Kindgen-Milles D, Slowinski T, Dimski T
Klinik für Anästhesiologie, Universitätsklinikum Düsseldorf, Operative Intensivstation im Zentrum für Operative Medizin I, Heinrich-Heine-Universität Düsseldorf, Moorenstr. 5, 40225, Düsseldorf, Deutschland.
Medizinische Klinik mit Schwerpunkt Nephrologie, Campus Mitte, Charité Universitätsmedizin Berlin, Berlin, Deutschland.
Med Klin Intensivmed Notfmed. 2020 Feb;115(1):37-42. doi: 10.1007/s00063-017-0400-z. Epub 2018 Jan 11.
Acute kidney injury (AKI) occurs in 30-50% of all intensive care patients. Renal replacement therapy (RRT) has to be initiated in 10-15%. The early in-hospital mortality is about 50%. Up to 20% of all survivors develop chronic kidney disease after intensive care discharge and progress to end-stage kidney disease within the next 10 years. For timely initiation of prophylactic or therapeutic interventions, it is crucial to exactly determine the actual kidney function, i. e., glomerular filtration rate (GFR), and to gain insight into the further development of kidney function. Traditionally, renal function has been estimated using serum levels of creatinine or urea. Unfortunately, both are notoriously unreliable and insensitive in intensive care patients. Cystatin C has fewer non-GFR determinants when compared to creatinine and is more sensitive and accurate to detect early decreases of GFR. At present, new functional tests are discussed, namely the furosemide stress test (FST) and renal functional reserve (RFR). The FST consists of an intravenous infusion of 1.0-1.5 mg/kgBW furosemide to critically ill patients with AKI. An increase in urine output to >100 ml/h is indicative of a GFR >20 ml/min and almost certainly excludes progression to AKI stage III and need for RRT. Estimation of RFR can be made by short-term oral or intravenous administration of a high protein load. A subsequent increase in GFR defines the presence and the magnitude of functional reserve which can be activated. Loss of RFR is an indicator of loss of functioning nephron mass and incomplete recovery following AKI. Both FST and RFR can help to improve diagnosis and care of high-risk patients with acute and chronic kidney disease.
急性肾损伤(AKI)发生在30%至50%的重症监护患者中。10%至15%的患者必须开始肾脏替代治疗(RRT)。早期院内死亡率约为50%。所有幸存者中高达20%在重症监护出院后会发展为慢性肾脏病,并在接下来的10年内进展为终末期肾病。为了及时启动预防性或治疗性干预措施,准确测定实际肾功能,即肾小球滤过率(GFR),并深入了解肾功能的进一步发展情况至关重要。传统上,肾功能是通过血清肌酐或尿素水平来估算的。不幸的是,在重症监护患者中,这两者都极不可靠且不敏感。与肌酐相比,胱抑素C的非GFR决定因素较少,在检测GFR早期下降时更敏感、准确。目前,正在讨论新的功能测试,即速尿应激试验(FST)和肾功能储备(RFR)。FST包括对患有AKI的重症患者静脉输注1.0 - 1.5mg/kg体重的速尿。尿量增加至>100ml/h表明GFR>20ml/min,几乎可以肯定排除进展为AKI III期以及需要RRT的情况。RFR的估算可通过短期口服或静脉给予高蛋白负荷来进行。随后GFR的增加定义了可激活的功能储备的存在和程度。RFR的丧失是功能性肾单位数量丧失以及AKI后恢复不完全的指标。FST和RFR都有助于改善急性和慢性肾脏病高危患者的诊断和护理。