[TCT2008]影剂引起的急性肾损伤仍然是主要的安全问题

发布于:2008-10-17 09:35

Peter A. McCullough说，肾损伤仍然是造影剂使用中非常重要安全的问题，造影剂首先引起急性肾损伤或CI-AKI，而非造影剂肾病。CI-AKI的最新定义是指血清肌酸酐≥0.3 mg/dL 或上升1.5倍以上。

情况虽然很少见，但却会使患者危险性增加
McCullough说，CI-AKI比较少见，有时只是暂时性的，但是它与多数MACE率增加有关。其病理生理是多层次，“迄今为止，临床试验通常只给出一个层次”，他说，“我们可能需要有一个综合的办法；一方面来影响血管的收缩，另一方面是改善或减轻氧化应激反应，还有就是尽可能地减少造影剂在肾脏中的存留时间。”他补充道，一个重大的进步可能是发明CI-AKI的生物标记，迄今为止最有希望的竞争者就是NGAL，这是一种由肾产生的一种糖蛋白，并且可以在血液和尿中被检测到。

相关研究正在进行
McCullough概述了一些降低CI-AKI危险的策略：进行风险评分、使用IV碳酸氢钠、通过摄入大量的液体或少量利尿剂来增加排尿量或进行临床干预。

被调查研究的药无有N -乙酰半胱氨酸、多巴胺、非诺多泮和茶碱迄今的结果有好有坏。

McCullough说，医学最大的进步在于铁螯合剂的出现，一种在欧洲市场得到验证并且获得FDA特殊批准应用于临床的药物，另外一些研究如促进造影剂转运或者排除的导管，平衡输入和输出的IV fluids的设备，进行血液透析和应用等渗造影剂等等。

McCullough给出了关于CI-AKI危险管理建议（见图）。他强调：“我们迫切需要一种没有肾毒性的药物应用于临床，现在我们正在跟介入心脏病学家一起研究，希望我们最终能解决这些问题，为肾脏提供更好的保护。”

(医心评论：朱婧译马秀芹校）

Contrast-induced Acute Kidney Injury Remains Major Safety Issue

Key Points:

Several strategies are being explored for risk assessment, prevention, and treatment.

By TCT Daily Staff

Kidney injury remains an important safety issue associated with procedures involving administration of contrast media, said Peter A. McCullough, MD, MPH, of William Beaumont Hospital, Royal Oak, Mich., in his overview of the topic on Tuesday.

McCullough said that the preferred term is now contrast-induced acute kidney injury, or CI-AKI, rather than contrast-induced nephropathy.

The most recent definition for CI-AKI is a ≥0.3 mg/dL or ≥1.5-fold rise in serum creatinine.

Condition somewhat rare, but increases risk

CI-AKI is relatively rare and sometimes temporary, McCullough said, but it has been tied to increased risk of major adverse cardiac events. Its pathophysiology is multilevel and "so far, clinical trials have only addressed typically one layer of that," he said.

"We may need to have a multimodality approach; one therapy to affect the vasoconstriction, one therapy to ameliorate or attenuate the oxidative stress, another therapy to potentially reduce the amount of time that the contrast stays in the kidneys."

A major move forward would be development of a biomarker for CI-AKI, he added. The most promising contender thus far is neutrophil gelatinase-associated lipocalin (NGAL), a glycoprotein produced by the kidneys that can be measured in blood and urine.

Several options being investigated

McCullough outlined several strategies to minimize CI-AKI risk: using risk scores, giving IV sodium bicarbonate, increasing urine flow rate with large amounts of fluid or even small amounts of diuretics, or using medical prophylaxis.

Drugs under investigation include N-acetylcysteine, dopamine, fenoldopam, and theophylline, although results so far have been mixed.

The best chance for a medical advance is iron chelation with deferiprone, a drug currently approved in Europe and involved in an FDA-approved special protocol assessment, McCullough said. Other experimental techniques include various catheters to deliver drugs or to aspirate contrast agents, devices to balance input and output of IV fluids, hemofiltration, and the use of iso-osmolar contrast agents.

McCullough gave his recommendations for managing CI-AKI risk (see Figure). "New contrast agents that have no renal toxicity are needed," he stressed.

"Right now we’re wedded in interventional cardiology to iodine-based contrast agents, and we have to work through these strategies to ultimately provide better renal protection."

Disclosures: