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Vol. 26, No. 3, 2006
Issue release date: July 2006
Section title: In-Depth Topic Review
Am J Nephrol 2006;26:232–244
(DOI:10.1159/000093632)

Insulin Resistance, Hyperinsulinemia, and Renal Injury: Mechanisms and Implications

Sarafidis P.A. · Ruilope L.M.
aHypertension/Clinical Research Center, Department of Preventive Medicine, Rush University Medical Center, Chicago, Ill., USA; bHypertension Unit, Hospital 12 de Octubre, Madrid, Spain

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Article / Publication Details

First-Page Preview
Abstract of In-Depth Topic Review

Received: 4/24/2006
Accepted: 4/24/2006
Published online: 7/19/2006

Number of Print Pages: 13
Number of Figures: 2
Number of Tables: 0

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN

Abstract

Most of the basic components of the metabolic syndrome, namely type 2 diabetes mellitus, hypertension, obesity, or low high-density lipoprotein cholesterol levels, apart from being major risk factors for cardiovascular disease have been also associated with an increased risk of chronic kidney disease. However, several epidemiologic studies conducted over the past years suggest that the central component of the syndrome, insulin resistance, as well as compensatory hyperinsulinemia are independently associated with an increased prevalence of chronic kidney disease. In addition, background studies support the existence of several pathways linking insulin resistance and hyperinsulinemia with kidney damage. Insulin per se promotes the proliferation of renal cells and stimulates the production of other important growth factors such as insulin-like growth factor-1 and transforming growth factor beta. Insulin also upregulates the expression of angiotensin II type 1 receptor in mesangial cells, thus enhancing the deleterious effects of angiotensin II in the kidney, and stimulates production and renal action of endothelin-1. Moreover, insulin resistance and hyperinsulinemia are associated with decreased endothelial production of nitric oxide and increased oxidative stress which have been also implicated in the progression of diabetic nephropathy. This review analyzes the above and other potential mechanisms, through which insulin resistance and hyperinsulinemia can contribute to renal injury.


Article / Publication Details

First-Page Preview
Abstract of In-Depth Topic Review

Received: 4/24/2006
Accepted: 4/24/2006
Published online: 7/19/2006

Number of Print Pages: 13
Number of Figures: 2
Number of Tables: 0

ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)

For additional information: http://www.karger.com/AJN


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