What is it about?
Methods: Insulin, proinsulin, adiponectin, malondialdehyde, and hsCRP were measured by conventional techniques in 14 previous kidney donors and 25 healthy volunteers. Results: Estimated GFR from Cockcroft-Gault formula of 76.42 ± 19.39 ml/min/1.73 m2 in the nephrectomized group was significantly lower (p < 0.01) than that in the control group of 125 ± 32.9 ml/min/1.73 m2. Fasting serum insulin of 16.57 ± 16.86 mU/l and homeostasis model assessment of insulin resistance (HOMA-IR) of 4.86 ± 5.11 in the nephrectomized group were significantly higher (p < 0.01) than the insulin level of 6.02 ± 4.06 mU/l and HOMA-IR of 1.5 ± 1.06 in the control group. There was no significant difference in levels in inflammatory mediators between the two groups. None of the tested inflammatory mediators correlated significantly with IR.
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Why is it important?
In chronic kidney disease the contribution of decreased glomerular filtration rate (GFR) versus enhanced inflammation to cause insulin resistance (IR) is controversial. Aim: This pilot observational study examines, therefore, the prevalence of IR after kidney donation and factors that may determine its level.
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This page is a summary of: Susceptibility to Insulin Resistance after Kidney Donation: A Pilot Observational Study, American Journal of Nephrology, January 2009, Karger Publishers,
DOI: 10.1159/000232577.
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