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Role of obesity in renal pathological and structural changes remains poorly investigated, and this study was designed to examine the pathological effects of obesity on renal structural components in patients with chronic kidney diseases (CKD). The study subjects were obese (body mass index, BMI ≥ 25 kg/m2) patients with nonglomerulonephritis (non-GN, n = 26), IgA nephropathy (IgAN, n = 19), benign nephrosclerosis (BNS, n = 15), and thin basement membrane disease (TMD, n = 6), and 65 nonobese controls ( n = 20, 20, 10, and 15, respectively). Patients were evaluated for glomerular lesions (mesangial proliferation and focal segmental/global glomerulosclerosis), glomerular size, and thickness of glomerular basement membrane (GBM). Urinary protein was higher in obese non-GN, IgAN, and BNS groups than in the respective controls. Focal segmental glomerulosclerosis (FSGS) lesions were noted in all obesity groups. The glomeruli were larger in size in obese than in nonobese patients of the non-GN and IgAN groups. The glomeruli of nonobese TMD and BNS patients were significantly larger in size than those of nonobese non-GN patients. GBM were thicker in obese than in nonobese patients irrespective of types of glomerular diseases, but only significantly so in non-GN and BNS groups. In non-GN, IgAN, and BNS, obesity worsens proteinuria and is associated with structural changes such as glomerulomegaly and GBM thickening, similar to changes observed in obesity-related nephropathy. Obesity seems to worsen the renopathological state in CKD. [ABSTRACT FROM AUTHOR]

A 57-year-old Japanese female was admitted because of edema, hypoproteinemia and proteinuria. Her histopathological findings of renal biopsy specimen were quite unique. Light microscopic findings suggested membranous glomerulonephritis, but no significant deposition of immunoglobulins or complements was detected in glomeruli by immunofluorescence. Electron microscopic examination revealed irregular thickening of the glomerular basement membrane (GBM). The GBM had no electron-dense deposits, but numerous microparticles varying in shape and size were present in all the thickened GBM and occasionally in the mesangium. The microparticles were round or oval in shape, and the size varied widely, measuring 25–290 nm (mostly 40–120 nm). The cytoplasmic infolding into the GBM by podocytes was seen. The large-sized particles had microgranules, mimicking free ribosomes seen in podocytes or endothelial cells. We conclude that cytoplasmic infolding and subsequent degradation may, partly, contribute to the formation of microparticles in the GBM. [ABSTRACT FROM AUTHOR]