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梗阻性肾病的病理特征为肾小管萎缩、肾小管间质纤维化、间质炎性细胞浸润、血管稀疏。从细胞层面来讲,肾脏自身的细胞和骨髓来源的细胞共同作用参与了肾脏损伤的发生和发展。输尿管梗阻后,炎性介质促进骨髓单核细胞浸润肾脏间质。肾间质巨噬细胞源于骨髓髓系干细胞,在多种趋化因子作用下浸润到肾间质,在间质微环境中分化为M1和M2巨噬细胞。多项体内外实验表明,巨噬细胞能加重或缓解肾脏间质纤维化,能诱导肾小管上皮细胞凋亡,同时损伤小管周围毛细血管并造成血管稀疏。
The pathological features of obstructive nephropathy are tubular atrophy, tubulointerstitial fibrosis, interstitial inflammatory cell infiltration, and sparse blood vessels. From the cellular level, the kidney’s own cells and bone marrow-derived cells are involved in the occurrence and development of kidney damage. After ureteral obstruction, inflammatory mediators promote the infiltration of bone marrow mononuclear cells into the renal interstitium. Renal interstitial macrophages originate from bone marrow myeloid stem cells and infiltrate the renal interstitium under the action of various chemokines and differentiate into M1 and M2 macrophages in the interstitial microenvironment. A number of in vitro and in vivo experiments showed that macrophages can aggravate or alleviate renal interstitial fibrosis, induce apoptosis of renal tubular epithelial cells, damage the capillaries around the tubules and cause sparse blood vessels.