32 research outputs found
Molecular genetic approaches for studying the etiology of diabetic nephropathy
10.2174/1566524054553504Current Molecular Medicine55509-525CMMU
Identification of a common risk haplotype for diabetic nephropathy at the protein kinase C-β1 (PRKCB1) gene locus
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
10.1093/ndt/gfm946Nephrology Dialysis Transplantation2372260-2264NDTR
A disease haplotype for advanced nephropathy in type 2 diabetes at the ACE locus
10.2337/db06-0496Diabetes5592660-2663DIAE
To: Rippin JD, Patel A, Belyaev ND, Gill GV, Barnett AH, Bain SC (2003) Nitric oxide synthase gene polymorphisms and diabetic nephropathy. Diabetologia 46:426-428 [1] (multiple letters)
10.1007/s00125-003-1229-yDiabetologia46121706-1708DBTG
A genome-wide linkage scan for genes controlling variation in urinary albumin excretion in type II diabetes
10.1038/sj.ki.5000023Kidney International691129-136KDYI
Genome-Wide Association Study of Diabetic Kidney Disease Highlights Biology Involved in Glomerular Basement Membrane Collagen
Effect of irbesartan on streptozotocin induced diabetic nephropathy: An interventionary study
A signature of circulating inflammatory proteins and development of end-stage renal disease in diabetes
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