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目的 :探讨糖皮质激素 (GC)对肾脏的远期不利作用及其机制。方法 :将 60例难治性肾病随机分为A (长期激素 )、B(非长期激素 )两组 ,按治疗结果的不同将B组分为B1与B2 组 ,用放免法检测血尿皮质醇并结合尿蛋白 (UP)与肌酐清除率 (Ccr)等分析。结果 :治疗后B组中有 10例出现应激因素 (B1组 ) ,其血尿皮质醇浓度显著高于无应激因素的B2 ( 2 0例 )组 (P <0 .0 1) ,A +B1组UP明显高于B2 组 (P <0 .0 0 1) ,并以大分子蛋白增高为主 ,Ccr明显低于B2 组 (P <0 .0 0 1) ;B1组血、尿皮质醇与UP呈正相关 (r =0 .6968与 0 .85 3 2 ,P <0 .0 5与P <0 .0 0 1) ;当Ccr≥ 40ml/min时 ,A +B1组UP与Ccr呈正相关 (r =0 .75 91,P <0 .0 0 1) ,当Ccr <40ml/min时 ,UP与Ccr呈负相关 (r =-0 .783 6,P <0 .0 0 1)。结论 :体内外GC可加重难治性肾病UP的排泄 ,它可能改变肾小球基底膜的静电屏障 ,通过高灌注作用促进肾小球的硬化。
Objective: To investigate the long-term adverse effects of glucocorticoid (GC) on the kidney and its mechanism. Methods: Sixty cases of refractory nephropathy were randomly divided into two groups: A (long-term hormone) and B (non-long-term hormone). The patients in group B were divided into B1 and B2 groups according to the results of treatment. Combination of urinary protein (UP) and creatinine clearance (Ccr) analysis. Results: After treatment, 10 patients in group B had stress factors (group B1). The serum and urine cortisol concentrations in group B were significantly higher than those in group B2 without stress (P0.01) The level of UP in group B1 was significantly higher than that in group B2 (P <0.01). The increase of macromolecular protein was the main factor, and the level of Ccr in group B1 was significantly lower than that in group B2 (P0.01) Was positively correlated with UP (r = 0.6968 vs 0.8532, P <0.05 and P <0.001); when Ccr≥40ml / min, UP and Ccr were positively correlated in group A + B1 (r = 0.7591, P <0.001). When Ccr <40ml / min, UP was negatively correlated with Ccr (r = -0.7383, P <0.01). CONCLUSION: GC excretion of UP in refractory nephropathy in vitro and in vivo may change the electrostatic barrier of glomerular basement membrane and promote the glomerular sclerosis through hyperperfusion.