warfarin and Glomerulonephritis--Membranoproliferative

Topics: Adrenal Cortex Hormones; Angiotensin-Converting Enzyme Inhibitors; Anticoagulants; Autoantibodies; Complement Activation; Complement C3 Nephritic Factor; Complement System Proteins; Glomerulonephritis, Membranoproliferative; Hepacivirus; Heparin; Humans; Warfarin

A 57-year-old woman with pulmonary sarcoidosis was admitted to the hospital because of an elevation of serum creatinine and blood urea nitrogen. On admission, the laboratory data suggested interstitial nephritis without proteinuria and hematuria, whereas a renal biopsy showed granulomatous interstitial nephritis and mild mesangial proliferative glomerulonephritis. Immunoglobulin and C1q deposits were negative, but mannose-binding lectin, C3, C4d, and C5b-9 deposits were marked in the glomerular mesangial areas. The lectin pathway of complement activation may have contributed to the development of glomerular injury in this patient. DNA of Propionibacterium acnes , which is now strongly suspected as the pathogen of sarcoidosis, was detected in the patient's glomerular mesangial cells; tubular epithelial cells, which were involved in granulomatous inflammation; and mononuclear cells in epithelioid granulomas by in situ hybridization. These findings may add new insights to the pathogenesis of renal sarcoidosis, including its relation to infection, because mannose-binding lectin plays a crucial role in the host defense against various pathogens. From this case of renal sarcoidosis, it is hypothesized that P acnes may be involved in pathogenesis of granulomatous interstitial nephritis and that it plays a role in glomerular complement activation via the lectin pathway.

Topics: Anti-Inflammatory Agents; Anticoagulants; Complement Activation; Complement C3; Complement C4b; Complement Membrane Attack Complex; DNA, Bacterial; Drug Therapy, Combination; Female; Glomerular Mesangium; Glomerulonephritis, Membranoproliferative; Gram-Positive Bacterial Infections; Heparin; Histiocytosis, Langerhans-Cell; Humans; Lung; Lung Diseases, Interstitial; Mannose-Binding Lectin; Methylprednisolone; Middle Aged; Nephritis, Interstitial; Peptide Fragments; Prednisone; Propionibacterium acnes; Sarcoidosis; Warfarin

A 21-year-old man was admitted to Kure National Hospital with nephrotic syndrome in September 1996. He had suffered from an intractable pruritic skin rash and recurrent subcutaneous abscesses caused by the hyperimmunoglobulin E syndrome since the age of 18 months. Renal biopsy gave a diagnosis of membranoproliferative glomerulonephritis. Steroid therapy decreased urinary protein loss and hypoproteinemia, and his pruritic skin rash was improved. Patients with hyperimmunoglobulin E syndrome have a defective immune response, especially to Staphylococcus aureus infection. Continuous antigen stimulation may have caused this patient's renal histological damage as in immune complex glomerulonephritis.

Topics: Adult; Anticoagulants; Biopsy; Diagnosis, Differential; Dilazep; Drug Therapy, Combination; Follow-Up Studies; Glomerulonephritis, Membranoproliferative; Glucocorticoids; Humans; Job Syndrome; Male; Nephrotic Syndrome; Prednisolone; Vasodilator Agents; Warfarin

The authors describe a 46-year-old Japanese woman who had Takayasu's arteritis associated with nephrotic syndrome due to mesangial proliferative glomerulonephritis with crescent. Although a few cases of focal and segmental mesangial proliferative glomerulonephritis associated with Takayasu's arteritis have been reported, nephrotic syndrome has not been reported previously in this situation.

Topics: Anti-Inflammatory Agents; Anticoagulants; Carotid Artery Diseases; Female; Glomerulonephritis, Membranoproliferative; Heparin; Humans; Middle Aged; Nephrotic Syndrome; Prednisolone; Proteinuria; Takayasu Arteritis; Warfarin

We report here a case of severe membranoproliferative glomerulonephritis with a singular high titer of anticardiolipin antibody (aCL). A 19-year-old Japanese female was admitted to Tsukuba Gakuen Hospital after complaining of general edema for 5 months. She had no past history of thrombosis, thrombocytopenia, or spontaneous abortion. Laboratory findings revealed that she had nephrotic syndrome and moderate renal dysfunction. Immunological test showed a high titer of aCL with a high-normal limit of antinuclear antibody, negativity for anti-beta(2) glycoprotein I antibody and negativity for anti-DNA antibody. In the renal biopsy tissue, most glomeruli showed global sclerosis and the remaining glomeruli revealed membranoproliferative change with crescent formation. Steroid therapy with warfarin and dipyridamole was effective and her renal function improved gradually. This case lacked the typical symptoms of primary antiphospholipid syndrome and did not satisfy the criteria of SLE. In spite of these findings, the singular high titer of aCL with membranoproliferative glomerulonephritis characterized this case.

Topics: Adult; Anti-Inflammatory Agents; Antibodies, Anticardiolipin; Anticoagulants; Dipyridamole; Female; Glomerulonephritis, Membranoproliferative; Humans; Kidney Glomerulus; Methylprednisolone; Platelet Aggregation Inhibitors; Prednisolone; Warfarin

We followed the course of membranoproliferative glomerulonephritis (MPGN) type I after immunosuppressive therapy in 10 children. At diagnosis all patients had abnormal urinary findings. After a mean follow-up of 14 years all but one patient showed normal urinalysis and renal function. Glomerular morphometry revealed an increase in the ratio of mesangial matrix area to glomerular area (M/G%) in all patients. After immunosuppressive treatment, a second biopsy was performed, which showed a significantly decreased M/G% in 4 patients. In 3 of the remaining 6, the mean M/G% was significantly lower in a third biopsy when compared with the first. In addition, there was a negative correlation between M/G% and duration from onset disease to biopsy (r = -0.46, p <0.05). Fifteen biopsies (6 initial and 9 repeat biopsies) were examined for the staining of various extracellular matrices. In the initial biopsy type IV collagen, type V collagen and fibronectin were increased in expanded mesangial areas. Type III collagen was found segmentally in a few biopsies only. M/G% correlated with the grade of type IV collagen, type V collagen and fibronectin staining. These findings suggest that a reversible clinical course of MPGN type I in children is paralleled by a decrease of mesangial matrix expansion.

Topics: Adolescent; Adult; Biopsy; Child; Cyclophosphamide; Dipyridamole; Extracellular Matrix; Extracellular Matrix Proteins; Female; Follow-Up Studies; Glomerular Mesangium; Glomerulonephritis, Membranoproliferative; Heparin; Humans; Immunosuppression Therapy; Male; Microscopy, Electron; Microscopy, Fluorescence; Prednisolone; Time Factors; Urokinase-Type Plasminogen Activator; Warfarin

We report the case of a 15-year-old Japanese female with severe mesangial proliferative IgA glomerulonephritis who showed a dramatic response to cocktail therapy for nephrotic syndrome. She had suddenly developed massive proteinuria and microscopic hematuria. The first renal biopsy at one month after onset revealed severe mesangial hypercellularity and podocytic detachment from the glomerular basement membrane (GBM). The cocktail therapy resulted in a decrease of proteinuria clinically, and a second biopsy demonstrated repair of the podocytic detachment. We suggest that the massive proteinuria in this case was due to destruction of the size barrier by detachment of podocytes from the GBM, and the repair of the podocytic covering on the GBM was accelerated by the cocktail therapy.

Topics: Adolescent; Basement Membrane; Cyclophosphamide; Dipyridamole; Drug Therapy, Combination; Female; Furosemide; Glomerulonephritis, IGA; Glomerulonephritis, Membranoproliferative; Humans; Kidney Glomerulus; Prednisolone; Warfarin

Treatment of idiopathic membranoproliferative glomerulonephritis remains an unsettled issue. The results of five randomized clinical trials have not provided convincing evidence for the effectiveness of any treatment. Follow-up periods in these trials were relatively short-term, ranging from 1 to 4 years. In three recently published long-term clinical studies of patients with membranoproliferative glomerulonephritis, 10-year cumulative survival free of renal failure improved by 20% to 35% over that described in studies published 5 to 10 years earlier. In each study, survival was estimated using life-table analysis. The survival curve in the treated group was then compared with that of a historical control group using the date of clinical onset as time zero. The survival curve in the treatment group was spuriously shifted to the right. By definition, those in the treatment groups had to survive from clinical onset to initiation of treatment, but the historical control group did not have such a constraint. The problem in this comparison is that treatments were not started in a large number of patients for years after clinical onset, resulting in a biased comparison in favor of the treatment groups. (Also, the conclusions drawn from the survival data were that the improvement related directly to various treatments that were used.) Survival was similarly improved in patients treated with dipyridamole and aspirin when survival was plotted against time after clinical onset. However, when the data were replotted and the platelet-inhibitor-treated group was compared with a contemporary randomized control group, no difference in either patient survival or survival free of renal disease was demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aspirin; Child; Cyclophosphamide; Dipyridamole; Drug Therapy, Combination; Glomerulonephritis, Membranoproliferative; Humans; Life Tables; Meta-Analysis as Topic; Prednisone; Survival Rate; Time Factors; United States; Warfarin