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目的探讨肾间质微血管病变在关木通致急性肾小管坏死肾间质纤维化中的作用及发生机制。方法取4例关木通致急性肾小管坏死患者(A组)、5例抗生素致急性肾小管坏死患者(B组)、5例非IgA型轻度系膜增生性肾小球肾炎患者(C组)肾活检标本,免疫组化SP法观察肾小管上皮血管内皮生长因子(VEGF)表达及肾小管周围毛细血管(PTC)密度及形态改变,电镜观察微血管内皮细胞和基底膜的结构变化。结果(1)A组PTC数目明显少于B组及C组(P<0.01),并可见管腔扩张变形或缩小、血管壁断裂。(2)A组电镜见PTC内皮细胞肿胀,有胞质空泡、致密颗粒,细胞局部与基底膜分离。基底膜有皱缩及增厚。(3)A组肾小管上皮VEGF表达明显少于B组,但2组VEGF表达均多于C组。(4)A、B组PTC密度与肾小管VEGF表达呈正相关(均r=0.793,P<0.01),与肾小管上皮再生呈正相关(r分别为0.880、0.802,P值均小于0.01)。结论关木通致急性肾小管坏死存在原发性肾间质微血管损伤,肾小管VEGF低表达可能参与了损伤过程。关木通致急性肾小管坏死中的微血管病变可能是肾小管中毒性损伤后修复不良及病变慢性化进展的原因之一。
Objective To investigate the role and mechanism of renal interstitial microangiopathy in renal tubulointerstitial fibrosis induced by Alzheimer’s disease. Methods Four patients with acute tubular necrosis (Group A), five patients with acute tubular necrosis caused by antibiotics (Group B) and five patients with mild non-IgA mesangial proliferative glomerulonephritis (Group C) The renal biopsy specimens and immunohistochemical SP method were used to observe the expression of vascular endothelial growth factor (VEGF) and the density and morphology of renal tubular epithelial cells (PTC). The ultrastructural changes of microvessel endothelial cells and basement membrane were observed by electron microscopy. Results (1) The number of PTC in group A was significantly less than that in group B and C (P <0.01), and the lumen expansion deform or reduced and the vessel wall ruptured. (2) A group of electron microscope see PTC endothelial cell swelling, cytoplasmic vacuoles, dense particles, cells separated from the basement membrane. Basement membrane shrinkage and thickening. (3) The expression of VEGF in group A was less than that in group B, but the expression of VEGF in group 2 was more than that in group C. (4) PTC density in group A and group B was positively correlated with the expression of VEGF (all r = 0.793, P <0.01), and positively correlated with renal tubular epithelial regeneration (r = 0.880,0.802, P <0.01). Conclusions There is primary renal interstitium microvascular injury in acute tubular necrosis and low expression of VEGF in renal tubules may be involved in the injury process. Microencapsulation in acute tubular necrosis may be one of the causes of poor repair and chronic pathological changes after tubulointerstitial injury.