The Clinical And Experimental Study Of The Chronic Ischemic Renal Injury And It's Mechanism

The progressing renal interstitial fibrosis and chronic renal function failure are the common pathway of all kinds of renal diseases coming to the end stage. Chronic renal ischemia is one of the most important factors leading to this pathological phenomenon. The pathogenesis of chronic ischemic renal disease has not been clearly elucidated so far, so the generally accepted diagnostic criteria has not been established. The persistant and nonfatal renal hypoperfusion, local rennin-angiotensin, the cascade of cellular and molecular responses that can lead to renal interstitial fibrosis, focal segmental glomerular sclerosis, tubular epithelial injury and tubular epithelial transformation may be the important pathogenesis of chronic ischemic renal disease.In this article, we have studied the morphologic alteration in 60 samples from the patients with chronic renal diseases and in the tissues of Goldblatt animal model that has a unilateral renal artery stenosis, after 60 days from the stenosis, observed the transformation of tubular epithelial and interstitial cell within the patients and animal model by the method of immunohistochemistry. finally, we analyzed these results by statistics. We concluded that:1 The arterilole stenosis and interstitial inflammation is an important agent that cause the tubule atrophy.2 The interstitial fibrosis may be result from the congenerous actions of arteriole stenosis, interstitial inflammation, and tubule atrophy.3 The degree of interstitial fibrosis has a significant positive correlation with the expression of a -SMA and vimentin.4 The phenotype transdifferentiations from tubular epithelial cell to interstitial cell (expression of viraentin and/or a -SMA) surrounding the atrophied tubues suggest that tubular epithelial cell may directly or indirectly play a role in the pathogenesis of interstitial fibrosis.5 The findings from animal model that the injured tubular epithelial cell expressed vimentin confirmed that ischemia can injure the tubule.6 The mechanism of chronic ischemic renal disease is likely to be that ischemic tubule injury leads to the interstitial fibrosis and inflammation.7 The expression of vimentin and a -SMA may be an useful indicator that predicate the degree of renal interstitial injury in chronic ischemic renal disease.