We reviewed the diagnostic features and clinical course of 140 patients with idiopathic membranous nephropathy who had their index renal biopsies performed at the Mayo Clinic between 1972 and 1984. There were 93 males and 47 females (average age, 50.8 +/- 17 years); 116 patients (83%) had the nephrotic syndrome and 42 (30%) were hypertensive at diagnosis. Eighty-nine patients were not treated with corticosteroid or immunosuppressive drugs and 51 patients were treated mainly with short-term courses of prednisone alone; a minority of patients also received meclofenamate, cyclophosphamide, azathioprine, or chlorambucil. Five-year survival, including patients who received dialysis or a renal transplant, was 85%, 75% at 10 years, and no different from expected survival; there was no difference between untreated and treated groups. Also, there were no differences in the outcomes of renal function and protein excretion between untreated and treated patients. Among 28 patients (20%) who developed end-stage renal disease, 17 showed rapid progression within 2.5 years after diagnosis. Fifteen of the 17 patients were males; all were severely nephrotic and had impaired renal function at diagnosis. Only 1 of 24 patients with nonnephrotic proteinuria at index renal biopsy progressed to end-stage renal disease. Overall, a level of baseline proteinuria of 10 g or more per 24 hours and variable blood pressure control in hypertensive patients were associated with renal progression.
The point prevalence and clinical significance of renal vein thrombosis (RVT) was evaluated in 27 of 33 consecutive nephrotic patients with idiopathic membranous glomerulopathy. A technique of retrograde venography after the injection of epinephrine into the main renal artery to decrease renal blood flow was used. Two patients had histories compatible with a thromboembolic event, and the excretory urogram was not suggestive of RVT in any patient. RVT was noted in 13 patients; in eight it was bilateral. All patients with RVT received anticoagulant drugs for a minimum of 1 year after the study, and no thromboembolic events occurred in this group. No patient was treated with corticosteroids. Follow-up observation of an average of 2.5 years has not revealed a significant difference in the rate of renal function deterioration or change in degree of proteinuria between patients with and without RVT. Coagulation abnormalities included elevated platelet counts and plasma fibrinogen levels and prolonged reptilase and thrombin times. These were noted in all 14 patients studied, six of whom had RVT. In patients experiencing a nephrotic remission, coagulation abnormalities reverted to normal. RVT is common in idiopathic membranous glomerulopathy with nephrosis and is associated with few clinical markers. Its influence on renal function and proteinuria is of questionable significance. Coagulation abnormalities may be a causative factor of RVT in this setting.
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