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Publication : Hereditary nephrotic syndrome with progression to renal failure in a mouse model (ICGN strain): clinical study.

First Author  Ogura A Year  1994
Journal  Nephron Volume  68
Issue  2 Pages  239-44
PubMed ID  7830863 Mgi Jnum  J:21051
Mgi Id  MGI:69101 Doi  10.1159/000188264
Citation  Ogura A, et al. (1994) Hereditary nephrotic syndrome with progression to renal failure in a mouse model (ICGN strain): clinical study. Nephron 68(2):239-44
abstractText  The clinical course of murine hereditary nephrotic syndrome (ICGN strain) was determined by examining 201 animals under different conditions. In the early stage, significant hypoproteinemia and hypoalbuminemia developed (p < 0.001) in parallel with a progressive rise in urinary protein concentration (p < 0.001). In the middle stage, the concentrations of total cholesterol, triglyceride, and beta-lipoprotein markedly increased (p < 0.01, p < 0.001, and p < 0.001, respectively), suggesting that type IIb hyperlipoproteinemia developed as in human nephrotic patients. Systemic edema appeared in 8 of 24 animals. In the terminal stage, both BUN and creatinine values greatly increased (p < 0.001), indicating rapid deterioration of renal function. The present study suggests that ICGN mice could be a useful model to study the pathophysiology of human nephrotic syndrome and its progression to renal failure.
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