Reichel Ronald R
Department of Nephrology, Ochsner Health Center-Baton Rouge, Baton Rouge, LA.
Ochsner J. 2014 Fall;14(3):359-68.
Acute kidney injury (AKI) is frequently encountered in the nephrology practice. Serum creatinine, with its many shortcomings, is still the main biomarker used to detect AKI.
This review focuses on recent advances in definition, diagnosis, risk factors, and molecular mechanisms of AKI. In addition, specific AKI syndromes such as contrast-induced AKI, hepatorenal syndrome, and acute decompensated heart failure are discussed. The connection between AKI and subsequent chronic kidney disease and recent developments in renal replacement therapy are also covered.
Novel biomarkers such as cystatin C and neutrophil gelatinase-associated lipocalin (NGAL) are being investigated to replace serum creatinine in the detection of AKI. Recent studies suggest that intravenous (IV) fluid use is beneficial for the prevention of contrast-induced AKI, while N-acetylcysteine use is not as well established. Diuretics are clearly beneficial in the treatment of acute decompensated heart failure. Ultrafiltration is less promising and can lead to adverse side effects. Although terlipressin use in hepatorenal syndrome is associated with reduced mortality, it is not available in the United States; combination therapy with midodrine, octreotide, and albumin provides an alternative. Fluid resuscitation is frequently used in critically ill patients with AKI; however, overly aggressive fluid resuscitation is frequently associated with an increased risk of mortality. A 3-step approach that combines guided fluid resuscitation, establishment of an even fluid balance, and an appropriate rate of fluid removal may be beneficial. If fluid resuscitation is needed, crystalloid solutions are preferred over hetastarch solutions. Renal replacement therapy is the last resort in AKI treatment, and timing, modality, and dosing are discussed. Research suggests that AKI leads to an increased incidence of subsequent chronic kidney disease. However, this relationship has not been fully established and additional studies are needed for clarification.
Despite major advances in AKI research, serum creatinine remains the major biomarker for the detection of AKI. The following interventions have shown to be beneficial: IV fluids for contrast-induced AKI; diuretics for acute decompensated heart failure/cardiorenal syndrome; and combination therapy with midodrine, octreotide, and albumin for hepatorenal syndrome. Fluid resuscitation in a patient with AKI should be used with caution because too liberal use of fluids can be associated with increased mortality. AKI appears to be related to increased rates of subsequent chronic kidney disease, and patients with AKI should therefore be monitored closely. Recent studies on renal replacement therapy have neither revealed an optimal timing for initiation of dialysis nor a clear advantage for a specific dialysis modality.
急性肾损伤（AKI）在肾脏病临床实践中经常遇到。血清肌酐虽有诸多缺点，但仍是用于检测AKI的主要生物标志物。
本综述重点关注AKI在定义、诊断、危险因素及分子机制方面的最新进展。此外，还讨论了特定的AKI综合征，如造影剂所致AKI、肝肾综合征和急性失代偿性心力衰竭。还涵盖了AKI与后续慢性肾脏病之间的联系以及肾脏替代治疗的最新进展。
正在研究诸如胱抑素C和中性粒细胞明胶酶相关脂质运载蛋白（NGAL）等新型生物标志物，以在检测AKI时替代血清肌酐。近期研究表明，静脉输液对预防造影剂所致AKI有益，而使用N - 乙酰半胱氨酸的效果尚未明确确立。利尿剂对急性失代偿性心力衰竭的治疗显然有益。超滤的前景较差且可导致不良副作用。尽管特利加压素用于肝肾综合征与死亡率降低相关，但在美国无法获得；米多君、奥曲肽和白蛋白联合治疗提供了一种替代方案。液体复苏常用于AKI的危重症患者；然而，过度积极的液体复苏常与死亡率增加风险相关。一种结合指导性液体复苏、维持液体平衡及适当液体清除率的三步法可能有益。如果需要液体复苏，晶体溶液优于羟乙基淀粉溶液。肾脏替代治疗是AKI治疗的最后手段，并对时机、方式和剂量进行了讨论。研究表明，AKI会导致后续慢性肾脏病的发病率增加。然而，这种关系尚未完全确立，需要更多研究予以阐明。
尽管AKI研究取得了重大进展，但血清肌酐仍是检测AKI的主要生物标志物。以下干预措施已证明是有益的：静脉输液用于造影剂所致AKI；利尿剂用于急性失代偿性心力衰竭/心肾综合征；米多君、奥曲肽和白蛋白联合治疗用于肝肾综合征。AKI患者的液体复苏应谨慎使用，因为过度大量使用液体可能与死亡率增加相关。AKI似乎与后续慢性肾脏病发病率增加有关，因此应对AKI患者进行密切监测。近期关于肾脏替代治疗的研究既未揭示开始透析的最佳时机，也未明确特定透析方式的明显优势。
