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Lookup NU author(s): Dr Kathryn White, Professor Rudy Bilous
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Background. The podocyte is believed to play a key role in maintaining the integrity of the glomerular filtration barrier, and damage or loss has been linked to the development of albuminuria. Methods. Renal biopsies from 16 type 2 diabetic patients with nephropathy and 28 non-diabetic controls were analysed using light and electron microscopy. Results. Podocyte number per glomerulus was significantly lower in the type 2 patients compared with controls [mean (95% confidence interval) 464 (382-546) vs 589 (543-635), P=0.004]. Mean glomerular volume was significantly increased in diabetic patients compared with controls [5.5 (4.9-6.1) vs 3.1 (2.7-3.5) x 10(6) mum(3), P<0.001], thus the diabetic patients demonstrated an even greater proportional reduction in podocyte density pier glomerulus [88 (68-108) vs 201 (182-220)/10(6) mum(3), P<0.001]. Podocyte foot process width on both the filtration surface (FPWgbm) and mesangial surface (FPWmes) was significantly increased compared with controls [796 (708-884) vs 556 (460-908)nm, P=0.001; 1108 (821-1394) vs 760 (555-1078)nm, P=0.029, respectively]. There was a significant negative correlation between proteinuria and both podocyte number and podocyte density per glomerulus (r=-0.63, P=0.009; r=-0.58, P=0.018, respectively). There was a significant positive correlation between proteinuria and both FPWgbm and FPWmes (r=0.64, P=0.008, for both). Conclusion. Podocyte loss occurs in type 2 diabetic nephropathy and is related to increasing proteinuria. Whether the accompanying glomerular enlargement and widening of foot processes are a cause of podocyte loss is uncertain. Longitudinal studies are required to determine the sequence of events leading to podocyte loss in diabetic nephropathy.
Author(s): White KE, Bilous RW, Diabiopsies Study Group
Publication type: Article
Publication status: Published
Journal: Nephrology Dialysis Transplantation
Year: 2004
Volume: 19
Issue: 6
Pages: 1437-1440
ISSN (print): 0931-0509
ISSN (electronic): 1460-2385
Publisher: Oxford University Press
URL: http://dx.doi.org/10.1093/ndt/gfh129
DOI: 10.1093/ndt/gfh129
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