慢性肾脏疾病患者尿SOD排泄变化

Urinary SOD Excretion in Patients with Chronic Renal Disease

为了探讨肾脏超氧化物歧化酶（ＳＯＤ）在慢性肾脏疾病发生、发展中的作用，采用放免方法测定了６０例慢性肾小球疾病患者尿ＳＯＤ的排泄变化，其中慢性肾炎１２例、肾病综合征２６例、轻中度慢性肾衰（Ｃｃｒ＞２０ｍＬ／ｍｉｎ）１０例、重度慢性肾衰（Ｃｃｒ≤２０ｍＬ／ｍｉｎ）１２例。结果发现，四组患者尿ＳＯＤ排泄均高于正常对照组，而肾病综合征组明显高于其它三组；慢性肾炎组明显高于轻、中度和重度慢性肾衰组，而轻、中度慢性肾衰组与重度组无显著差异。血ＳＯＤ除肾病综合征组高于正常对照组外，其它三组与正常对照组无显著差异。未发现尿ＳＯＤ排泄与尿钠、尿蛋白和尿肌酐排泄之间有相关关系。在轻、中度和重度慢性肾衰组，尿ＳＯＤ与Ｃｃｒ的比值显著高于正常对照组和慢性肾炎组，说明残存肾单位产生ＳＯＤ明显增加以清除氧自由基。本文结果提示。

To evaluate the role of renal superoxide dismutases (SOD) in development of chronic renal disease,urinary SOD excretion was measured using radioimmunoassay in 60 patients with chronic glomerular diseases,including 12 patients with chronic glomerulonephritis,26 with nephrotic syndrome in nephrotic stages,10 with mild and moderate chronic renal failure(Ccr>20mL/min) and 12 with severe chronic renal failure(Ccr20mL/min).Urinary SOD excretion in patients of the four groups was significantly increased compared with that in normal controls.Urinary SOD excretion in nephrotic syndrome was more increased than that in other three groups.Urinary SOD and Ccr ratio was highly increased in patients with chronic renal failure.No significant correlation was found between urinary SOD excretion and urinary protein, sodium and creatinine.It was suggested remnant nephrons produce much more SOD to clear free radicals.Although kidney produce more SOD,it can not protect renal tissues from damage by active oxygen.The reaso n might be that SOD could not clear enough active oxygen but on the contray increased the damage by activce oxygen sometimes.