安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
3期
350-353
,共4页
阿托伐他汀%经皮冠脉介入治疗%肾功能%对比剂%急性肾损伤
阿託伐他汀%經皮冠脈介入治療%腎功能%對比劑%急性腎損傷
아탁벌타정%경피관맥개입치료%신공능%대비제%급성신손상
atorvastatin%percutaneous coronary intervention%kidney function%contrast medium%acute kidney in-jury
目的探讨强化剂量的阿托伐他汀能否减轻经皮冠脉介入术( PCI)对患者肾功能的影响及减少对比剂致急性肾损伤( CI-AKI)的发生率。方法将128例接受PCI治疗的患者随机分为2组：强化组(n=64)和对照组(n=64)。强化组术前12~24 h、术后第1天及第2天均口服80 mg阿托伐他汀,对照组术前及术后口服20 mg阿托伐他汀。主要终点事件是CI-AKI的发生率,并观察患者术前24 h和术后24、48、72 h的血清肌酐( Scr)、胱抑素C、肾小球滤过率( eG-FR)、尿白蛋白、尿β-2微球蛋白水平。结果强化组3.1%(n=2)的患者发生CI-AKI,对照组为4.7%(n=3),两组间差异无统计学意义( P=1.00)；术后两组间Scr、胱抑素C、eGFR、尿白蛋白、尿β-2微球蛋白和肌酸激酶( CK)差异均无统计学意义。术后3 d两组谷丙转氨酶( ALT)升高,强化组谷草转氨酶(AST)亦升高(P<0.05),但均在正常参考值范围内。结论 PCI术前强化阿托伐他汀治疗与常规剂量比较在减轻肾功能损伤和降低CI-AKI发生率方面差异无统计学意义。
目的探討彊化劑量的阿託伐他汀能否減輕經皮冠脈介入術( PCI)對患者腎功能的影響及減少對比劑緻急性腎損傷( CI-AKI)的髮生率。方法將128例接受PCI治療的患者隨機分為2組：彊化組(n=64)和對照組(n=64)。彊化組術前12~24 h、術後第1天及第2天均口服80 mg阿託伐他汀,對照組術前及術後口服20 mg阿託伐他汀。主要終點事件是CI-AKI的髮生率,併觀察患者術前24 h和術後24、48、72 h的血清肌酐( Scr)、胱抑素C、腎小毬濾過率( eG-FR)、尿白蛋白、尿β-2微毬蛋白水平。結果彊化組3.1%(n=2)的患者髮生CI-AKI,對照組為4.7%(n=3),兩組間差異無統計學意義( P=1.00)；術後兩組間Scr、胱抑素C、eGFR、尿白蛋白、尿β-2微毬蛋白和肌痠激酶( CK)差異均無統計學意義。術後3 d兩組穀丙轉氨酶( ALT)升高,彊化組穀草轉氨酶(AST)亦升高(P<0.05),但均在正常參攷值範圍內。結論 PCI術前彊化阿託伐他汀治療與常規劑量比較在減輕腎功能損傷和降低CI-AKI髮生率方麵差異無統計學意義。
목적탐토강화제량적아탁벌타정능부감경경피관맥개입술( PCI)대환자신공능적영향급감소대비제치급성신손상( CI-AKI)적발생솔。방법장128례접수PCI치료적환자수궤분위2조：강화조(n=64)화대조조(n=64)。강화조술전12~24 h、술후제1천급제2천균구복80 mg아탁벌타정,대조조술전급술후구복20 mg아탁벌타정。주요종점사건시CI-AKI적발생솔,병관찰환자술전24 h화술후24、48、72 h적혈청기항( Scr)、광억소C、신소구려과솔( eG-FR)、뇨백단백、뇨β-2미구단백수평。결과강화조3.1%(n=2)적환자발생CI-AKI,대조조위4.7%(n=3),량조간차이무통계학의의( P=1.00)；술후량조간Scr、광억소C、eGFR、뇨백단백、뇨β-2미구단백화기산격매( CK)차이균무통계학의의。술후3 d량조곡병전안매( ALT)승고,강화조곡초전안매(AST)역승고(P<0.05),단균재정상삼고치범위내。결론 PCI술전강화아탁벌타정치료여상규제량비교재감경신공능손상화강저CI-AKI발생솔방면차이무통계학의의。
Objective To investigate whether intensive atorvastatin treatment in patients after percutaneous coro-nary intervention ( PCI) could decrease the effect of contrast medium on kidney function and the incidence of con-trast-induced acute kidney injury( CI-AKI) . Methods A total of 128 patients with PCI were randomly divided into two groups:the enhanced treatment group (n=64) and the control group(n=64). The enhanced treatment group received 80 mg atorvastatin at 12~24 h before PCI and 24,48 h after PCI. The control group was given 20 mg ator-vastatin respectively before and after PCI. The primary end point was the incidence of CI-AKI. Serum creatinine (Scr), cystatin C, glomerular filtration rate(eGFR), urinary albumin and urinary β-2 microglobulin levels were observed at 24 h before PCI and 24, 48, 72 h after PCI. Results In the enhanced treatment group 3. 1 % (n=2) of patients developed CI-AKI versus 4. 7 % (n=3) in the control group, without statistical difference (P=1.00). There was no significant difference between two groups in postoperative Scr, cystatin C, eGFR, urinary al-bumin, urinary β-2 microglobulin and creatine kinase(CK). Three days after the operation, alanine aminotrans-ferase ( ALT) elevated in two groups, and aspartate aminotransferase ( AST) increased in the enhanced treatment group (P<0. 05), but they were all in the normal range. Conclusion There has been no significant difference in decreasing the incidence of CI-AKI and the damage of contrast medium on renal function between the enhanced treatment group and the control group before PCI.
