Podocyte Depletion Causes Glomerulosclerosis

Wharram, Bryan L.; Goyal, Meera; Wiggins, Jocelyn; Sanden, Silja K.; Hussain, Sabiha M.; Filipiak, Wanda E.; Saunders, Thomas L.; Dysko, Robert C.; Kohno, Kenji; Holzman, Lawrence B.; Wiggins, Roger C.

doi:10.1681/asn.2005010055

articleJournal of the American Society of NephrologyAug 18, 2005Closed access

Podocyte Depletion Causes Glomerulosclerosis

BLBryan L. Wharram MGMeera Goyal JWJocelyn Wiggins SKSilja K. Sanden SMSabiha M. Hussain

Pediatric Nephrology of Alabama · Michigan Medicine · +4 more institutions

PubMed

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Abstract

Glomerular injury and proteinuria in diabetes (types 1 and 2) and IgA nephropathy is related to the degree of podocyte depletion in humans. For determining the causal relationship between podocyte depletion and glomerulosclerosis, a transgenic rat strain in which the human diphtheria toxin receptor is specifically expressed in podocytes was developed. The rodent homologue does not act as a diphtheria toxin (DT) receptor, thereby making rodents resistant to DT. Injection of DT into transgenic rats but not wild-type rats resulted in dose-dependent podocyte depletion from glomeruli. Three stages of glomerular injury caused by podocyte depletion were identified: Stage 1, 0 to 20% depletion showed mesangial…

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Topics

Keywords

Podocyte
Glomerulosclerosis
Focal segmental glomerulosclerosis
Proteinuria
Diabetic nephropathy
Endocrinology
Internal medicine
Nephropathy

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