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目的探讨罗格列酮对环孢素A(Cyclosporine,CsA)早期肾损伤的保护作用。方法选择2013年1月至2014年5月在郑州大学第一附属医院和南阳市中心医院经肾活检确诊的膜性肾病患者61例,采用随机数字表法分为对照组和罗格列酮干预组(干预组)。对照组30例,服用常规量激素泼尼松1 mg·kg~(-1)·d~(-1),环孢素胶囊2~3 mg·kg~(-1)·d~(-1);干预组31例,在对照组基础上服用罗格列酮片4 mg/d。分别在服用罗格列酮前、服用后第3、6个月时检测患者动脉压、组织型金属蛋白酶抑制剂1(tissue inhibitor of metallo-proteinase-1,TIMP-1)、尿胆微球白蛋白(β2-microspheres,β2-MG)、禁水12 h尿渗透压数值。结果与治疗前比较,对照组和干预组治疗后第3个月的血清TIMP-1分别为(248.1±48.6)ng/ml和(179.4±38.2)ng/ml,尿β2-MG分别为(253.2±39.7)μg/L和(190.8±35.4)μg/L,动脉压分别为(115.8±10.3)mm Hg和(101.5±8.7)mm Hg,2组均较治疗前升高(P<0.05);治疗后第3个月时,对照组和干预组禁水12 h尿渗透压分别为(542.6±79.3)mosm/L和(615.4±68.7)mosm/L,2组均较治疗前下降(P<0.05)。治疗后第6个月时,对照组和干预组血清了IMP-1分别为(401.3±52.1)ng/ml和(212.7±43.6)ng/ml,尿β2-MG分别为(382.7±41.2)μg/L和(221.3±36.7)μg/L,2组均高于治疗后第3个月(P<0.05),呈时间依赖性。治疗后第6个月时,对照组和干预组动脉压分别为(128.6±8.9)mm Hg和(114.4±12.6)mm Hg,均高于治疗后第3个月(P<0.05);治疗后第6个月时,对照组和干预组禁水12 h尿渗透压分别为(461.3±62.7)mosm/L和(531.2±72.6)mosm/L,均低于治疗后第3个月(P<0.05)。干预组与同时间段的对照组比较,血清了IMP-1、尿β2-MG和动脉压均低于对照组(P<0.05),禁水12 h尿渗透压高于对照组(P<0.05)。结论 CsA能够上调肾病综合征患者血清TIMP-1和尿β2-MG表达,使患者动脉压升高,禁水12 h尿渗透压下降。罗格列酮可以明显降低CsA诱导的血清了IMP-1和尿β2-MG的表达,改善CsA导致的动脉压升高和尿渗透压下降,减少CsA导致的患者高血压和肾脏间质小管纤维化的风险。
Objective To investigate the protective effect of rosiglitazone on early renal injury induced by cyclosporine A (CsA). Methods Sixty-one patients with membranous nephropathy diagnosed by renal biopsy in the First Affiliated Hospital of Zhengzhou University and Central Hospital of Nanyang from January 2013 to May 2014 were randomly divided into control group and rosiglitazone intervention Group (intervention group). The control group received 30 mg · kg -1 d · g -1 of conventional hormones prednisone and 2 ~ 3 mg · kg -1 d -1 of cyclosporine capsules ); Intervention group of 31 patients, taking rosiglitazone tablets 4 mg / d on the basis of the control group. The arterial pressure, tissue inhibitor of metallo-proteinase-1 (TIMP-1), urinary bladder microsphere white Protein (β2-microspheres, β2-MG), water for 12 h urine osmolality values. Results Compared with those before treatment, the levels of TIMP-1 in the control group and the intervention group were (248.1 ± 48.6) ng / ml and (179.4 ± 38.2) ng / ml, respectively, and urinary β2-MG were The arterial pressures were (115.8 ± 10.3) mm Hg and (101.5 ± 8.7) mm Hg, respectively, both of which were significantly higher than those before treatment (P <0.05). At the third month after treatment, the urine osmotic pressure of the control group and the intervention group for 12 h were (542.6 ± 79.3) mosm / L and (615.4 ± 68.7) mosm / L, respectively, 0.05). At the 6th month after treatment, the levels of IMP-1 in the control group and the intervention group were (401.3 ± 52.1) ng / ml and (212.7 ± 43.6) ng / ml, respectively, and the urinary β2-MG values were (382.7 ± 41.2) / L and (221.3 ± 36.7) μg / L, respectively. Both groups were higher than the third month after treatment (P <0.05) in a time-dependent manner. At 6 months after treatment, arterial pressure was (128.6 ± 8.9) mm Hg and (114.4 ± 12.6) mm Hg in the control and intervention groups, respectively, which were higher than those in the 3rd month after treatment (P <0.05) At 6 months, the urine osmolality of the control group and the intervention group for 12 h were (461.3 ± 62.7) mosm / L and (531.2 ± 72.6) mosm / L, respectively, both of which were lower than the 3rd month after treatment (P < 0.05). Compared with the control group, the levels of IMP-1, β2-MG and arterial pressure in the intervention group were lower than those in the control group (P <0.05) ). Conclusions CsA can up-regulate the expression of TIMP-1 and β2-MG in patients with nephrotic syndrome, and increase the arterial pressure and reduce the urine osmolality for 12 hours. Rosiglitazone significantly decreased CsA-induced serum expression of IMP-1 and urinary β2-MG, improved arterial pressure induced by CsA and decreased osmotic pressure, and decreased CsA-induced hypertension and renal interstitial fibrosis The risk of change.