Division of Nephrology, Hospital Juan A Fernández, Universidad de Buenos Aires, Paraguay 5259 Floor 3, Apt A, C1425BTG, Buenos Aires, Argentina.
Clin Exp Nephrol. 2013 Jun;17(3):396-404. doi: 10.1007/s10157-012-0722-3. Epub 2012 Nov 10.
The occurrence of contrast-induced acute kidney injury (CIAKI) has paralleled the increased number of diagnostic interventions requiring radiographic contrast media (CM). Several strategies aimed at preventing renal injury following iodine have been carried out over the last several years. The aim of this study was to evaluate the impact of three different strategies aimed at preventing CIAKI in patients with renal dysfunction (serum creatinine >1.25 mg/dl or estimated creatinine clearance <45 ml/min) receiving low osmolar CM for diagnostic-therapeutic procedures.
Candidates received 154 mmol NaHCO3 solution (B0) at a rate of 3 ml/kg/h from at least 2 h before the procedure and at 1 ml/kg/h during and for the next 6-12 h; the same schedule plus N-acethyl-cysteine (NAC) 600 mg twice daily the day before and the day of the procedure (BN) or NAC as above plus 154 mmol NaCl solution at a rate of 3 ml/kg/h from at least 2 h before the procedure and at 1 ml/kg/h during and for the next 6-12 h (SN). Serum creatinine (SCr) was measured at baseline and on days 2 or occasionally 3 after CM. The main outcome measure was the occurrence of CIAKI, defined as a ≥25% increase in SCr within 2-3 days of CM.
The three groups were similar with regard to age, gender distribution, weight, baseline serum levels of creatinine, sodium, potassium, urate and estimated creatinine clearance. A larger proportion of individuals received ACEIs/ARAs in the BN group (p < 0.05), but in the SN group, more patients declared a past history of acute myocardial infarction or had high blood pressure, and few displayed mild-moderate left ventricular dysfunction (p < 0.05). CIAKI occurred in 24/123 (19.5%) assessable patients (15/42 in the B0 group, 3/43 in the BN group and 6/38 in the SN group; p < 0.01). Thus, 15/42 patients who did not receive NAC developed CIAKI in contrast to 9/81 who did (p < 0.01). Multivariate logistic regression models showed that the use of NAC was the unique factor associated with a statistically significant influence for the occurrence of CIAKI (OR: 0.18; 95% CI: 0.04-0.72; p = 0.016).
The results from this study show that: (1) the occurrence of CIAKI after low-osmolar CM administration is similar to that reported worldwide. (2) NAC-based renoprotective measures are superior for the prevention of CIAKI in patients with previous renal dysfunction. (3) They also demonstrate that bicarbonate expansion alone has limited value in preventing CIAKI. For those individuals at risk, combination prophylaxis including volume expansion plus NAC should be recommended to reduce the chance of overt kidney injury following CM administration.
对比剂诱导的急性肾损伤(CIAKI)的发生与需要放射性对比剂(CM)的诊断性介入的数量增加相平行。在过去的几年中,已经提出了几种旨在预防碘后肾损伤的策略。本研究的目的是评估三种不同策略在接受低渗 CM 进行诊断-治疗程序的肾功能障碍(血清肌酐> 1.25 mg/dl 或估计肌酐清除率<45 ml/min)患者中预防 CIAKI 的影响。
候选人在程序前至少 2 小时以 3 ml/kg/h 的速度接受 154 mmol NaHCO3 溶液(B0),并在程序期间和之后以 1 ml/kg/h 的速度继续 6-12 小时;同样的方案加上 N-乙酰半胱氨酸(NAC)600 mg 每天两次在程序前一天和当天(BN)或如上所述加上 154 mmol NaCl 溶液以 3 ml/kg/h 的速度从程序前至少 2 小时开始,并在程序期间和之后以 1 ml/kg/h 的速度继续 6-12 小时(SN)。在基线和 CM 后第 2 天或偶尔第 3 天测量血清肌酐(SCr)。主要观察终点是 CIAKI 的发生,定义为 CM 后 2-3 天内 SCr 增加≥25%。
三组在年龄、性别分布、体重、基线血清肌酐、钠、钾、尿酸和估计肌酐清除率方面相似。BN 组接受 ACEI/ARB 的人数比例较大(p < 0.05),但在 SN 组中,更多的患者有急性心肌梗死或高血压病史,少数患者有轻度至中度左心室功能障碍(p < 0.05)。在 123 名可评估患者中,24/123 名(B0 组 15/42,BN 组 3/43,SN 组 6/38)发生 CIAKI(p < 0.01)。因此,与接受 NAC 的 9/81 名患者相比,未接受 NAC 的 15/42 名患者发生 CIAKI(p < 0.01)。多变量逻辑回归模型显示,使用 NAC 是 CIAKI 发生的唯一与统计学显著相关的因素(OR:0.18;95%CI:0.04-0.72;p = 0.016)。
本研究结果表明:(1)低渗 CM 给药后 CIAKI 的发生与全球报道的相似。(2)基于 NAC 的肾脏保护措施对预防先前肾功能障碍患者 CIAKI 更有效。(3)它们还表明,碳酸氢盐扩张单独在预防 CIAKI 方面的价值有限。对于那些有风险的个体,应推荐包括容量扩张加 NAC 的联合预防措施,以降低 CM 给药后肾脏损伤的机会。