| PrefaceChronic interstitial nephritis (CIN) is a major cause of end -stage renal failure. More and more studies have demonstrated that the degree of tubulointerstitial injury rather than the extent of glomerular involvement determines the final outcome. The pathologic characteristics of chronic interstitial nephritis are renal interstitial fibrosis(RIF) , tubular atrophy, inflammatory cells infiltration and glomerulosclerosis. Fibrogenesis can be divided into three phrases. The first phrase of fi-brogenesis is the induction phrase , in which renal tubular epithelial cells receive different stimulations, they activate and release all kinds of cytokines and inflammatory media, various inflammatory cells infiltrate , among which macrophrages (CD68 + cells) play an important role for their infiltration on the renal tubular epitheliums and tubular basement membranes. In 1994 France et al verified that activated macrophage can secret transforming growth factor beta (TGF-1), basic fibroblast growth factor ( bFGF) , platelet - derived growth factor (PDGF) which can promote fibroblasts proliferation and extracellular matrix (ECM) synthesis and then lead to the progression of renal interstitial fibrosis. In 2001 Yang Li et al observed that the infiltration of macrophages was close negatively correlated with the level of serumcreatinine in the phenotypic characteristics of infiltrated inflammatory cells, renal tubular epithelial cells and interstitial cells in human drug -associated interstitial nephritis.With the deep research of the mechanisms of RIF, people gradually notice that microcirculation injury and various microthrombus in the GIN may be an critical facor in RIF. In 2000 Choi et al proposed that human chronic interstitial diseases, regardless of the initial cause, all exist peri - tubular microcirculation injury. vWF is an important adhering protein synthesized by endothelial cells and megakaryocytes. When vascular endothelial cells injure, vWF may mediate platelet to adhere to the exposing extracellular matrix and initiate coagulation mechanism to form thrombosis, causing microcirculation impairment. The role of vWF antigen in the microcirculation impartment in the GIN has not been reported and calls for investigation.To study the role of macrophage and vWF in the progression of GIN, we detect the expression of macrophage and vWF in renal biopsies of GIN patients by immunohistochemistory two stages method.Materials and Methods30 patients with GIN in trail group admitted to the Department of Nephrology First Affilicated Hospital of China Medical University from Dem 2000 to Aug 2002, 15 cases were diagnosed as aristolochic acid nephropathy (AAN) , 6 analgesic nephropathy (AN) , 4 chronic pyelonephritis (CPN) , 2 Grout, 3 obstructive nephropathy. All patients have performed renal biopsies and the pathologic diagnosis is GIN by light and electron microscope. Macrophage and vWF expression in renal biopsies were detected by immunohistochemistry two stages meth-od. We detect serum creatinine in the same patients before renal biopsies and calculate endogenous creatinine clearance rate ( Ccr) according to standard formula.Results1. The amounts of CD68 + cells in renal biopsies of the GIN patients in trial group were significantly higher than that in the control group (p<0.01)2. The expression of vWF in renal biopsies of the GIN patients in trial group were remarkedly higher than that in the control group ( p < 0.001).3. There is a significant negative correlation between the amount of CD68 + cells in biopsies of the GIN patients in trial group and endogenous creatinine clearance rate (Ccr)4. There is a strong negative correlation between the expression of vWF in biopsies of the GIN patients in trial group and endogenous creatinine clearance rate (Ccr)DiscussionRecent studies about the injury of different kinds of renal tubular interstitial by animal models have found that macrophages have more correlation with RIF. The first phase of fibrogenesis is induction...
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