Open AccessChronic allograft nephropathy: expression and localization of PAI-1 and PPAR-γ
Author(s) -
Mónica P. Revelo,
Charles F. Federspiel,
Harold Helderman,
Agnes B. Fogo
Publication year - 2005
Publication title -
nephrology, dialysis, transplantation/nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfi172
Subject(s) - medicine , glomerulosclerosis , fibrosis , nephropathy , chronic allograft nephropathy , population , diabetic nephropathy , pathology , transplantation , creatinine , renal biopsy , renal function , kidney , endocrinology , kidney transplantation , diabetes mellitus , proteinuria , environmental health
Chronic allograft nephropathy (CAN) is a major cause of loss of renal allografts. Mechanisms postulated to be involved include sequelae of rejection, warm ischaemia time, drug toxicity, ongoing hypertension and dyslipidaemia. Plasminogen activator inhibitor-1 (PAI-1) is implicated not only in thrombosis, but also in fibrosis, by inhibiting matrix degradation, and is expressed in renal parenchymal cells as well as in macrophages. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a member of the steroid receptor superfamily, and plays a major beneficial role in lipid regulation, insulin sensitivity and macrophage function, factors that may play a role in CAN. We therefore studied the expression of these molecules in CAN.