Abstract
CHRONIC TRANSPLANT NEPHROPATHY (CTN) of renal allografts is distinguished histologically by vascular fibrointimal thickening, tubular atrophy, interstitial fibrosis, chronic transplant glomerulopathy, and altered composition and quantity of extracellular matrix (ECM) proteins. It has been suggested that certain cytokines, such as transforming growth factor beta-1 (TGF-b1), which promotes graft fibrosis, play significant roles in the CTN process. Changes in circulating TGF-b1 occur in humans after renal transplantation, but levels are no higher in patients with CTN than in those who have acute rejection (AR) or stable graft function (STx). TGF-b1 is known to promote the production of ECM components by upregulating inhibitors of degradation or downregulating promoters of ECM degradation. Tissue matrix metalloproteinases (MMP) are a family of homologous proteinases that plays an important role in the turnover of ECM components. Excessive or inappropriate expression of MMP is known to contribute to the pathogenesis of several processes, such as rheumatoid arthritis, cardiovascular disease, or tumor progression. Also, reports have shown the involvement of MMP in renal pathology, as a contributors to interstitial fibrosis and abnormal glomerular matrix turnover. To date, there has been no investigation of the role of circulating MMP in kidney transplantation, or of its relationship with TGF-b1. With this study we determined and analyzed the serum levels of MMP-1, MMP-2, MMP-3, and TGF-b1 levels in kidney transplant recipients with STx, CTN, and AR.
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