Focal glomerulosclerosis: a clinico-pathological analysis of 36 adult patients with idiopathic nephrotic syndrome

Wei, C.H.; Chen, A.; Fan, C.D.; Tu, Y.C.

Zhonghua Yi Xue Za Zhi 46(4): 225-231

1990


ISSN/ISBN: 0578-1337
PMID: 2178056
Document Number: 353147
A retrospective study was conducted to determine the clinicopathological correlation of focal glomerulosclerosis in 36 adult patients with idiopathic nephrotic syndrome. All cases were divided into two groups, focal segmental glomerulosclerosis (FSGS, 23 cases) and focal global glomerulosclerosis (FGBG, 13 cases), on the basis of pathological findings. Most patients with FSGS were non-responsive/partial-responsive (22/22) to the corticosteroid treatment. By contrast, those with FGBG gave a relatively high responsive rate of 7/12 to the same therapy. The 5 non-responders with FGBG, however, were noted to have intensive interstitial fibrosis/mononuclear cell infiltrate of the renal lesions (4 cases), or diffusely glomerular Clq deposition without other coexisting immune deposits (1 case). Most cases of FSGS (20/23) became steroid dependent or remained heavy proteinuria resistant to corticosteroids/other immunosuppressive agents over a mean of 3.4 (ranged, 1 to 7) years after renal biopsy. Three of the 5 patients of FGBG initially non-responsive/partial-responsive to corticosteroids turned out to have protein-free urine (less than 4 mg/hr/m2) (2 patients) 1 month after leaving the hospital and became mildly proteinuric (1 patient) two months after discharge, respectively. The remainders of FGBG (10/13) were free of protein in their urine sample or had occasional episodes of proteinuria over a mean duration of 4.1 (ranged, 1 to 7) years. In addition, chronic renal insufficiency on discharge was noted in 2 cases of FSGS (2/23) and 1 case of FGBG (1/13). Only two cases of FSGS (2/23) progressed into a uremic status 3 and 5 years, respectively, after the time of the presumed clinical onset of their disease. These findings suggest that FGBG clinically behaves similar to a minimal change disease.

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