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目的测定肾素、血管紧张素Ⅱ(AngⅡ)在慢性环孢素(CsA)肾病肾移植患者肾组织、血浆中的水平,探讨肾素-血管紧张素系统(RAS)在慢性CsA肾病中的作用。方法 (1) 采用免疫组化、放射免疫和荧光偏振法,测定13例慢性CsA肾病患者肾组织中肾素表达及血浆 AngⅡ、CsA早晨服药后2 h血浓度(C2)水平,并结合临床表现进行分析。(2)体外培养人脐静脉内皮细胞株(HUVEC)、大鼠系膜细胞株(MC),经不同浓度CsA(0、250、500、1000μg／L)孵育细胞后,用免疫组化和放免方法测定肾素的表达及AngⅡ的含量。结果慢性CsA肾病组肾素指数与对照组比较显著增高(P<0．01);血浆AngⅡ、C2水平高于对照组,但无显著性差异 [(122．69±26．73)pg／ml比(121．88±36．35)pg／ml,P=0．977,(719．04±55．89)pg／ml比(658．80± 90．78)pg／ml,P=0．196]。CsA在一定浓度范围内呈剂量依赖刺激HUVEC、MC分泌AngⅡ及上调肾素的表达。结论移植肾活检可避免慢性CsA肾病漏诊或误诊。慢性CsA肾病肾移植患者肾组织局部RAS活化,导致血浆AngⅡ水平与肾组织局部表达不一致。CsA刺激血管内皮细胞、肾小球系膜细胞分泌AngⅡ,上调肾素的表达。阻断RAS可能有益于延缓慢性CsA肾病的进程。
Objective To determine the level of renin and angiotensin Ⅱ (AngⅡ) in renal tissue and plasma of patients with chronic renal transplantation of CsA nephropathy and explore the role of renin-angiotensin system (RAS) in chronic CsA nephropathy . Methods (1) The expression of renin and plasma Ang Ⅱ in renal tissue of 13 patients with chronic CsA nephropathy were measured by immunohistochemistry, radioimmunoassay and fluorescence polarization. The blood concentration (C2) at 2 h after CsA administration in morning was determined. Combined with clinical manifestations Analyze. (2) Human umbilical vein endothelial cell line (HUVEC) and rat mesangial cell line (MC) were cultured in vitro. The cells were incubated with different concentrations of CsA (0,250,500,1000μg / L) Methods Renin expression and Ang Ⅱ content were measured. Results The renin index in chronic CsA nephropathy group was significantly higher than that in control group (P <0.01), and the levels of plasma AngⅡ and C2 were higher than those in control group [(122.69 ± 26.73) pg / ml P (121.88 ± 36.35) pg / ml, P = 0.977, (719.04 ± 55.89) pg / ml ratio (658.80 ± 90.78) pg / ml, P = 0. 196]. CsA stimulated HUVEC in a dose-dependent manner in a certain concentration range, and the secretion of AngⅡ and the up-regulation of renin in MCs were observed. Conclusion Transplant renal biopsy can avoid the misdiagnosis or misdiagnosis of chronic CsA nephropathy. Local RAS activation in renal tissue of patients with chronic CsA nephropathy resulted in inconsistent plasma AngⅡ levels and local expression in renal tissues. CsA stimulated vascular endothelial cells, mesangial cells secrete Ang II, upregulated renin expression. Blocking RAS may be beneficial in delaying the progression of chronic CsA nephropathy.