Serial Studies On Kidney Disease With C4d By Immunohistochemical Staining

【Objective】1. The deposition of C4d in common kidney disease of 11 species and humoralrejection of renal transplantation (RT-HR) was studied to found out the diagnosisbetween the humoral rejection of renal transplantation and nephropathy relapse..2. The deposition of C4d in HBV-N of different types contrast to that in primaryglomerulonephritis, and the relationship between the deposition of HBsAg, HBcAgand C4d were investigated to explore the pathopoiesis of HBV-Ag to HBV-N ofdifferent type.3. The deposition of C4d in FSGS of different types was studied to explore thepathopoiesis of humoral-mediated immunity to FSGS.【Methods】1. C4d immunohistologic staining for biopsies of the humoral rejection of renaltransplantation, FSGS of different types, HBV-N and other common kidney diseases,HBsAg and HBcAg immunohistologic staining for HBV-N biopsies, observingpositive stain distributed in nephridial tissue including Glomemlar mesangium (GM),glomerular capillary(GC), vasa recta(VR) in the inner stripe of the outer medulla andrecord the extent and intensity of positive stain.2. Serial sections and CD34 and CK7 immunohistologic staining carried out inbiopsies of respectively 5 cases from different types HBV-N so that making locationfor depositionin precise; IgA/C4d and IgM/C4d double immunohistochemisticalstaining for 10 cases of IgAN and FSGS to observe the distribution of IgA and IgMcontrast to C4d.3. PASM-C4d double stain for 25 cases of FSGS to ensure the relationship between the deposition C4d and basement membrane.【Results】1. The deposition of C4d was presented with the shape of fine grain and falseline in the endothelial cell of the RT-HR' glomerular, and respectively granules,girdle and false line in the vicinity of glomerular basement membrane of othernephritis; It was presented with the shape of encircling renal tubule because of C4ddeposited in both narrow and broad interstitium and the shape of flower because ofC4d deposited in endothelial cellular swelling of tiny arteriola, which phenomenondidn't occur in other common nephritis. Compared to other groups, there was thehighest average scores of positive intensity significantly (P＜0.01).2. There was some deposition of HBsAg and HBcAg to some extent inglomerular mesangium, blood capillary, the distal tubule of juxtaglomerular apparatus,the arteriole of interstitial substance, the wall of straight vessels and the capillary wallbetween tubule. Statistics analysis indicated the deposition of C4d correlated withHBsAg (P＜0.05) in GM and VR and correlated with HBcAg respectively in GC,GM and VR (P＜0.01). By serial sections, we observe the deposition position of C4dconformity to HBsAg and HBcAg. The average scores of positive intensity ofHBV-IgAN and HBV-MSPGN was higher significantly than the same group PGN(P＜0.05), there were no statistical significance among other groups.3. In FSGS, the deposition of C4d was presented with line-form in basalmembrane of glomerular sclerosis. The stain of PASM—C4d show the deposition ofC4d overlapped with staining of basal membrane of glomerular sclerosis. In cellularvariant, collapsing variant and classic type FSGS, the average scores of positiveintensity of C4d deposition in GC was higher significantly than GM of (P＜0.05);inperihilar variant FSGS, GM was higher significantly than GC of (P＜0.05); there wereno statistical significance between GC and GM of tip variant FSGS.【Conclusion】1. The morphological difference of the deposition of C4d in glomerulus, PTCand vasa recta between RT-HR and other common nephritis was important to thedifferential diagnosis between RT-HR and nephropathy relapse.2. In HBV-N, the deposition of HBsAg and HBcAg resulted in the damage to notonly glomerulus but nephric tubule and interstitium.There was obviously different pathogenesis between HBV-IgAN and IgAN, so it was necessary to distinguish thetwo on diagnosis and treatment.3. The segment sclerosis of glomerulus maybe result from the formation ofbasement membrane antibody and antigen-antibody complex in situ damage to basalmembrane, and pathological changes of foot cells maybe occurred after the damage tobasal membrane. There were the same pathogenesy in tip variant, cellular variant,collapsing variant and classic type FSGS, but there were different pathogenesybetween perihilar variant FSGS and other variant FSGS.