AN IMPORTANT ROLE OF GLOMERULAR SEGMENTAL LESIONS ON PROGRESSION OF IGA NEPHROPATHY - A MULTIVARIATE-ANALYSIS

The independent predictors of progression of IgA nephropathy (IgAN) we re investigated by multivariate life table analysis, using Cox's propo rtional hazard model, in 225 patients with IgAN diagnosed by renal bio psy (Bx). There were 105 men and 120 women. Mean age at Bx was 32.5 ye ars. The follow-up period following Bx was 4.0 +/- 2.6 yrs, ranging fr om 5 months to 11 yrs. The clinical parameters analyzed were age at th e time of discovery of the disease, age at Bx, intervals from discover y to Bx, presence or absence of macrohematuria, and clinical data at B x such as presence or absence of hypertension, the degree of hematuria , the amount of urinary protein excretion, serum creatinine and serum IgA concentration. The following immunopathological parameters were al so examined; glomerular hypercellularity index, percentage of glomerul i associated with segmental lesions such as tuft adhesions, crescents and segmental sclerosis, percentage of obliterated glomeruli by global sclerosis, severity of interstitial infiltration, fibrosis, arterial wall thickening, arterial hyaline changes, and intensity of the deposi tions of IgG, IgA, IgM, C3, C1q and fibrinogen by immunofluorescent st udy. Among all clinical and pathologic parameters examined, the follow ing parameters were proved to be significant independent predictors of progression of IgAN: serum creatinine exceeding 1.5 mg/dl in men and 1.3 mg/dl in women, proteinuria over 2 g/day, segmental lesions involv ing more than 25% of glomeruli and interstitial fibrosis occupying mor e than 25% of cortical area. Since the interstitial fibrosis is an irr eversible sclerotic change which is the secondary abnormality to glome rular change, glomerular segmental lesions such as tuft adhesion, cres cent or segmental sclerosis, all of which are frequently found to be a ssociated with each other, seems to be the most important primary path ological change, indicating ongoing inflammation and subsequent progre ssion to irreversible obliteration of glomerular capillaries.