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目的 :探讨血管紧张素转换酶 (ACE)基因插入 /缺失 (I/D)多态性、血管紧张素Ⅱ 1型受体 (AT1R)基因A116 6 /C多态性和血管紧张素原 (AGT)基因M2 35T多态性是否影响血管紧张素Ⅱ 1型受体阻断剂 (ARB)治疗IgA肾病 (IgAN)患者尿蛋白的疗效。 方法 :6 4例原发性IgAN患者 ,符合以下条件 :尿蛋白 1～ 3 5g/d ,尿RBC <5 0 0万 /ml,SCr<133μmol/L ,血清白蛋白 >30g/L ;肾活检示肾小球系膜增生性病变或局灶节段性肾小球硬化 ,无新月体及袢坏死 ,小管间质病变轻。治疗方法 :口服缬沙坦 80mg/d 8周。PCR法检测ACE基因I/D多态性、AT1R基因A116 6 /C多态性和AGT基因M2 35T多态性。比较不同基因型患者治疗前后尿蛋白、血压及肾功能变化。 结果 :缬沙坦治疗 8周后 ,患者血压由 (119± 8 10 ) / (78 7± 8 71)mmHg降至 (113± 13 5 ) / (73 0± 10 7)mmHg ,尿蛋白由 (2 0 8± 0 72 )g/d降至 (1 5 8± 0 70 )g/d ,血清白蛋白相应上升 ,但血肌酐及肌酐清除率无明显变化。本试验未观察到AT1R基因型为CC型者。AT1R基因AA型、AC型患者尿蛋白较治疗前分别下降了 (2 4 5± 2 0 1) %,(2 8 5±2 0 0 ) %;ACE基因II型、DI型、DD型患者尿蛋白分别下降了 (2 7 5± 18 4 ) %,(2 3 8± 2 2 6 ) %,(2 2 4± 12 6 ) %;AGT基
Objective: To investigate the association of angiotensin converting enzyme (ACE) gene insertion / deletion (I / D) polymorphism, AT1R gene A116 6 / C polymorphism and angiotensinogen ) Gene M235T polymorphism affects the efficacy of angiotensin Ⅱ type 1 receptor blocker (ARB) in the treatment of urinary protein in IgA nephropathy patients. Methods: Totally 64 primary IgAN patients were enrolled in this study. The following conditions were fulfilled: urinary protein 1 ~ 35g / d, urine RBC <50 million / ml, SCr <133μmol / L and serum albumin> 30g / Shows mesangial proliferative lesions or focal segmental glomerulosclerosis, no crescent and necrosis, tubulointerstitial lesions. Treatment: oral valsartan 80mg / d for 8 weeks. The ACE gene I / D polymorphism, AT1R gene A116 6 / C polymorphism and AGT gene M235T polymorphism were detected by PCR. Urine protein, blood pressure and renal function changes in different genotypes before and after treatment were compared. Results: After 8 weeks of valsartan treatment, the blood pressure decreased from (119 ± 8 10) / (78 7 ± 8 71) mmHg to (113 ± 13 5) / (73 0 ± 10 7) mmHg, 2 08 ± 0 72) g / d to (1 58 ± 0 70) g / d, serum albumin increased accordingly, but the serum creatinine and creatinine clearance rate did not change significantly. No AT1R genotype was observed in this study. The proteinuria of AT1R gene type AA and AC patients decreased by (2 45 ± 2 0 1)% and (28 5 ± 2 0 0)% respectively before treatment; (2 7 5 ± 18 4)%, (2 3 8 ± 2 2 6)%, (2 2 4 ± 12 6)%, respectively; AGT