STUDY OF SOME MARKERS OF PROGRESSION IN SCHISTOSOMAL NEPHROPATHY

Abstract

In Egypt, the incidence of schistosomiasis in one village in the Nile delta was 74 %, with renal affection in 12-15% of cases. Tissue fibrosis is a series of dynamic interactive processes to effect nmmal repair of injured tissue. Renal fibrosis is characterized by a progressive loss of specialized renal parenchymal cells with a disturbance of the delicate balance regulating extra-cellular matrix (ECM) production towards the accumulation of excessive fibrous tissue. A better understanding of the mechanisms involved in the process of renal fibrosis, the fmal common pathway of all advanced forms of renal pathology, is a valuable aid in the development of strategies of hampering this progressive deterioration of renal stmcture and function. The validity of markers of fibroblasts differentiation (Alpha smooth muscle actin I aSMA and Vimentin) in renal fibrosis in some experimental and clinical models have been recently highlighted. A role for Mast cells (MC) (that have been implicated in the pathogenesis of atherosclerosis and tissue fibrosis) in the development of renal fibrosis has not been fully elucidated. Stem cell factor (SCF) (the ligand for MC c-kit receptor) is thought to attract and activate MC. Studies in experimental models of renal scruTing demonstrated that tissue transglutaminase (tTg) may be a key enzyme involved in the accumulation of ext:ra-cellulru• matrix, through the fonnation of c(y-glutamyl) lysine di-peptide bonds leading to increased ECM deposition and resistance breakdown. The previously mentioned markers/mediators where investigated in an attempt to detennine their possible role in progression of schistosoma.! associated neplrropathy in compru•ison with other fmms of secondruy glomerulonephritis.