John Stefan
Medical Intensive Care, Medical Department 8, Klinikum Nuernberg-Sued, Paracelsus Medical University and University of Erlangen-Nuernberg, Breslauerstr. 201, 90471, Nuernberg, Germany.
Med Klin Intensivmed Notfmed. 2020 May;115(Suppl 1):21-27. doi: 10.1007/s00063-020-00659-2. Epub 2020 Feb 12.
Acute kidney injury (AKI) is a common and severe complication in patients in the intensive care unit with a significant impact on patient's mortality and morbidity. Therefore renal protective therapy is very important in these severely ill patients.
Several renal protective strategies have been postulated during recent decades, which came from pathophysiologic concepts and have been contradicted or changed during the last few years. So lessons had to be learned in AKI, leading to new, in many cases completely reversed preventive and therapeutic concepts which may also be important for protection in other organs.
Most important for renal protection is the early identification of patients at risk for AKI or with acute kidney damage before renal function further deteriorates. A stage-based management of AKI comprises more general measures like discontinuation of the nephrotoxic agent but most importantly early hemodynamic stabilization. Recent research has contradicted that AKI is renal ischemia caused by vasoconstriction with consecutive tubular necrosis. In septic AKI, renal blood flow is even increased. Intrarenal vasodilation together with microcirculatory changes and redistribution of blood flow lead to a drop in glomerular filtration by functional changes. Accordingly it had to be learned that not vasodilators but vasoconstrictors are beneficial in AKI. A mean arterial blood pressure target of >65 mm Hg is often recommended but exact targets are not known, and patients with pre-existing hypertension even need higher perfusion pressure. Also the concept that fluid therapy is always beneficial for the kidney in shock states had to be revised. A volume restrictive therapy with only balanced crystalloids is also becoming more important in AKI. Still no specific pharmacological therapy for renal protection is available. Inflammation and mitochondrial dysfunction appear to play a significant role in AKI. Anti-inflammatory strategies are under investigation and may become more important for AKI prevention and therapy in the future. (This article is freely available.).
急性肾损伤(AKI)是重症监护病房患者常见且严重的并发症,对患者的死亡率和发病率有重大影响。因此,肾脏保护治疗在这些重症患者中非常重要。
近几十年来提出了几种肾脏保护策略,这些策略源于病理生理学概念,在过去几年中受到了反驳或改变。因此,必须从急性肾损伤中吸取教训,从而形成新的、在许多情况下完全相反的预防和治疗概念,这对其他器官的保护也可能很重要。
对肾脏保护最重要的是在肾功能进一步恶化之前早期识别有急性肾损伤风险或急性肾损伤的患者。急性肾损伤的分期管理包括更一般的措施,如停用肾毒性药物,但最重要的是早期血流动力学稳定。最近的研究反驳了急性肾损伤是由血管收缩导致肾小管坏死引起的肾脏缺血这一观点。在脓毒症相关性急性肾损伤中,肾血流量甚至增加。肾内血管舒张以及微循环变化和血流重新分布导致肾小球滤过率因功能改变而下降。因此,人们认识到在急性肾损伤中有益的不是血管扩张剂而是血管收缩剂。通常建议平均动脉血压目标>65 mmHg,但确切目标尚不清楚,已有高血压的患者甚至需要更高的灌注压力。此外,液体治疗在休克状态下对肾脏总是有益的这一概念也必须修正。在急性肾损伤中,仅使用平衡晶体液的容量限制性治疗也变得越来越重要。目前仍没有针对肾脏保护的特异性药物治疗方法。炎症和线粒体功能障碍似乎在急性肾损伤中起重要作用。抗炎策略正在研究中,未来可能对急性肾损伤的预防和治疗更为重要。(本文可免费获取。)