Abstract
Diabetic nephropathy is presently the first reason of end stage renal failure in Europe and the USA and its worldwide prevalence is rapidly increasing. Several studies have demonstrated that diabetes per se is not sufficient to induce nephropathy and a genetic predisposition has to be present as well. Looking for genetic markers, investigators have been helped by the finding that a predisposition to hypertension facilitates the development of nephropathy in diabetic patients. Prompted by the evidence that essential hypertension is characterized by a number of defects at cellular level, similar dysfunctions have been searched also in cells obtained from diabetic patients with nephropathy. Increased Na-Li countertransport and Na-H exchange activities, slower Ca pump and faster cell proliferation rate have been found in cells obtained from patients affected by diabetic nephropathy. The definition of these intermediate phenotypes represents a necessary step toward the identification of the molecular dysfunction(s) underlying the development of diabetic nephropathy. The present review will focus on the description of the different cell dysfunctions identified in patients affected by diabetic nephropathy, their pathophysiologic meaning and will try to define an unifying hypothesis that, by linking together the different dysfunctions, will highlight a few areas "at risk", candidate to home the primitive genetic abnormality.
Keywords: Diabetic nephropathy, Na-Li countertransport, Na-H exchange, Ca pump, Cell proliferation rate, Cell matrix
Current Diabetes Reviews
Title: Dysfunction of Cellular Transporters and Predisposition to Diabetic Nephropathy
Volume: 2 Issue: 2
Author(s): Gianpaolo Zerbini, Daniela Gabellini, Dora Ruggieri and Anna Maestroni
Affiliation:
Keywords: Diabetic nephropathy, Na-Li countertransport, Na-H exchange, Ca pump, Cell proliferation rate, Cell matrix
Abstract: Diabetic nephropathy is presently the first reason of end stage renal failure in Europe and the USA and its worldwide prevalence is rapidly increasing. Several studies have demonstrated that diabetes per se is not sufficient to induce nephropathy and a genetic predisposition has to be present as well. Looking for genetic markers, investigators have been helped by the finding that a predisposition to hypertension facilitates the development of nephropathy in diabetic patients. Prompted by the evidence that essential hypertension is characterized by a number of defects at cellular level, similar dysfunctions have been searched also in cells obtained from diabetic patients with nephropathy. Increased Na-Li countertransport and Na-H exchange activities, slower Ca pump and faster cell proliferation rate have been found in cells obtained from patients affected by diabetic nephropathy. The definition of these intermediate phenotypes represents a necessary step toward the identification of the molecular dysfunction(s) underlying the development of diabetic nephropathy. The present review will focus on the description of the different cell dysfunctions identified in patients affected by diabetic nephropathy, their pathophysiologic meaning and will try to define an unifying hypothesis that, by linking together the different dysfunctions, will highlight a few areas "at risk", candidate to home the primitive genetic abnormality.
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Cite this article as:
Zerbini Gianpaolo, Gabellini Daniela, Ruggieri Dora and Maestroni Anna, Dysfunction of Cellular Transporters and Predisposition to Diabetic Nephropathy, Current Diabetes Reviews 2006; 2 (2) . https://dx.doi.org/10.2174/157339906776818550
DOI https://dx.doi.org/10.2174/157339906776818550 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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