluid retention and tissue swelling (edema), low urine volume, and dark urine that contains blood. Edema may first appear as puffiness of the face and eyelids but later is prominent in the legs. Blood pressure increases as kidney function becomes impaired. In turn, high blood pressure and swelling of the brain may produce headaches, visual disturbances, and more serious disturbances of brain function. In older people, nonspecific symptoms, such as nausea and a general feeling of illness (malaise), are more common.

When rapidly progressive glomerulonephritis develops, weakness, fatigue, and fever are the most obvious early symptoms. Loss of appetite, nausea, vomiting, abdominal pain, and joint pain are also common. About 50% of people had a flu-like illness in the month before kidney failure started to develop. These people have edema and usually produce very little urine. High blood pressure is uncommon and rarely severe when it does occur.

Because chronic nephritic syndrome usually causes only very mild or subtle symptoms for years, it goes undetected in most people. Fluid retention (edema) may occur. High blood pressure is common. The disease may progress to kidney failure, which can cause itchiness, fatigue, decreased appetite, nausea, vomiting, and difficulty breathing.

Diagnosis

Doctors investigate the possibility of acute nephritic syndrome in people who develop symptoms of the disorder after having had strep throat or another infection and whose laboratory test results indicate kidney dysfunction. Laboratory tests show variable amounts of protein and blood cells in the urine and a high concentration of urea and creatinine (metabolic waste products) in the blood.

In people with rapidly progressive glomerulonephritis, protein clumps (casts) of red blood cells or white blood cells are almost always visible under a microscope, and blood tests detect anemia and often an abnormally high number of white blood cells. When doctors suspect nephritic syndrome, a biopsy is usually performed to confirm the diagnosis, help determine the cause, and determine the amount of scarring and potential for reversibility.

Additional tests are sometimes helpful for identifying the cause of nephritic syndrome. For example, a throat culture may provide evidence of streptococcal infection. Blood levels of antibodies against streptococci may be higher than normal or progressively increase over several weeks. Acute nephritic syndrome that follows an infection other than strep throat is usually easier to diagnose, because its symptoms often begin while the infection is still obvious. Cultures and blood tests that help identify the organisms that cause these other types of infections are sometimes needed to confirm the diagnosis.

Chronic nephritic syndrome develops gradually, and therefore, a doctor may not be able to tell exactly when it began. It may be discovered when a urine test performed as part of a medical examination reveals the presence of protein and blood cells in a person who is feeling well, has normal kidney function, and has no symptoms. A kidney biopsy is the most reliable way to distinguish chronic nephritic syndrome from other kidney diseases. A biopsy, however, is rarely performed in advanced stages, when the kidneys are shrunken and scarred, because the chance of obtaining specific information about the cause is small.

Prognosis

Acute nephritic syndrome resolves completely in about 80 to 90% of children and about 60% of adults.

The prognosis for people with rapidly progressive glomerulonephritis depends on the severity of glomerular scarring and whether the underlying cause, such as infection, can be cured. In about half of the people who are treated early (within weeks to a few months), kidney function is preserved and dialysis is not needed. However, because the early symptoms can be subtle and vague, many people who have rapidly progressive glomerulonephritis are not aware of the underlying disease and do not seek medical care until kidney failure develops. People with advanced kidney failure die within a few weeks unless they undergo dialysis. The prognosis also depends on the cause, the person's age, and any other diseases the person might have. When the cause is unknown or the person is older, the prognosis is worse.

In some children and adults who do not recover completely from acute nephritic syndrome, other types of kidney disorders develop, such as asymptomatic proteinuria and hematuria syndrome or nephrotic syndrome. Other people with acute nephritic syndrome, especially older adults, develop chronic nephritic syndrome.

Treatment

No specific treatment is available in most cases of acute nephritic syndrome. Following a diet that is low in protein and sodium may be necessary until kidney function recovers. Diuretics may be prescribed to help the kidneys excrete excess sodium and water. High blood pressure needs to be treated.

When a bacterial infection is suspected as the cause of acute nephritic syndrome, antibiotics are usually ineffective because the nephritis begins 1 to 6 weeks (average, 2 weeks) after the infection. However, if a bacterial infection is still present when acute nephritic syndrome is discovered, antibiotic therapy is started. Antimalarial drugs may be beneficial if the cause of the syndrome is malaria.

For rapidly progressive glomerulonephritis, drugs to suppress the immune system are started promptly. High doses of corticosteroids are usually given intravenously for about a week, followed by a variable period of time when they are taken by mouth. Cyclophosphamide, an immunosuppressant, may also be given. In addition, plasmapheresis is sometimes used to remove antibodies from the blood. If treatment is delayed, there is an increased likelihood of kidney failure and the need for dialysis. Kidney transplantation is sometimes considered for people who have chronic kidney failure, but rapidly progressive glomerulonephritis may recur in the transplanted kidney.

Angiotensin-converting enzyme (ACE) inhibitors often slow progression of chronic nephritic syndrome. Taking drugs to reduce high blood pressure and reducing sodium intake are considered beneficial. Restricting the amount of protein in the diet is modestly helpful in reducing the rate of kidney deterioration. Kidney failure must be treated with dialysis or a kidney transplant
 
« Last Edit: June 02, 2006, 09:04:53 am by Kathy » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #4 on: July 01, 2006, 08:51:29 am »

New Drugs Offer Relief for Lupus Patients with Kidney Problems

One of the more common and potentially serious complications for patients with systemic lupus erythematosus (also called SLE or lupus) is kidney involvement, called lupus nephritis. Until recently, such patients were typically prescribed cyclophosphamide, a chemotherapy drug that relieved symptoms for some, but was also accompanied by such side effects as hair loss, nausea, infection and infertility.

So when the New England Journal of Medicine reported in November 2005 that CellCept, an immune-suppression drug, worked significantly better than cyclophosphamide and with fewer side effects, there was rejoicing by patients with SLE and by some physicians. In an accompanying editorial, however, the Journal noted that CellCept (generic name: mycophenolate mofetil) would not become the standard of care until a larger, more definitive study is completed. The editorial did say that it was reasonable for doctors to prescribe the drug to patients worried about preserving fertility.

"We've been using CellCept here for at least the past two or three years," says Mary E. Cronin, MD, an Associate Professor of Medicine at the Medical College of Wisconsin, "but we've also had good results from cyclophosphamide." Dr. Cronin - a rheumatologist whose specialty areas include systemic lupus erythematosus - says CellCept is just one of a number of promising new drug treatment options being investigated for lupus nephritis patients. Dr. Cronin practices at the Froedtert & The Medical College of Wisconsin Rheumatology Clinic.

Study Not Definitive
Dr. Cronin has concerns about patients' reading too much into the New England Journal report: In addition to the fact that the study was small - just 140 patients, with 70 receiving CellCept and 70 being administered cyclophosphamide - it wasn't definitive for other reasons, she says. The patients used in the study apparently were not as severely affected by lupus nephritis as the typical patient caseload seen in a large medical center. Second, the study's findings did not concur with the experience Dr. Cronin and her colleagues have found in their patients.

"We have had better results here with intravenous cyclophosphamide," she says. "We typically use it as the drug of choice to begin with, and if the patient has a remission, we'll switch to CellCept to maintain the remission. In certain cases with patients concerned about fertility, we do use CellCept as the primary drug. If the patient is quite ill, we go directly to cyclophosphamide."

Dr. Cronin says about 50% of lupus patients do have clinical kidney disease - although not all cases are severe - and another 20% have "subclinical" kidney problems. The subclinical patients are often not diagnosed, she says, and if suspected would have to be referred to a nephrologist (kidney specialist) for a kidney biopsy. Symptoms of nephritis can include increased blood pressure readings, swelling of the legs, and protein in the urine, as determined by a urine test.

Lupus Symptoms Vary within Populations
Lupus is a vague and vexing autoimmune disease. According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), lupus can affect many parts of the body. "Everyone reacts differently," NIAMS notes. "One person with lupus may have swollen knees and fever. Another person may be tired all the time or have kidney trouble. Someone else may have rashes. Lupus can involve the joints, the skin, the kidneys, the lungs, the heart or the brain. If you have lupus, it may affect two or three parts of your body. Usually, one person doesn't have all the possible symptoms."

NIAMS also notes that, although anyone can get lupus, 9 out of 10 people who have it are women. It is most common in women between 15 and 44 years old. African American women are three times more likely to get lupus than white women. It's also more common in Hispanic/Latino, Asian, and American Indian women. They tend to develop lupus at a younger age and have more symptoms at diagnosis, including kidney problems. African American women also tend to have more severe disease than whites, including seizures and strokes, while Hispanic/Latino patients have more heart problems.

Kidney Complications: Lupus Nephritis Trials and Treatments
For the past 30 years, chemotherapy has been the standard treatment for the kidney complications of lupus. Before cyclophosphamide was widely used, lupus patients were treated with steroids. Unlike treatments used today, patients flared earlier, and their flares lasted longer. Cyclophosphamide changed that, Dr. Cronin said.

CellCept is now being studied in a multicenter, controlled trial using a larger number of patients than were tested in the study described in the New England Journal. In addition, other drugs are currently undergoing testing in patient trials, Dr. Cronin notes. One active trial is underway at Froedtert & the Medical College, but it is no longer enrolling patients. At other sites, a monoclonal antibody drug, rituximab - originally used to treat lymphoma patients and now approved by the Food and Drug Administration (FDA) to treat rheumatoid arthritis - is being tested for its effects on lupus nephritis. "We're using it here off-label for patients with both lupus nephritis and lupus with other serious manifestations," she says.

"It's nice to have new medications for lupus," Dr. Cronin says. "It's been decades since we've had anything new to offer our patients. Finally, years of support for basic science research through the National Institutes of Health and other funding agencies have resulted in discoveries that are now bearing the fruit of new treatments. And that's giving new hope to lupus patients."

Article Created: 2006-06-29
Article Reviewed: 2006-06-29
« Last Edit: July 04, 2006, 01:24:34 pm by Kathy » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #5 on: July 04, 2006, 07:22:19 pm »

Renal Tubular Acidosis
 
 In renal tubular acidosis, the kidney tubules cannot adequately remove acids from the blood to excrete them in the urine.

Normally, the breakdown of food produces acids that circulate in the blood. The kidneys remove acids from the blood and excrete them in the urine. This function is predominantly performed by the kidney tubules.

In renal tubular acidosis, one of several causes of metabolic acidosis, the ability of the kidneys to excrete acids is partially impaired, and acid levels build up in the blood. The balance of electrolytes is also affected. Renal tubular acidosis may lead to the following problems:

Low or high potassium levels in the blood
Calcium deposits in the kidneys
Dehydration
Painful softening and bending of the bones (osteomalacia or rickets)
Renal tubular acidosis may be hereditary or may be caused by drugs, such as acetazolamide and amphotericin B; poisoning by some heavy metals; or an autoimmune disease, such as systemic lupus erythematosus or Sjögren's syndrome.

Symptoms and Diagnosis

Three types of renal tubular acidosis exist: type 1, type 2, and type 4. Each type produces slightly different symptoms. When potassium levels in the blood are low, as occurs in types 1 and 2, neurologic problems may develop, including muscle weakness, diminished reflexes, and even paralysis. In type 4, potassium levels typically increase, although it is uncommon for the level to rise high enough to cause symptoms.

 If the level becomes too high, irregular heartbeats and muscle paralysis may develop. In type 1, kidney stones may develop, causing damage to kidney cells and, in some cases, chronic kidney failure.

A doctor considers the diagnosis of type 1 or type 2 renal tubular acidosis when a person has certain characteristic symptoms (muscle weakness, diminished reflexes) and when tests reveal high levels of acid and low levels of bicarbonate and potassium in the blood. Type 4 renal tubular acidosis is usually suspected when high potassium levels accompany high acid levels and low bicarbonate levels in the blood. Special tests help to determine the type of renal tubular acidosis.

   
Types of Renal Tubular Acidosis 
Type
 Cause
 Unerlying Abnormality
 Resulting Symptoms and Metabolic Abnormalities
 
1  May be hereditary; may be triggered by an autoimmune disease or certain drugs; cause usually not known, especially in women  Inability to excrete acid into the urine  High blood acidity; mild dehydration; low potassium levels in the blood, leading to muscle weakness and paralysis; fragile bones; bone pain; kidney stones (calcium deposits); kidney failure
 
2  Usually caused by a hereditary disease such as Fanconi's syndrome, hereditary fructose intolerance, Wilson's disease, or Lowe's syndrome; may also be caused by heavy metal poisoning or certain drugs  Inability to reabsorb bicarbonate from the urine, so bicarbonate is lost  High blood acidity, mild dehydration, and low potassium levels in the blood 

4  Not hereditary; caused by diabetes, an autoimmune disease, sickle cell disease, or an obstruction in the urinary tract  Deficiency of or inability to respond to aldosterone, a hormone that helps regulate potassium and sodium excretion in the kidneys  High blood acidity and high potassium levels in the blood that rarely cause symptoms, unless the potassium level is so high that irregular heartbeats and muscle paralysis develop 
Note: There is no type 3.
 
 

Treatment

Treatment depends on the type. Types 1 and 2 are treated by drinking a solution of sodium bicarbonate (baking soda) every day to neutralize the acid that is produced from food. This treatment relieves the symptoms and prevents kidney failure and bone disease or keeps these problems from becoming worse. Other specially prepared solutions are available, and potassium supplements may also be required.

In type 4, the acidosis is so mild that bicarbonate may not be needed. High potassium levels in the blood can usually be kept in check by restricting the potassium intake and, if necessary, taking diuretics.

 
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #6 on: July 06, 2006, 09:10:12 pm »

Smoking linked to autoantibodies associated with lupus nephritis

April 24, 2006
San Francisco, California - Current smoking raises the level of autoantibodies to double-stranded DNA (dsDNA) in patients with systemic lupus erythematosus (SLE), which suggests that lupus patients who continue to smoke might be setting themselves up for more severe disease manifestations such as lupus nephritis, according to a report in the May 2006 issue of Annals of the Rheumatic Diseases [1].

"There is an association between smoking and dsDNA antibodies, which are usually seen in SLE patients with more severe disease (eg, renal disease). The effect of smoking, if it is a causal association, is short-lived. Therefore, it is in SLE patients' best interest to quit smoking as soon as possible. Their smoking may worsen their disease (in addition to the multitude of other health risks of smoking)," lead author Dr Michelle Freemer (University of California, San Francisco) told rheumawire.



Current but not former smoking associated with dsDNA autoantibodies
There is an association between smoking and dsDNA antibodies, which are usually seen in SLE patients with more severe disease.
 
Freemer and colleagues reviewed medical records of 410 SLE patients from the University of California, San Francisco Lupus Genetics Project to evaluate dsDNA-antibody status and smoking status to determine whether dsDNA seropositivity (dsDNA+) is more common in lupus patients who smoke than in lupus patients who do not smoke. "Possibly," they write, "DNA damage in smokers leads to dsDNA-autoantibody formation and may have a role in the development of SLE."

They found:

An association of dsDNA seropositivity with current smoking but not with never or former smoking.
In tests of 92 of the 410 patients, no relationship between dsDNA-autoantibody titer level and smoking status in SLE patients.
No significant interaction between smoking and age at SLE diagnosis.
No significant effect of cumulative amount smoked on dsDNA status.
No significant effect of age of smoking onset on dsDNA status.
The message is that current smoking is likely to create additional risk for SLE patients, but that it appears to be a relatively short-term risk that abates within months after smoking cessation. The authors note that smoking-related DNA adducts have a half-life of only nine to 13 weeks.

The investigators' hypothesis was that smoking might increase DNA-adduct formation and dsDNA-autoantibody production in patients with SLE, which might increase susceptibility to or worsen SLE.

In regard to the clinical significance of the association between current smoking and dsDNA seropositivity, Freemer said, "The statistical analysis limits the 'chance' association (between smoking and dsDNA positivity) to less than 2.5% that there is not at least a 1.6-fold increase in the risk of dsDNA+ in current (vs never smokers).

"With respect to whether this association is clinically significant, the association between dsDNA seropositivity and disease severity has been established previously. In this study, one might pursue an assessment of SLE severity ([Systemic Lupus International Collaborating Clinics] SLICC or [Systemic Lupus Erythematosus Disease Activity Index] SLEADAI depending on when you want to or are able to assess severity) and compare the dsDNA-positive vs -negative individuals and smoking status."


Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #7 on: July 15, 2006, 08:06:51 am »




One of the more common and potentially serious complications for patients with systemic lupus erythematosus (also called SLE or lupus) is kidney involvement, called lupus nephritis. Until recently, such patients were typically prescribed cyclophosphamide, a chemotherapy drug that relieved symptoms for some, but was also accompanied by such side effects as hair loss, nausea, infection and infertility.

So when the New England Journal of Medicine reported in November 2005 that CellCept, an immune-suppression drug, worked significantly better than cyclophosphamide and with fewer side effects, there was rejoicing by patients with SLE and by some physicians. In an accompanying editorial, however, the Journal noted that CellCept (generic name: mycophenolate mofetil) would not become the standard of care until a larger, more definitive study is completed. The editorial did say that it was reasonable for doctors to prescribe the drug to patients worried about preserving fertility.

"We've been using CellCept here for at least the past two or three years," says Mary E. Cronin, MD, an Associate Professor of Medicine at the Medical College of Wisconsin, "but we've also had good results from cyclophosphamide." Dr. Cronin - a rheumatologist whose specialty areas include systemic lupus erythematosus - says CellCept is just one of a number of promising new drug treatment options being investigated for lupus nephritis patients. Dr. Cronin practices at the Froedtert & The Medical College of Wisconsin Rheumatology Clinic.

Study Not Definitive
Dr. Cronin has concerns about patients' reading too much into the New England Journal report: In addition to the fact that the study was small - just 140 patients, with 70 receiving CellCept and 70 being administered cyclophosphamide - it wasn't definitive for other reasons, she says. The patients used in the study apparently were not as severely affected by lupus nephritis as the typical patient caseload seen in a large medical center. Second, the study's findings did not concur with the experience Dr. Cronin and her colleagues have found in their patients.

"We have had better results here with intravenous cyclophosphamide," she says. "We typically use it as the drug of choice to begin with, and if the patient has a remission, we'll switch to CellCept to maintain the remission. In certain cases with patients concerned about fertility, we do use CellCept as the primary drug. If the patient is quite ill, we go directly to cyclophosphamide."

Dr. Cronin says about 50% of lupus patients do have clinical kidney disease - although not all cases are severe - and another 20% have "subclinical" kidney problems. The subclinical patients are often not diagnosed, she says, and if suspected would have to be referred to a nephrologist (kidney specialist) for a kidney biopsy. Symptoms of nephritis can include increased blood pressure readings, swelling of the legs, and protein in the urine, as determined by a urine test.

Lupus Symptoms Vary within Populations
Lupus is a vague and vexing autoimmune disease. According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), lupus can affect many parts of the body. "Everyone reacts differently," NIAMS notes. "One person with lupus may have swollen knees and fever. Another person may be tired all the time or have kidney trouble. Someone else may have rashes. Lupus can involve the joints, the skin, the kidneys, the lungs, the heart or the brain. If you have lupus, it may affect two or three parts of your body. Usually, one person doesn't have all the possible symptoms."

NIAMS also notes that, although anyone can get lupus, 9 out of 10 people who have it are women. It is most common in women between 15 and 44 years old. African American women are three times more likely to get lupus than white women. It's also more common in Hispanic/Latino, Asian, and American Indian women. They tend to develop lupus at a younger age and have more symptoms at diagnosis, including kidney problems. African American women also tend to have more severe disease than whites, including seizures and strokes, while Hispanic/Latino patients have more heart problems.

Kidney Complications: Lupus Nephritis Trials and Treatments
For the past 30 years, chemotherapy has been the standard treatment for the kidney complications of lupus. Before cyclophosphamide was widely used, lupus patients were treated with steroids. Unlike treatments used today, patients flared earlier, and their flares lasted longer. Cyclophosphamide changed that, Dr. Cronin said.

CellCept is now being studied in a multicenter, controlled trial using a larger number of patients than were tested in the study described in the New England Journal. In addition, other drugs are currently undergoing testing in patient trials, Dr. Cronin notes. One active trial is underway at Froedtert & the Medical College, but it is no longer enrolling patients. At other sites, a monoclonal antibody drug, rituximab - originally used to treat lymphoma patients and now approved by the Food and Drug Administration (FDA) to treat rheumatoid arthritis - is being tested for its effects on lupus nephritis. "We're using it here off-label for patients with both lupus nephritis and lupus with other serious manifestations," she says.

"It's nice to have new medications for lupus," Dr. Cronin says. "It's been decades since we've had anything new to offer our patients. Finally, years of support for basic science research through the National Institutes of Health and other funding agencies have resulted in discoveries that are now bearing the fruit of new treatments. And that's giving new hope to lupus patients."
 
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #8 on: July 31, 2006, 09:21:33 pm »

Mycophenolate Mofetil Approved for Treatment of Lupus Nephritis in Malaysia
   
VICTORIA, BC, July 19 /CNW/ - Aspreva Pharmaceuticals Corporation
reports that Mycophenolate Mofetil (MMF,
CellCept(R)) has been approved for the treatment of lupus nephritis in
Malaysia. On July 11, 2006, Roche Malaysia received a letter of approval from
the Drug Control Authority (DCA) in Malaysia granting them approval to include
lupus nephritis as an additional indication for MMF in the induction and
maintenance treatment of lupus nephritis (used concomitantly with
corticosteroids). Malaysia is the first country to have regulatory approval of
MMF in any autoimmune disease.
    The supporting documents used in the application consisted of published
clinical papers and the expert clinical report prepared by key opinion leader
Dato Dr. Zaki Morad, Head of Nephrology at Hospital Kuala Lumpur. Dato Dr.
Morad's report on the clinical trial of MMF in lupus nephritis was published
in the October 2005 issue of the journal Nephrology. The trial was conducted
at eight centres in Malaysia, comparing intravenous cyclophosphamide to MMF in
the induction therapy of proliferative lupus nephritis.
    Aspreva is conducting a global phase III study to assess the efficacy and
safety of MMF in inducing response and maintaining remission in patients with
lupus nephritis. Aspreva's two-phase induction and maintenance study is a
randomized, open label comparison of MMF to intravenous cyclophosphamide in
the first six months or induction phase, followed by a double-blind comparison
of MMF to azathioprine for up to three years during the maintenance phase. The
first patient in the Aspreva study was treated in July 2005, and completion of
the induction phase of the trial is expected in early 2007.

    About Lupus Nephritis

    Systemic lupus erythematosus (SLE), commonly called lupus, is a chronic
autoimmune disease that causes the body to attack its own tissues and joints.
    Lupus nephritis is the most serious manifestation of the disease, which,
if left untreated, can lead to kidney failure, requiring dialysis. It is a
complicated disease as patients typically fluctuate between periods of intense
disease activity when the patient's own immune system is actively attacking
and causing damage in their kidney, interspersed with periods of remission.
Clinicians estimate that one third to one half of lupus patients have lupus
nephritis.
    There has been no new approved treatment for SLE or lupus nephritis in
the United States in over thirty years. Current treatments involve the
off-label use of existing cancer drugs such as cyclophosphamide, steroids, and
other immunosuppressant drugs such as azathioprine.
    About CellCept

    CellCept is F. Hoffmann-La Roche's (Roche) leading immunosuppressant or
"anti-rejection" drug used in combination with other immunosuppressive drugs
(cyclosporine and corticosteroids) for the prevention of rejection in patients
receiving heart, kidney and liver transplants. CellCept was first approved for
use in combination therapy for the prevention of acute organ rejection in
kidney transplantation in 1995 and has since been approved worldwide for
prevention of organ rejection in adult kidney, heart and liver
transplantation. In some countries, it has also been approved for paediatric
kidney transplantation. This therapeutic success represents 10 years of
clinical experience and patient benefits, including reduced toxicities and
prolonged graft and patient survival. Over the last decade, CellCept has
become the world's most widely studied immunosuppressant and research is
ongoing both in organ transplantation and related areas, such as autoimmune
disease, to help provide clinical benefit to a wider range of patients.
    In July 2003, Aspreva signed a collaboration agreement with Roche for the
exclusive worldwide rights (excluding Japan) to develop and, upon regulatory
approval, commercialize CellCept for all autoimmune disease applications.

    About Aspreva Pharmaceuticals

    Aspreva is an emerging pharmaceutical company focused on identifying,
developing and, upon regulatory approval, commercializing new indications for
approved drugs and late stage drug candidates for patients living with less
common diseases. Aspreva is listed on the NASDAQ Global Select Market under
the trading symbol "ASPV" and on the Toronto Stock Exchange under the trading
symbol "ASV". For further information on Aspreva, please visit
www.aspreva.com.
    This press release contains forward-looking statements or information
within the meaning of the Private Securities Litigation Act of 1995 and
applicable Canadian Securities Legislation. These include, without limitation,
statements or information related to our strategy, future operations, clinical
trials, prospects and plans of management. Words such as "anticipates,"
"believes," "estimates," "expects," "intends," "may," "plans," "projects,"
"will," "would" and similar expressions are intended to identify
forward-looking statements or information, although not all forward-looking
statements or information contain these identifying words. These
forward-looking statements or information are based upon our current
expectations and we may not actually achieve the plans, approvals, intentions
or expectations disclosed in our forward-looking statements or information.
Forward-looking statements or information involve risks and uncertainties. Our
actual results and the timing of events could differ materially from those
anticipated in such forward-looking statements or information as a result of
these risks and uncertainties, which include, without limitation, risks
related to difficulties or delays in the progress, timing and results of our
clinical trials, our ability to attract and retain collaborations relating to
the development and commercialization of new indications, difficulties or
delays in obtaining regulatory approval, the FDA may finally determine that
the design and planned analysis of our clinical trials do not adequately
address the trial objectives in support of our regulatory submission,
competition from other pharmaceutical or biotechnology companies, and other
risks detailed in our filings with the Securities and Exchange Commission and
Canadian securities regulatory authorities. You are cautioned not to place
undue reliance on these forward-looking statements or information, which speak
only as of the date of this press release. All forward-looking statements or
information are qualified in their entirety by this cautionary statement, and
Aspreva undertakes no obligation to revise or update any forward-looking
statements or information as a result of new information, future events or
otherwise after the date hereof.
    %SEDAR: 00021534E



For further information: Sage Baker, Executive Director, Corporate &
Investor Affairs, Aspreva Pharmaceuticals, (250) 744-2488, sbaker@aspreva.com
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #9 on: September 04, 2006, 08:49:51 am »

Orange Juice Is Better Than Lemonade At Keeping Kidney Stones Away

A daily glass of orange juice can help prevent the recurrence of kidney stones better than other citrus fruit juices such as lemonade, researchers at UT Southwestern Medical Center have discovered.


The findings indicate that although many people assume that all citrus fruit juices help prevent the formation of kidney stones, not all have the same effect. The study is available online and is scheduled to be published in the Oct. 26 issue of the Clinical Journal of the American Society of Nephrology.

Medically managing recurrent kidney stones requires dietary and lifestyle changes as well as treatment such as the addition of potassium citrate, which has been shown to lower the rate of new stone formation in patients with kidney stones.

But some patients can't tolerate potassium citrate because of gastrointestinal side effects, said Dr. Clarita Odvina, assistant professor of internal medicine at the Charles and Jane Pak Center for Mineral Metabolism and Clinical Research and the study's lead author. In those cases, dietary sources of citrate -- such as orange juice -- may be considered as an alternative to pharmacological drugs.

"Orange juice could potentially play an important role in the management of kidney stone disease and may be considered an option for patients who are intolerant of potassium citrate," Dr. Odvina said.

All citrus juices contain citrate, a negatively charged form of citric acid that gives a sour taste to citrus fruits. Researchers compared orange juice and lemonade -- juices with comparable citrate contents -- and found that the components that accompany the citrate can alter the effectiveness of the juice in decreasing the risk of developing new kidney stones.

Kidney stones develop when the urine is too concentrated, causing minerals and other chemicals in the urine to bind together. Over time, these crystals combine and grow into a stone.

In the UT Southwestern study, 13 volunteers -- some with a history of kidney stones and some without -- underwent three phases, each lasting one week. Chosen in random order, the phases included: a distilled water or control phase; an orange juice phase; and a lemonade phase. There was a three-week interval between phases.

During each phase, volunteers drank 13 ounces of orange juice, lemonade or distilled water three times a day with meals. They also maintained a low-calcium, low-oxalate diet. Urine and blood samples were taken at intervals during each phase. The study was done at UT Southwestern's General Clinical Research Center.

Orange juice, researchers found, boosted the levels of citrate in the urine and reduced the crystallization of uric acid and calcium oxalate -- the most frequently found ingredient in kidney stones.

But lemonade did not increase the levels of citrate, an important acid neutralizer and inhibitor of kidney stone formation.

"One reason might be the different constituents of various beverages," Dr. Odvina said.

For instance, the citrate in orange and grapefruit juice is accompanied by a potassium ion while the citrate in lemonade and cranberry juice is accompanied by a hydrogen ion. Ions of hydrogen, but not potassium, counteract the beneficial effects of the high citrate content.

"There is an absolute need to consider the accompanying positive charge [of hydrogen ions] whenever one assesses the citrate content of a diet," Dr. Odvina said.

Thank You Karyl, As Always,
Kathy
« Last Edit: January 29, 2007, 10:04:49 am by ♥Admin♥ » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #10 on: September 12, 2006, 01:23:53 pm »

Simpler Measures for Predicting Kidney Function May Be Useful

 
In order to measure how well the kidneys are functioning, doctors frequently use a measurement called the creatinine clearance (CrCl). Creatinine is a breakdown product of creatine, a component of muscles in the body. The way that the kidney eliminates creatinine reflects how well the kidneys are working.

 

The CrCl test compares the level of creatinine in the urine with the creatinine level in the blood. The classic way of doing this takes measurements on a sample of urine that has been collected over a 24-hour period, and compares this to a blood sample drawn at the end of that time. Because creatinine is freely filtered through a well-functioning kidney and not reabsorbed into the bloodstream the way some other proteins are, creatinine clearance can be used to estimate how fast the kidney is filtering out wastes from the body (known as the glomerular  filtration rate (or GFR). This is the gold standard by which kidney function is assessed. As kidneys become damaged, the GFR goes down and less creatinine is filtered out, leaving more creatinine in the bloodstream, along with other potentially toxic waste products.

 

Researchers wanted to know whether creatinine clearance (CrCl) that is estimated by different, easier methods agreed with the CrCl measured, using a 24-hour collection of urine. Forty-three lupus patients with mild to moderate kidney disease were studied. For this study, the methods used to estimated creatinine clearances were (1) the Cockcroft-Gault (CG) equation, (2) the Modification of Diet in Renal Disease (MDRD) study equation, and (3) the abbreviated MDRD (aMDRD) study equation. These methods each were compared to the measured CrCl by 24-hour urine collection.

 

The results were that the MDRD and aMDRD methods seemed more accurate than the CG equation. However, there seemed to be a tendency for the MDRD and aMDRD study equations to underestimate CrCl, making the kidneys appear to be functioning more poorly that was indicated using the 24-hour urine collection data. Some, however, would argue that there are some inaccuracies in all of the methods, including the 24-hour urine collection. The take-home message from these studies is that easier methods for measuring kidney function, although not perfect, are reasonably reliable. They certainly can be used and understood in evaluating how patients with kidney disease are doing and in examining the progress over time of people undergoing treatments. This could be of significant benefit in treating patients and also in running clinical trials of new medications.

 

Read the Abstract:

http://www.ingentaconnect.com/content/sage/lu/2006/00000015/00000005/art00004

 

 
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #11 on: September 12, 2006, 01:27:37 pm »

Lupus Patients with Potential for Kidney Disease Need to be Monitored Carefully

 
 Researchers have long attempted to develop some framework to sort patients into subgroups so predictions could be made about who might do better with one treatment approach versus another.  A study conducted in the United Kingdom has provided some statistical verification that subsets of lupus exist, with kidney involvement (renal disease) occurring frequently on its own, while skin (mucocutaneous) and joint and muscle (musculoskeletal) diseases may represent a possible subset by flaring together. In addition, the study also shows that a history of previous lupus flares and the involvement of other organ systems affect a patient’s chance of developing additional flares.

 

The researchers studied the symptoms and test results of 440 lupus patients over 10 years who had a history of active mucocutaneous, musculoskeletal, or renal disease. Lupus disease activity was evaluated every three months and the side effects of lupus or its treatments (damage to joints or organs) were assessed about every six months.

 

The researchers found that patients who had previous history of active disease in a given part of the body were at greater risk for having future disease activity of the same type. The higher the number of previous visits in which patients reported active disease of a given type, the greater the likelihood of having new reports of active disease of that type as well. This was true for mucocutaneous, musculoskeletal, and renal system involvement.

 

A history of renal disease appeared to decrease a patient’s chances of developing active mucocutaneous and musculoskeletal disease. However, it should be pointed out that people with a history of renal disease likely are taking immunosuppressive medications for longer periods of time than people without any threat to the kidney, and this might keep rashes and joint pain/swelling from flaring. On the other hand, patients in the study with previous active musculoskeletal disease were less likely to present with renal disease activity. Patients with a history of mucocutaneous activity and musculoskeletal damage had an increased risk of presenting with musculoskeletal disease, as did those who had a history of severe mucocutaneous and musculoskeletal disease.

 

These findings lead the researchers to suggest that mucocutaneous disease and musculoskeletal disease may represent one subset of lupus, and renal disease another subset. The most important finding in this study is regarding past damage to the kidney and renal disease. A patient’s chance of developing active renal disease was increased if there was evidence of renal damage. That, the researchers point out, may be a result of renal disease activity being “clinically silent” — which means it is occurring, but without being detected by the patient or a doctor. As a result, the patient may already have encountered significant permanent damage to the kidney before an obvious flare is discovered. This finding points to the need for lupus patients with potential for kidney disease to be monitored carefully, in order to uncover disease activity that is “under the radar” but nonetheless capable of producing significant harm.

 

Read the Abstract:

http://rheumatology.oxfordjournals.org/cgi/content/abstract/45/3/308
 
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #12 on: September 18, 2006, 11:10:22 am »

HEALTH ANSWERS
Does cranberry juice prevent urinary tract infections?
September 18, 2006

Yes, say researchers who study the gorgeous berry -- although the National Center for Complementary and Alternative Medicine, which is sponsoring several clinical studies, says the data are ``not conclusive."

The queen of cranberry science, Amy Howell , an associate research scientist at Rutgers University in Chatsworth, N.J., said that overall, research suggests that eight to 10 ounces a day of cranberry juice doodle dootail drink, sweetened with either sugar or artificial sweetener, has been shown clinically to reduce urinary tract infections by 50 percent.

For years, people thought cranberry juice might combat urinary tract infections by making urine more acidic, thus making it harder for bacteria to grow.

Now, thanks to the work of Howell and others, it is known that a chemical in cranberries called proanthocyanidin blocks infections by coating E. coli, the major culprit, so that it cannot stick to cells in the bladder. ``If you prevent the adhesion, the bacteria won't multiply and cause infection," Howell said.

That's why it's no big deal, she said, that there were ``negative" findings in a recent study published in the American Journal of Health-System Pharmacy. That study showed that drinking cranberry juice was no more effective at preventing bacterial growth in urine than drinking water, said Sophie Chang , a clinical pharmacist at Cedars-Sinai Medical Center in Los Angeles and one of the authors.

Since the cranberry compounds don't kill bacteria, there is less of a chance that the bacteria will become resistant, as they would with the antibiotics that are used to treat infections, said Howell.

A similar version of proanthocyanidin is found in blueberries, said Dr. Kalpana Gupta , assistant professor of medicine at Yale University School of Medicine.

Until recently, scientists thought that once you get a urinary infection, you need antibiotics. But data released last week suggest that cranberry juice may help treat, as well as prevent, urinary infections.
« Last Edit: September 18, 2006, 11:42:11 am by Kathy » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #13 on: September 21, 2006, 07:27:20 am »

Urinary tract infection (UTI) overview



Introduction

A urinary tract infection (UTI) is an infection that begins in your urinary system. UTIs limited to your bladder can be painful and annoying. But serious consequences can occur if the infection spreads to your kidneys.

Women are most at risk of developing a UTI. In fact, half of all women will develop a UTI during their lifetimes, and many will experience more than one.

The urinary system is composed of the kidneys, ureters, bladder and urethra. All play a role in removing waste from your body. The kidneys, a pair of bean-shaped organs in your upper posterior abdomen, filter waste from your blood. Tubes called ureters carry urine from your kidneys to your bladder, where it is stored until it exits the body through the urethra. All of these components can become infected, but most infections involve the lower tract — the urethra and the bladder.

Antibiotics are the typical treatment for urinary tract infections. But you can take steps to reduce your chance a getting a UTI in the first place.


Signs and symptoms

Not everyone with a UTI develops recognizable signs and symptoms, but most people have some. These can include:

A strong, persistent urge to urinate
A burning sensation when urinating
Passing frequent, small amounts of urine
Blood in the urine (hematuria) or cloudy, strong-smelling urine
Each type of UTI may result in more specific signs and symptoms, depending on which part of your urinary tract is infected:

Acute pyelonephritis. Infection of your kidneys may occur after spreading from an infection in your bladder. Kidney infection can cause upper back and flank pain, high fever, shaking chills, and nausea or vomiting.
Cystitis. Inflammation or infection of your bladder may result in pelvic pressure, lower abdomen discomfort, frequent, painful urination and strong-smelling urine.
Urethritis. Inflammation or infection of the urethra leads to burning with urination. In men, urethritis may cause penile discharge.


Blood in urine


Cystitis overview

Causes

Urinary tract infections typically occur when bacteria enter the urinary tract through the urethra and begin to multiply in the bladder. The urinary system has infection-fighting properties that inhibit the growth of bacteria and is designed to keep out such microscopic invaders. However, certain factors increase the chances that bacteria will enter the urinary tract, take hold and multiply into a full-blown infection.

Having bacteria in the urine doesn't always signify an infection. Some people, especially older adults, may have bacteria in the urine without any signs or symptoms of infection. This condition, known as asymptomatic bacteriuria, doesn't need treatment.

Cystitis may occur in women after sexual intercourse. But even girls and women who aren't sexually active are susceptible to lower urinary tract infections because the anus is so close to the female urethra. Most cases of cystitis are caused by Escherichia coli (E. coli), a species of bacteria commonly found in the gastrointestinal tract.

In urethritis, the same organisms that infect the kidney and bladder can infect the urethra. In addition, because of the female urethra's proximity to the vagina, sexually transmitted diseases (STDs), such as herpes simplex virus and chlamydia, also are possible causes of urethritis.

In men, urethritis often is the result of bacteria acquired through sexual contact. The majority of such infections are caused by gonorrhea and chlamydia.


Risk factors

Some people appear to be more likely than others to develop UTIs. Up to half of all women will develop a bladder infection over a lifetime. A key reason is their anatomy. Women have a shorter urethra than men have, which cuts down on the distance bacteria must travel to reach the bladder.

Women who are sexually active tend to have more UTIs. Sexual intercourse can irritate the urethra, allowing germs to more easily travel through the urethra into the bladder. Women who use diaphragms for birth control also may be at higher risk, as are women who use spermicidal agents. After menopause, UTIs may become more common because tissues of the vagina, urethra and the base of the bladder become thinner and more fragile due to loss of estrogen.

Other risk factors include:

Anything that impedes the flow of urine, such as an enlarged prostate in men or a kidney stone
Diabetes and other chronic illnesses that may impair the immune system
Medications that lower immunity, such as chronic cortisone therapy or chemotherapy for cancer
Prolonged use of tubes (catheters) in the bladder
A woman's immune system may play a role in her risk of recurrent UTIs. Bacteria may be able to attach to cells in the urinary tract more easily in women lacking protective factors that normally allow the bladder to shed bacteria. More research is needed to determine the exact factors involved and how such factors can be manipulated to benefit women with frequent UTI

Screening and diagnosis

If you have symptoms of a urinary infection, contact your doctor promptly. If your doctor suspects you have a UTI, he or she may ask you to turn in a urine sample to determine if pus, red blood cells or bacteria are present in your urine. Laboratory analysis of the urine (urinalysis), sometimes followed by a urine culture, can reveal whether you have an infection. Although no simple test can differentiate between an upper and lower urinary tract infection, the presence of fever and flank pain indicate that the infection likely involves your kidneys.


Complications

When treated promptly and properly, UTIs rarely lead to complications. But left untreated, a urinary tract infection can become something more serious than a set of uncomfortable symptoms.

Untreated UTIs can lead to acute or chronic kidney infections (pyelonephritis), which could permanently damage your kidneys. Young children and older adults are at the greatest risk of kidney damage due to UTIs because their symptoms are often overlooked or mistaken for other conditions. Women who have UTIs while pregnant may also have an increased risk of delivering low birth weight or premature infants.



Treatment

If your symptoms are typical of a UTI and you're generally in good health, antibiotics are the first line of treatment. Which drugs are prescribed and for how long depends on your health condition and the type of bacteria found in your urine. Drugs most commonly recommended for simple UTIs include amoxicillin (Amoxil, Trimox), nitrofurantoin (Furadantin, Macrodantin), trimethoprim (Proloprim) and the antibiotic combination of trimethoprim and sulfamethoxazole (Bactrim, Septra). Make sure your doctor is aware of any other medications you're taking or any allergies you have. This will help him or her select the best treatment.

Usually, UTI symptoms clear up within a few days of treatment. But you may need to continue antibiotics for a week or more. Take the entire course of antibiotics recommended by your doctor to ensure that the infection is completely eradicated. For an uncomplicated UTI that occurs when you're otherwise healthy, your doctor may recommend a shorter course of treatment, such as taking an antibiotic for three days. But whether this short course of treatment is adequate to treat your UTI depends on your particular symptoms and medical history.

If you have recurrent UTIs, your doctor may recommend a longer course of antibiotic treatment or a self-treatment program with short courses of antibiotics at the outset of your urinary symptoms. For infections related to sexual activity, your doctor may recommend taking a single dose of antibiotic after sexual intercourse.

For severe UTIs, hospitalization and treatment with intravenous antibiotics may be necessary. When recurrences are frequent or a kidney infection becomes chronic, your doctor will likely refer you to a doctor who specializes in urinary disorders (urologist) or a doctor whose specialty is kidneys (nephrologist) for an evaluation to determine if urologic abnormalities may be causing the infections.


Prevention

You can take steps to reduce your risk of urinary tract infections. Women in particular may benefit from the following:

Drink plenty of liquids, especially water. Cranberry juice may have infection-fighting properties. However, don't drink cranberry juice if you're taking the blood-thinning medication warfarin. Possible interactions between cranberry juice and warfarin can lead to bleeding.
Urinate promptly when the urge arises. Avoid retaining your urine for a long time after you feel the urge to void.
Wipe from front to back. Doing so after urinating and after a bowel movement helps prevent bacteria in the anal region from spreading to the vagina and urethra.
Empty your bladder as soon as possible after intercourse. Also, drink a full glass of water to help flush bacteria.
Avoid potentially irritating feminine products. Using deodorant sprays or other feminine products, such as douches and powders, in the genital area can irritate the urethra.


Self-care

UTIs can be painful, but you can take steps to ease your discomfort until antibiotics clear the infection. Follow these tips:

Drink plenty of fluids. Drinking plenty of water dilutes your urine and may help flush out bacteria. Avoid coffee, alcohol, and soft drinks containing citrus juices and caffeine until your infection has cleared. They can irritate your bladder and tend to aggravate your frequent or urgent need to urinate.
Use a heating pad. Sometimes a heating pad placed over the abdomen can help minimize feelings of bladder pressure or pain.
If you have recurrent bladder infections, let your doctor know. Together you can determine a strategy to reduce recurrences and the discomfort UTIs can bring.

www.LupusMCTD.com
« Last Edit: September 21, 2006, 07:29:34 am by Kathy » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #14 on: September 23, 2006, 07:20:28 am »

New directions in the management of severe lupus nephritis.




Systemic lupus erythematosus, which predominantly affects young women, frequently is complicated by renal involvement.
The presence of acute glomerulonephritis significantly adds to morbidity and mortality.

Based on currently published clinical trials, induction therapy with cyclophosphamide combined with pulse corticosteroids is an efficacious treatment option to preserve renal function, and long-term data are available to support this choice.

Mycophenolate mofetil is a promising new agent, and recent data suggest that it is at least as efficacious as cyclophosphamide in the induction and maintenance phase, but with fewer side effects.

Cell-depleting agents may be added in patients who fail the traditional regimens, preferentially in the setting of one of the ongoing clinical trials. The number of treatment regimens that the clinician can choose from when confronted with a patient with severe lupus nephritis has increased significantly, and more options are on the horizon.

This promises more efficacious and better tolerable therapies, but it also puts an additional obligation on the physician to consider risk-to-benefit ratio, patient preference and adherence, feasibility, and cost; and to engage the patient in an active discussion about the different alternatives.
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #15 on: October 06, 2006, 06:16:06 pm »

Membranous lupus glomerulonephritis is one of six commonly recognized forms of glomerulonephritis due to lupus. Many people who have lupus eventually develop kidney problems, such as glomerulonephritis. About 10 percent to 20 percent of those with lupus glomerulonephritis have the membranous form of the disease.

Each kidney contains about a million nephrons. A nephron is made up of a ball of small capillary blood vessels (glomerulus) that filter your blood and tubules that determine which of the filtered substances are returned to your bloodstream and which are excreted in your urine.

Membranous lupus glomerulonephritis causes the capillary walls of the glomeruli to thicken and leak substances, such as the protein albumin, into your urine. Often, the result is nephrotic syndrome, which is characterized by:

High levels of protein in the urine (proteinuria)
Low levels of albumin in the blood
Elevated levels of cholesterol and triglycerides in the blood
Some people with membranous lupus glomerulonephritis maintain adequate kidney function for years. Others may develop persistent nephrotic syndrome, high blood pressure and further loss of kidney function. Periodic evaluation is needed to adjust or start treatments to prevent deterioration of your kidney function.

www.LupusMCTD.com
« Last Edit: October 09, 2006, 09:22:19 am by ♥ Supreme Queen Goddess ♥ » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #16 on: October 09, 2006, 08:18:53 am »

Urinary Stones Passage Enhanced by Medical Therapy
 
October 02, 2006

 
ANN ARBOR, Mich., Oct. 2 -- The likelihood of spontaneous urinary stone passage can be increased significantly by treatment with calcium channel blockers or α blockers, according to pooled data on nearly 700 patients with urinary calculi.

A nine-trial meta-analysis found that patients treated with calcium channel blockers or α blockers were 65% more likely to spontaneously pass the stones (95% confidence interval 1.45-1.88 P<0.001), reported John M. Hollingsworth, M.D., of the University of Michigan and the Veterans Affairs Center here, and colleagues, in the Sept.30 issue of The Lancet.


In four studies in which patients were treated with the α blocker Flomax (tamsulosin) the pooled risk ratio was 1.52 (95% CI 1.23-1.86, P<0.001).


In three trials in which corticosteroids were added to calcium channel blockers the pooled risk ratio was 1.90 (95% CI 1.51-2.40 P<0.0001).


The number of patients needed to treat in order to achieve one spontaneous stone expulsion with calcium channel blockers or α blockers was four.


Although the authors included the caveat that the a large confirmatory trial is needed, they concluded that "with the low- risk profile of these drugs and their wide therapeutic window, our results suggest that treating physicians should consider a new algorithm for the management of urolithiasis, in which treatment begins with a course of medical therapy, unless medically contraindicated."


Moreover, they pointed out that medical treatment costs just a fraction of the average cost of ureteroscopy ($2,645) or shock wave lithotripsy ($4,225). The estimated cost for medical treatment ranged from $10 to $74 for a 28-day course of Cardura (doxazosin) to $104 to $141 for a 42-day course of Flomax, the only non-generic drugs included in the meta-analysis.


The analysis included data from 693 patients with ureteral stones. The studies compared treatment with calcium channel blockers and/or α blockers, or standard therapy (control group).


In seven of the nine studies, both treatment and control groups received on-demand nonsteroidal anti-inflammatory drugs for relief of acute renal colic. In three, trials corticosteroids were given along with the calcium channel blocker nifedipine.


The mean age of patients ranged from 34.4 to 46.5 years and number of women in the trials ranged from 25% to 60%. The mean stone size ranged from 3.9 mm to 7.8 mm.


Treatment duration ranged from seven days to six weeks and follow-up ranged from 15 days to 48 days.


Among the findings:

When data from all five studies in which patients were treated with α blockers were pooled the risk ratio was 1.54 (95%CI 1.29-1.85, P<0.001).
In the two studies in which patients were treated with nifedipine without α blockers the risk ratio was 1.51 (95% CI 1.18-1.94 P=0.001).
The risk ratio in a subgroup analysis that pooled data from two studies in which neither treatment nor control group received NSAIDs was 1.74 (95% CI 1.29-2.33 P<0.0001)
Pooled risk in seven studies in which NSAIDs were used in treatment and control arms was 1.63 (1.41-1.88 P<0.001).

The authors noted that their findings might be limited by publication bias, because positive trials are more likely to have been published. Another potential limitation is the possibility of clinical heterogeneity, which they said they have addressed by conducting separate analysis of each drug class.

 

www.LupusMCTD.com
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #17 on: November 17, 2006, 06:59:14 am »

Higher Hemoglobin Targets for Chronic Kidney Disease Linked to Heart Complications
     
BOSTON, Nov. 16 -- When treating anemia in chronic kidney disease, it's best not to shoot for too high a hemoglobin target, suggested U.S. and European researchers in separate studies.

Early complete correction of anemia with a recombinant erythropoietin in patients with chronic kidney disease does not reduce the risk of cardiovascular events, reported European investigators in the Cardiovascular Risk Reduction by Early Anemia Treatment with Epoetin Beta (CREATE) trial. Action Points

Explain to patients who ask that anemia is a common complication of chronic kidney disease, and that treatment with recombinant human erythropoietin can help to reduce the associated fatigue and improve quality of life for many patients.


Explain that the studies described here indicate that an overly-aggressive approach to treating anemia in patients with chronic kidney disease does not help more than standard treatment, and may be associated with an increased risk for cardiovascular complications.
In fact, aiming for a target hemoglobin of 13.5 g/dL may increase the risk for cardiovascular events compared with a target of 11.3 g/dL, without adding any apparent quality-of-life benefit, according to U.S. and Irish investigators in the Correction of Hemoglobin and Outcomes in Renal Insufficiency (CHOIR) trial.


Results of both the CREATE and CHOIR trials were published in the Nov. 16 issue of the New England Journal of Medicine.


In an accompanying editorial, Giuseppe Remuzzi, M.D., of the Mario Negri Institute for Pharmacological Research in Bergamo, Italy, and Julie R. Ingelfinger, M.D., deputy editor of NEJM, wrote, "The most surprising finding is that high target hemoglobin levels did not ameliorate left ventricular hypertrophy in the CREATE study and, indeed, they increased the risk of congestive heart failure in both trials."


Anemia caused by erythropoietin deficiency is a common complication in patients with chronic kidney disease, and is therefore frequently treated with recombinant human erythropoietin alfa, sold as either Epogen or Procrit. Package inserts for both products say that the maximum hemoglobin target should not exceed 12 g/dL.


Correction of anemia in patients with chronic kidney disease has been associated with improved quality of life, but the optimal target hemoglobin levels have not been clearly established, noted Ajay K. Singh, M.B., of Brigham and Women's Hospital here, and CHOIR colleagues at other centers.


"Evidence suggesting that the correction of anemia improves cardiovascular outcomes has largely been derived from observational studies and small interventional trials associating a high level of hemoglobin (>12.0 g/dL) with a lower rate of complications and death from cardiovascular causes," Dr. Singh and colleagues wrote.


Other studies have suggested that anemia correction to a high target level might improve left ventricular hypertrophy and other cardiovascular complications.


"However, in a randomized, controlled study comparing a hematocrit target of 42% with that of 30% among patients with heart disease who were undergoing hemodialysis, the former group had higher rates of nonfatal myocardial infarction and death, but not significantly so," Dr. Singh and colleagues noted.


In an effort to determine the optimal hemoglobin level in patients with stage III or stage IV chronic kidney disease (estimated glomerular filtration rate (GFR) of 15-50 ml/min/1.73m² of body surface area), the investigators conducted an open-label trial in 1,432 patients were randomly assigned to receive epoietin afla targeted to achieve a hemoglobin level of 13.5 g/dL (175 patients), or 11.3 g/dL (717 patients).


The patients were followed for a mean of 16 month for a primary composite end point of death, myocardial infarction, hospitalization for congestive heart failure (without renal replacement therapy), and stroke.


In all, there were significantly more events in the high-hemoglobin group compared with the low hemoglobin group: 125 vs. 97. The hazard ratio for a cardiovascular event with a high vs. lower hemoglobin target was 1.34 (95% confidence interval, 1.03 to 1.74; P=0.03).


"On the basis of data from the intention-to-treat population, but including all events from randomization to study termination or 30 days after the last administration of study medication, the hazard ratio for the primary outcome in the high-hemoglobin group, as compared with the low-hemoglobin group, was 1.30 (95% CI, 1.01 to 1.68, P=0.04)," Dr. Singh and colleagues wrote. "When the analysis included all events from randomization to 90 days after study termination, the hazard ratio was also 1.30 (95% CI, 1.01 to 1.66; P=0.04)."


They concluded that "the use of a target hemoglobin level of 13.5 g per deciliter (as compared with 11.3 g per deciliter) was associated with increased risk and no incremental improvement in the quality of life."


In the CREATE trial, Tilman B. Drüeke, M.D., of Necker Hospital in Paris, and colleagues in other European centers conducted a study to determine whether correction of anemia in patients with stage 3 or 4 chronic kidney disease could improve cardiovascular outcomes.


Their study included 603 patients with an estimated GFR of 15.0 to 35.0 ml/minute/1.73 m2 and mild-to-moderate anemia (hemoglobin level, 11.0 to 12.5 g/dL).


The patients were randomly assigned to receive therapy to a target hemoglobin value in the physiologically normal range (13.0 to 15.0 g/dL), or to the subnormal range (10.5 to 11.5 g/dL).


Patients in the normal hemoglobin group were started on subcutaneous epoietin beta (NeoRecormon) at randomization, while those in the subnormal hemoglobin group were given erythropoietin only when their hemoglobin levels fell below 10.5 g/dL.


The primary endpoint was a composite of eight cardiovascular events: time to first cardiovascular event, a category that included sudden death, myocardial infarction, acute heart failure, stroke, transient ischemic attack, angina pectoris resulting in hospitalization for 24 hours or more or prolongation of hospitalization, complication of peripheral vascular disease (amputation or necrosis), or cardiac arrhythmia resulting in hospitalization for 24 hours or more.


Secondary endpoints included left ventricular mass index, quality-of-life scores, and chronic kidney disease progression.


They found that during the three-year study, correction of anemia to normal lowers the risk of a first cardiovascular event. There were 58 events among patients in the normal hemoglobin group, and 47 among patients in the low hemoglobin group (hazard ratio, 0.78, 95% CI, 0.53 to 1.14, P=0.20). In addition, the left ventricular mass index remained stable in both groups.


The mean estimated baseline GFR was 24.9 ml/minute in the normal hemoglobin group, decreasing by 3.6 ml/min per year. The decline was similar among patients treated to the low hemoglobin target, who had an estimated mean baseline GFR of 24.2 ml/minute, which decreased by 3.1 ml/minute per year (P=0.40).


Significantly more patients in the higher target group went on to require dialysis (127 vs. 111, P=0.03), although patients in the higher target group had significantly better general health (P=0.003) and physical function (P<0.001).


There were no significant differences in the combined incidence of adverse events between the two groups.


Dr. Drüeke and colleagues concluded that "in patients with chronic kidney disease, early complete correction of anemia does not reduce the risk of cardiovascular events."


"Taken together, these two studies suggest caution in the full correction of anemia in patients with chronic kidney disease," Dr. Remuzzi and Dr. Ingelfinger wrote in their editorial.


"Currently, there are several additional multicenter trials of complete as compared with partial correction of anemia in patients with chronic kidney disease; Dr. Remuzzi is participating in one of them," they continued. "Although we need more information about the ideal target level and should consider the present guidelines incomplete, it seems wisest to refrain from complete correction of anemia in persons with chronic kidney disease."

 
 

www.LupusMCTD.com
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #18 on: November 24, 2006, 04:42:56 pm »

New folder for all information related to kidneys, Lupus,MCTD, autoimmune disorders
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #19 on: November 24, 2006, 06:42:49 pm »

CV Risk With Erythropoietic Agents and Higher Haemoglobin
Treatment Of Anemia Associated With Chronic Renal Failure, Including Patients On Dialysis And Patients Not On Dialysis

BETHESDA, MD -- November 24, 2006 -- The U.S. Food and Drug Administration notified healthcare professionals of a newly published clinical study showing that patients treated with an erythropoiesis-stimulating agent (ESA) and dosed to a target hemoglobin concentration of 13.5 g/dL are at a significantly increased risk for serious and life threatening cardiovascular complications, as compared to use of the ESA to target a hemoglobin concentration of 11.3 g/dL.

The "Correction of Hemoglobin and Outcomes in Renal Insufficiency" study, published November 16, 2006 in the New England Journal of Medicine, reports the adverse cardiovascular complications as a composite of the occurrence of one of the following events: death, myocardial infarction, hospitalization for congestive heart failure, or stroke.

The study findings underscore the importance of following the currently approved prescribing information for Procrit, Epogen, and Aranesp, including the dosing recommendation that the target hemoglobin not exceed 12 g/dL.

www.LupusMCTD.com
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #20 on: November 30, 2006, 10:18:43 am »

November 30, 2006
Treatment of Anemia Questioned

An expert panel of doctors for the National Kidney Foundation plans to assess whether hundreds of thousands of patients with kidney disease are being dangerously overtreated with drugs for anemia.

The decision to convene the panel comes two weeks after studies in The New England Journal of Medicine suggested that kidney patients whose anemia was more aggressively treated were more likely to die or suffer heart problems than those who were allowed to remain more anemic.

As a result, the panel, which will meet early next year, may recommend less aggressive treatment of anemia, potentially hurting sales for Amgen and Johnson & Johnson, which market the drugs, which are among the world’s best-selling prescription medicines.

“There are substantial sums of money involved here,” said Kerry Willis, vice president for medical and scientific activities of the National Kidney Foundation. The foundation, in response to a reporter’s question, confirmed the panel’s plans to meet. The panel’s recommendations would not have the force of law. But they are certain to be closely watched by kidney doctors as well as administrators of the federal Medicare program, which is by far the largest buyer of the drugs worldwide.

Sold under the brand names Epogen, Procrit, and Aranesp, the anemia drugs will reach almost $10 billion in sales worldwide in 2006. Medicare will spend $2 billion on them for kidney dialysis patients alone, and a similar amount for cancer patients and patients with kidney disease not yet on dialysis.

Nearly one million Americans, including 500,000 kidney patients, receive the drugs every year.

But some independent scientists say they believe that kidney patients are receiving too much of the drugs, in part because dialysis clinics make bigger profits for providing higher doses. The clinics make little profit on the actual dialysis services they provide for Medicare enrollees, who are the vast majority of dialysis patients.

The foundation’s panel will probably meet in January or early February and could release new treatment recommendations for public review a few weeks later, the foundation said.

The anemia panel consists of 15 nephrologists who meet under the auspices of the foundation, a private nonprofit group based in New York that provides financing for kidney researchers. The panel is one of several panels sponsored by the foundation that make recommendations about how to improve treatment for kidney patients.

But some scientists complain that Amgen has until now had too much influence on the creation of the foundation’s guidelines. The most recent version of the anemia guidelines, released earlier this year, encourages more aggressive treatment than the Food and Drug Administration recommends.

“The guidelines are funded through the National Kidney Foundation by industry, by and large,” said Dr. Daniel Coyne, professor of medicine at Washington University in St. Louis. “They write guidelines that are opinion-based, by and large, and favor industry or would appear to favor industry.”

While Amgen sponsors the creation of the guidelines and donated $4 million to the foundation last year, both the foundation and the company say that the company does not control which doctors are chosen for the panel or influence their choice of treatment.

Dr. Rob Brenner, senior director of medical affairs at Amgen, said the company had always promoted use of its drugs in accordance with the more cautious F.D.A. label, not the more aggressive guidelines created by the foundation.

The anemia drugs are proteins that stimulate bone marrow cells to produce hemoglobin, the main component of red blood cells. They must be given via injection, either intravenously or through the skin.

The original drug, called epoetin, is made by Amgen, which markets it under the brand name Epogen. Johnson & Johnson sells the identical drug, also produced by Amgen, as Procrit.

The other drug, darbepoetin, is sold under the name Aranesp. It was introduced in 2001 by Amgen and is a slightly modified version of epoetin that can be given less frequently.

Neither the National Kidney Foundation panel nor the F.D.A. suggest how much of the drugs patients should receive. Instead, they have guidelines for hemoglobin targets in the blood.

In general, healthy adults have hemoglobin levels of 14 grams or more per deciliter of blood, while patients are considered to need treatment if their levels are below 10 grams. Severe anemia can be devastating, leaving patients unable to work, walk for more than a few minutes, or even think clearly, while also increasing their risk of infection and heart disease.

But high levels of hemoglobin can cause high blood pressure, strokes and heart attacks, even in healthy adults. Now some scientists say they believe that kidney doctors need to become more conservative about treating anemia, which probably means using less of the drugs.

The prescribing label for Epogen, as approved by the F.D.A., says dialysis patients should have a target hemoglobin level of 10 to 12 grams per deciliter of blood. In its most recent guideline, the panel of doctors overseen by the kidney foundation said a target of 11 to 13 grams was appropriate. It is that target that will now be under review.

In practice, almost all dialysis patients receive the drugs, and almost none have hemoglobin levels below 11 grams after treatment. About half have levels of more than 12 grams, according to data from the United States Renal Data System, a federally sponsored group that monitors kidney patient care. Almost 20 percent of patients have levels above 13 grams.

The differences may seem small, but one of the studies published in The New England Journal found that patients treated to an average hemoglobin level of 12.6 grams had a 34 percent higher risk of death or serious heart problems than those treated to a level of 11.3 grams.

And the average patient at the higher level required about twice as much of the anemia drug to get to that level.

www.LupusMCTD.com
« Last Edit: November 30, 2006, 10:20:53 am by Kathy » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #21 on: December 04, 2006, 12:46:44 pm »


Mycophenolate mofetil may be more effective in inducing lupus nephritis remission

 
"This is the first nationwide randomized clinical trial comparing the newer agent, approved for about 10 years for kidney transplant patients, with the long-time standard of care, which has been Cytoxan"
 
Treating lupus patients suffering from kidney inflammation with a medicine known as mycophenolate mofetil may be more effective in inducing remission than treating them with the standard regimen of intravenous cyclophosphamide (Cytoxan), a new clinical trial indicates.

The study, published in Thursday’s issue (Nov. 24) of the New England Journal of Medicine, also showed that mycophenolate mofetil produced fewer complications, researchers found.

Such results could be an important step forward in protecting patients from Cytoxan’s side effects, including loss of child-bearing ability, the doctors say. Since 90 percent of lupus patients are women, and the average age when the disease is diagnosed is 32 years old, loss of fertility remains an important concern.

Authors of the report include Drs. Ellen M. Ginzler, chief of rheumatology at SUNY Downstate Medical Center in Brooklyn, and Mary Anne Dooley, associate professor of medicine and a Thurston Arthritis Research Center investigator at the University of North Carolina at Chapel Hill School of Medicine.

"This is the first nationwide randomized clinical trial comparing the newer agent, approved for about 10 years for kidney transplant patients, with the long-time standard of care, which has been Cytoxan," said Dooley, who helped design the FDA orphan disease branch-funded study, get it approved and recruit medical centers and patients. "Our results are very promising, but we need to do longer follow-up to see if the new medicine produces long-lasting improvement."

Oral mycophenolate mofetil worked faster in relieving inflamed kidneys, a condition doctors call nephritis, in half of the 140 patients enrolled in the trial, she said. At the end of the six months, patients taking it were doing significantly better than the other half, who were getting monthly intravenous doses of the standard medication.

"Lupus nephritis is a severe manifestation of lupus, which is an autoimmune disease that affects nine times as many women as men," Dooley said. "It also is three times more likely to occur in African-Americans than in Caucasians, and it is an increasing cause of end-stage renal disease.

"Among African-American patients we see, 40 percent progress to dialysis within five years," she said. "That’s despite being treated with Cytoxan, and so we are very motivated to find new drugs to better treat these patients."

For unknown reasons, blacks tend to get lupus earlier in life and suffer severe kidney damage much more frequently, the UNC physician said. African patients get it, too, but not with nearly the same severity as blacks in the U.S. and Europe.

A major issue for future studies of mycophenolate mofetil will be whether it protects as well as, or better than, Cytoxan does against nephritis relapses among lupus patients, Dooley said.

In an accompanying editorial in the New England Journal of Medicine, Dr. W. Joseph McCune of the University of Michigan said, "In an era of industry-sponsored research, this investigator-initiated and investigator-directed clinical trial makes an important contribution to patient care."
www.LupusMCTD.com
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Adminஐﻬ
"Pay It Forward" ஐﻬ
Site Owner
******
Offline Offline

Gender: Female
Posts: 10407


LupusMCTD Founder ஐﻬ


WWW
« Reply #22 on: December 26, 2006, 02:16:25 pm »


FDA Issues Alert on Gadolinium-Based Contrast Agent for Kidney Patients
     

 
 Dec. 26 -- The FDA updated a public health advisory today about a serious new kidney disease that is apparently associated with a gadolinium-based contrast agent used with MRI or MR angiography.
The agency said that as of Dec. 21 it had received reports of 90 patients with moderate to end-stage kidney disease who developed the new disease, called nephrogenic systemic fibrosis or nephrogenic fibrosing dermopathy (NSF/NFD), after they had an MRI or MRA with a gadolinium-based contrast agent.

The FDA recommended that whenever possible patients with moderate to end-stage kidney disease who need an imaging study, be given imaging methods other than MRI or MRA with a gadolinium-based contrast agent.

NSF/NFD began from two days to 18 months after exposure to the contrast agent, said the FDA. Many, but not all of these patients, received a high dose of the contrast agent, yet some received only one dose.

The signs of NSF/NFD also include: burning, itching, swelling, hardening and tightening of the skin; red or dark patches on the skin; yellow spots on the whites of the eyes; stiffness in joints with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness.

The FDA notified physicians and patients that:

Patients with moderate to end-stage kidney disease who receive an MRI or MRA with a gadolinium-based contrast agent may get NSF/NFD which is debilitating and may cause death.
Patients who believe they may have NSF/NFD should get in touch with their doctor. Patients who develop NSF/NFD have areas of tight, rigid skin and may have scarring of their body organs.
If these patients must receive a gadolinium-based contrast agent, prompt dialysis following the MRI or MRA should be considered.
It is not clear why NSF/NFD occurs in patients with moderate to end-stage kidney disease who receive a gadolinium-based contrast agent.
There are five FDA-approved gadolinium-based contrast agents, Magnevist, MultiHance, Omniscan, OptiMARK, and ProHance. These contrast agents are FDA approved for use during an MRI scan, but not for use during an MRA scan. Although NSF/NFD has been reported for only three of the five gadolinium-based contrast agents, the FDA said it believes that there is a potential for NSF/NFD to occur with the use of any of the approved gadolinium-based contrast agents.

The advisory was an update to an alert last June when the FDA said it had learned of 25 cases of NSF/NFD in patients with kidney failure who received Omniscan, and took the MRA test. "These reports provide more evidence for a causal relationship between gadolinium-based contrast agents and the development of NSF/NFD," the FDA said.

Worldwide, the re have been about 215 patients with NSF/NFD reported, said the FDA. The medical histories of 75 of these patients were reviewed in detail, and all of the patients had received a gadolinium-based contrast agent for an MRI or MRA. Researchers, the agency said, have identified gadolinium in skin biopsies of patients with NSF/NFD.

 
 

www.LupusMCTD.com
Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
www.LupusMCTD.com Represents:
1) We are patients helping researchers build a future for the lives of others...
2) Where HOPE is a WORK In Progress
3) Pay It Forward~Giving Back To The Future Lupus/MCTD Patients
Pages: 1   Go Up
  Print  
 
Jump to:  


© Page Contents, Layout, Graphics and Design All Copyrighted by Credited Artists and are Not Public Domain.



LupusMCTD Founder & Patient
Former Domestic Violence SURVIVOR
Kathy A. Patterson

Author of the Upcoming Memoir Book:
"Fighting From The Inside Out"..
A lupus patient fights the beast within her immune system and the beast at home....

e-Booklet filled with photos and videos of what abuse was, signs to look for,
where to turn to for help, and much more to help others like me...


For more information
Call the National Domestic Violence Hotline at 1−800−799−SAFE(7233)



"The Meaning of the Words in the Second Amendment .... "That the people have a right to freedom of speech, and of writing, and publishing their sentiments;"

PRIVACY NOTICE: Warning--any person and/or institution and/or Agent and/or Agency of any governmental structure including but not limited to the United States Federal Government also using or monitoring/using this website or any of its associated websites, you do NOT have my permission to utilize any of my profile information nor any of the content contained herein including, but not limited to my photos, and/ or the comments made about my photo's or any other "picture" art posted on my profile. You are hereby notified that you are strictly prohibited from disclosing, copying, distributing, disseminating, or taking any other action against me with regard to this profile and the contents herein. The foregoing prohibitions also apply to your employee(s), agent(s), student(s) or any personnel under your direction or control. The contents of this profile are private and legally privileged and confidential information, and the violation of my personal privacy is punishable by law
Photobucket
© 2008 LupusMCTD Foundation of America - All Rights Reserved
Est.November 11, 2005
"We Understand What You Are Going Through"™
Powered by EzPortal

Powered by MySQL Powered by PHP Powered by SMF 1.1.21 | SMF © 2015, Simple Machines
Twitter Mod created by 2by2host.com - a web hosting company