Mediatorsof Immune Glomerular Injury and Epithelial Cell Injury. A, Mediators of immuneglomerular injury, including effectorcells,molecules, and cells affected or injured. B, Visceral epithelial cell(podocyte) injury. The postulated sequence is a consequence of antibodiesagainst epithelial cell antigens, arriving in thecirculating blood (1) with subsequent activation of effector cells, includingpodocytes and mesangial cells (2). This leads to liberation of toxins,cytokines, or other effector molecules (3) that cause injury of podocytes,podocyte foot processes, and endothelial cells (4) with subsequent cell detachment, resulting inprotein leakage through the defective glomerular basement membrane andfiltration slits.
Antibody-MediatedGlomerular Injury. A,Normal structure of the glomerulus. Antibody-mediated glomerular injury canresult either from the deposition of circulating immunecomplexes (B) or from formation of complexes in situ (C and D). Usingimmunofluorescence microscopy (not shownhere),antiglomerularbasement membrane (anti-GBM) disease (C) and antiglomerular(visceral epithelial cell) disease (D) are characterized by linear patternsofimmunofluorescence deposition in glomeruli, whereas deposition of circulatingimmune complexes in glomeruli is characterized by granular (“lumpy-bumpy”)patterns
免疫介导的肾小球肾炎分类
•膜性肾小球肾炎 membranous glomerulonephritis
–Ig沉积在肾小球毛细血管基底膜，导致肾小球毛细血管基底膜弥漫性增厚
–PAS染色阳性、轻度纤维化
•膜增生性肾小球肾炎
membranoproliferative glomerulonephritis
–细胞增生（内膜细胞、上皮细胞、系膜细胞、炎症细胞）、基膜增厚
–增生性肾小球肾炎（如图）：细胞增生＞基膜增厚（犬）
–肾小球新月体
A. 增生性肾小球肾炎，猪。病变的特点主要是肾小球系膜细胞的增生B. 膜性肾小球肾炎，犬。病变特点是肾小球毛细血管基底膜的玻璃样增厚C. 膜增生性肾小球肾炎，马。膜增生性肾小球肾炎有明显增生性肾小球肾炎和膜性肾小球肾炎的病理特点。大量的球旁纤维围绕细胞增生（系膜细胞）的肾小球。系膜基质在肾小球右上角区域较为明显D. 肾小球硬化症，犬。由于纤维结缔组织和系膜基质的增加，导致细胞减少、收缩和透明变性，肾小球毛细血管几乎完全消失。当肾小球硬化时（慢性肾小球肾炎终末期），肾小球基本上丧失其功能。
