Nierenversagen

Der Begriff akutes Nierenversagen beschreibt eine abrupte Verschlechterung der exkretorischen Nierenfunktion. Da bereits eine nur milde Funktionsverschlechterung das Mortalitätsrisiko steigert, wandelt sich die Terminologie zur akuten Nierenschädigung (Acute Kidney Injury, AKI). Eine AKI ist eines der häufigsten Organversagen auf Intensivstationen mit signifikanten Folgen. Folgend wird die Wichtigkeit präventiver Maßnahmen in den Fokus gestellt.

Abstract

„Acute kidney injury“ (AKI) describes any acute deterioration in kidney function but also only injury to the kidneys without a severe loss of function. It is a common and severe complication in patients on the intensive care unit with a significant impact on patient’s mortality and morbidity. Since no specific pharmacological therapy exists, the early identification of patients at risk for AKI or with acute kidney damage is most important before renal function further deteriorates. A stage-based management of AKI comprises more general measures like discontinuation of 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 are leading 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 mmHg is often recommended but exact targets are not known and patients with preexisting hypertension do even need a 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 balanced, chloride restricted crystalloids only, is important also in AKI. Exposure to contrast material is often associated with AKI but less common the direct cause of AKI, so if indicated, contrast material should not be withheld in patients at risk for AKI.

Schlüsselwörter

Nierenversagen - hämodynamische Stabilisierung - Vasopressoren - Volumetherapie - Sepsis

Key words

acute kidney injury - hemodynamic stabilization - vasopressors - fluid therapy - sepsis

Publikationsverlauf

Artikel online veröffentlicht:
28. Dezember 2021

• Literatur

• 1 Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Intern 2012; 2 (01) 138
• 2 Susantitaphong P, Cruz DN, Cerda J. et al. World incidence of AKI: a metaanalysis. Clin J Am Soc Nephrol 2013; 8: 1482-1493
• 3 Uchino S, Kellum JA, Bellomo R. et al. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA 2005; 294: 813-818
• 4 Nisula S, Kaukonen KM, Vaara ST. et al. Incidence, risk factors and 90-day mortality of patients with acute kidney injury in Finnish intensive care units: the FINNAKI study. Intensive Care Med 2013; 39: 420-428
• 5 Joannidis M, Forni LG, Haase M. et al. Use of cell cycle arrest biomarkers in conjunction with classical markers of acute kidney injury. Crit Care Med 2019; 47: e820-e826
• 6 Tomasev N, Glorot X, Rae JW. et al. A clinically applicable approach to continuous prediction of future acute kidney injury. Nature 2019; 572: 116-119
• 7 Prowle JR, Bellomo R. Sepsis-associated acute kidney injury: macrohemodynamic and microhemodynamic alterations in the renal circulation. Semin Nephrol 2015; 35: 64-74
• 8 Arulkumaran N, Pollen S, Greco E. et al. Renal tubular cell mitochondrial dysfunction occurs despite perserved renal oxygen delivery in experimental septic acute kidney injury. Crit Care Med 2018; 46: e318-e325
• 9 Joannidis M, Druml W, Forni LG. et al. Prevention of acute kidney injury and protection of renal function in the intensive care unit: update 2017. Intensive Care Med 2017; 43: 730-749
• 10 Nagendran M, Russell JA, Walley KR. et al. Vasopressin in septic shock: an individual patient data meta-analysis of randomised controlled trials. Intensive Care Med 2019; 45: 844-855
• 11 Tumlin JA, Murugan R, Deane AM. et al. Outcomes in patients with vasodilatory shock and renal replacement therapy treated with intravenous angiotensin II. Crit Care Med 2018; 46: 949-957
• 12 Asfar P, Meziani F, Hamel JF. et al. High versus low blood-pressure target in patients with septic shock. N Engl J Med 2014; 370: 1583-1593
• 13 Perner A, Prowle JR, Joannidis M. et al. Fluid management in acute kidney injury. Intensive Care Med 2017; 43: 807-815
• 14 Woodward CW, Lambert J, Ortiz-Soriano V. et al. Fluid overload is associated with major adverse kidney events in critically ill patients with acute kidney injury requiring continuous renal replacement therapy. Crit Care Med 2019; 47: e753-e760
• 15 Hjortrup PB, Haase N, Bundgaard H. et al. Restricting volumes of resuscitation fluid in adults with septic shock after initial management: the CLASSIC randomized, parallel-group, multicenter feasibility trial. Intensive Care Med 2016; 42: 1695-1705
• 16 Corl KA, Prodromou M, Merchant RC. et al. The restrictive iv fluid trial in severe sepsis and septic shock (RIFTS): A randomized pilot study. Crit Care Med 2019; 47: 951-959
• 17 Murugan R, Kerti SJ, Chang CCH. et al. Association of net ultrafiltration rate with mortality among critically ill adults with acute kidney injury receiving continuous venovenous hemodiafiltration – a secondary analysis of the randomized evaluation of normal vs augmented level (RENAL) of renal replacement therapy trial. JAMA Network Open 2019; 2: e195418
• 18 Semler MW, Self WH, Wanderer JP et al for the SMART Investigators. Balanced crystalloids versus saline in critically ill adults. N Engl J Med 2018; 378: 829-839
• 19 Williams LMS, Walker GR, Loewenherz JW. et al. Association of contrast and acute kidney injury in the critically ill’. A propensity-matched study. Chest 2020; 157: 866-876