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目的 探讨肾缺血再灌注损伤与IGF 1表达的关系。方法 实验组采用RIA法研究 6 0只大鼠缺血再灌注损伤的肾组织IGF 1表达。临床组 :采用免疫组化SP法研究 2 0例肾移植病人移植肾组织中IGF 1表达。结果 实验组 :肾缺血再灌注损伤后 2 4h出现肾小管上皮细胞肿胀 ,肾小球及肾间质炎性细胞浸润。IGF 1呈阳性表达 (0 0 5 1± 0 0 1)ng mg ,术后 7d达高峰 (0 11± 0 0 1)ng mg ,与对照组比较P <0 0 5 ,肾组织学及IGF 1在 2周后恢复正常。临床组 :肾移植后 2 4hIGF 1呈阳性表达 ,AOD值为(0 31± 0 0 7) ,术后 7d达高峰 (0 5 0± 0 0 7) ,P <0 0 5 ,10～ 14d后逐渐下降至正常。术后发生CR3例 ,IGF 1升高达 (0 76± 0 0 7) ,P <0 0 5 ,而ATN6例中 ,IGF 1为 (0 5 6± 0 10 ) ,P <0 0 5。随着排斥控制 ,肾功能恢复IGF 1逐渐恢复正常。结论 移植肾缺血再灌注损伤不可避免会出现IGF 1表达。排斥反应时IGF表达明显高于ATN及正常肾组织。肾缺血再灌注损伤作为非免疫因素与免疫因素损伤相互协同 ,共同促进移植肾功能损害。
Objective To investigate the relationship between renal ischemia-reperfusion injury and IGF-1 expression. Methods The experimental group used RIA to study the expression of IGF-1 in the kidney of 60 rats with ischemia-reperfusion injury. Clinical group: Immunohistochemical SP method was used to investigate the expression of IGF-1 in renal transplant recipients of 20 renal transplant recipients. Results Experimental group: tubulointerstitial cell swelling, glomerular and interstitial infiltration of inflammatory cells occurred at 24 h after renal ischemia-reperfusion injury. The positive expression of IGF1 was (0 051 ± 0 0 1) ng mg and reached the peak at 7 days after operation (0 11 ± 0 0 1) ng mg, compared with the control group, P <0 05, renal histology and IGF 1 Returned to normal after 2 weeks. In the clinical group, the positive expression of IGF-1 was detected at 24 hours after renal transplantation, the AOD value was (0 31 ± 0 0 7) and reached the peak at 7d after operation (P 0 05, P 10 05) Gradually dropped to normal. There were CR3 cases and IGF1 up to (0 76 ± 0 0 7) P <0 05 after operation. In ATN 6 cases IGF 1 was (56 ± 0 10) P <0 05. With rejection control, recovery of renal function IGF 1 gradually returned to normal. Conclusion IGF-1 expression is inevitable in transplanted renal ischemia-reperfusion injury. Exclusion reaction IGF expression was significantly higher than ATN and normal kidney tissue. Renal ischemia-reperfusion injury as a non-immune and immune factors damage mutual cooperation, together to promote renal graft damage.