Abstract
Chronic allograft nephropathy (CAN) includes pathologic changes of interstitial fibrosis, tubular atrophy, and fibrous intimal thickening. Transforming growth factor (TGF)-β1 is a fibrogenic cytokine involved in renal allograft fibrosis. Hypoxia-inducible factor (HIF)-1α is induced as an adaptive response to hypoxia triggering the production of fibrogenic cytokines such as TGF-β1. Between January 1995 and February 2005, we performed 71 renal allograft biopsies in 61 recipients. Immunohistochemical studies were performed with an immunoperoxidase technique using as the primary antibody either a rabbit anti-human TGF-β1 polyclonal or a mouse anti-human HIF-1α monoclonal reagent. The glomerular TGF-β1 expression in recipients diagnosed with glomerulonephritis was significantly greater than other pathologic groups ( P < .05), and the glomerular TGF-β1 expression in the heavy proteinuria group (≥2.5 g/d) was significantly greater than the low proteinuria group (<1.0 g/d; P < .05). The tubular and interstitial TGF-β1 and HIF-1α expressions in CAN were greater than in other groups ( P < .05). The tubular TGF-β1 expression among the graft loss group was significantly greater than the graft function group ( P < .05).
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