Abstract
Renal disease in diabetic patients causes increased morbidity and mortality. About 30 to 40% of insulin-dependent diabetic patients develop end stage renal disease and require either dialysis or transplantation for survival. Several animal models of diabetes have been developed to understand the renal disease with regard to structural, biochemical and functional changes that occur in the diabetic kidney. Our interest has been to delineate these relationships in diabetic nephropathy using the KK mouse as an animal model. Therefore, we evaluated the kidney disease in KK mice from three perspectives. The first one is to demonstrate glomerulosclerosis in a reasonable number of animals. The second perspective is to establish the biochemical basis of diabetic glomerulosclerosis, and finally to correlate these structural and biochemical abnormalities with the functional defect, namely, proteinuria. This correlation has clinical relevance because of possible prevention of diabetic proteinuria through improvement in structural or biochemical abnormalities.
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© 1988 Plenum Press, New York
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Reddi, A.S., Wehner, H., Khan, M.Y., Camerini-Davalos, R.A. (1988). Kidney Disease in KK Mice: Structural, Biochemical and Functional Relationships. In: Camerini-Davalos, R.A., Cole, H.S. (eds) Prediabetes. Advances in Experimental Medicine and Biology, vol 246. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5616-5_17
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DOI: https://doi.org/10.1007/978-1-4684-5616-5_17
Publisher Name: Springer, Boston, MA
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