32 research outputs found

    Molecular genetic approaches for studying the etiology of diabetic nephropathy

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    10.2174/1566524054553504Current Molecular Medicine55509-525CMMU

    Identification of a common risk haplotype for diabetic nephropathy at the protein kinase C-β1 (PRKCB1) gene locus

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    10.1097/01.ASN.0000077347.27669.5CJournal of the American Society of Nephrology1482015-2024JASN

    Genetic variation at the SLC12A3 locus is unlikely to explain risk for advanced diabetic nephropathy in Caucasians with type 2 diabetes

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    10.1093/ndt/gfm946Nephrology Dialysis Transplantation2372260-2264NDTR

    A disease haplotype for advanced nephropathy in type 2 diabetes at the ACE locus

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    10.2337/db06-0496Diabetes5592660-2663DIAE

    A signature of circulating inflammatory proteins and development of end-stage renal disease in diabetes

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    Chronic inflammation is postulated to be involved in the development of end-stage renal disease in diabetes, but which specific circulating inflammatory proteins contribute to this risk remain unknown. To study this, we examined 194 circulating inflammatory proteins in subjects from three independent cohorts with type 1 and type 2 diabetes. In each cohort, we identified an extremely robust kidney risk inflammatory signature (KRIS), consisting of 17 proteins enriched in tumor necrosis factor-receptor superfamily members, that was associated with a 10-year risk of end-stage renal disease. All these proteins had a systemic, non-kidney source. Our prospective study findings provide strong evidence that KRIS proteins contribute to the inflammatory process underlying end-stage renal disease development in both types of diabetes. These proteins point to new therapeutic targets and new prognostic tests to identify subjects at risk of end-stage renal disease, as well as biomarkers to measure responses to treatment of diabetic kidney disease
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