Akute Nierenschädigung: Epidemiologie, Pathophysiologie, Reparaturmechanismen

Zusammenfassung

Eine akute Nierenschädigung tritt bei 25% aller Krankenhaus- und bei 50% der Intensivpatienten auf. Im Stadium 3 der akuten Nierenschädigung sterben auch bei optimaler Therapie etwa 40 – 50% der betroffenen Patienten. Die Langzeitprognose hängt ganz wesentlich von der Erholung der Nierenfunktion ab. Eine frühe Diagnostik und die konsequente Durchführung von Interventionen zur Prophylaxe und zur schnellen Wiederherstellung der Nierenfunktion sind essenziell [1].

Abstract

Acute kidney injury (AKI) is a major complication in critically ill patients and affects up to 50% of those admitted to intensive care units. Causes of AKI include patient specific factors (susceptibility: e.g. age, pre-existing chronic kidney disease, chronic heart failure, diabetes) and patient unspecific factors (exposure: e.g. sepsis, hypovolemia, cardiac surgery, nephrotoxin application). Mortality of severe AKI is in the range of 40 – 50%.

AKI is accompanied by volume overload, electrolyte disorders, acidosis, and uremia. The diagnosis of AKI is based on an increase of creatinine levels and/or a decrease in urine output within 7 days after an insult. These 2 markers are late und unspecific, especially with regard to early identification of patients at risk of AKI. New AKI markers have been investigated within the last decade including NGAL (neutrophil gelatinase-associated lipocalin), the product of IGFBP-7 (insulin like growth factor binding protein 7) and TIMP-2 (tissue inhibitor of metalloproteinase 2), KIM-1 (kidney injury molecule 1) and the cysteine-protease-inhibitor cystatin C. New markers or a panel of new markers might improve the diagnosis of patients at risk of AKI in the future.

There are currently no specific therapeutics in the treatment of AKI. Therefore, the prevention of AKI is of an utmost importance. The recommended preventive measures include optimization of hemodynamics and volume status, close monitoring of creatinine levels and urine output, avoidance or discontinuation of nephrotoxic drugs, normoglycemia and the application of alternatives to radiocontrast agents if possible.

As the long term prognosis of AKI highly depends on renal recovery, the 2 major goals for the future will be 1) the early identification of patients at AKI risk and 2) the support of renal recovery of AKI patients.

Schlüsselwörter

akute Nierenschädigung - Pathophysiologie - renale Erholung

Key words

acute kidney injury - pathophysiology - renal recovery

• Literatur

• 1 Zarbock A, John S, Jorres A. et al. Neue KDIGO-Leitlinien zur akuten Nierenschädigung – Praktische Handlungsempfehlungen. Anaesthesist 2014; 63: 578-588 doi:10.1007/s00101-014-2344-5
• 2 KDIGO. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International 2012; 2 (Suppl. 01) 1-138
• 3 Steinke T, Moritz S, Beck S. et al. Estimation of creatinine clearance using plasma creatinine or cystatin C: a secondary analysis of two pharmacokinetic studies in surgical ICU patients. BMC Anesthesiol 2015; 15: 62 doi:10.1186/s12871-015-0043-7
• 4 Hoste EA, Bagshaw SM, Bellomo R. et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med 2015; 41: 1411-1423 doi:10.1007/s00134-015-3934-7
• 5 Hoste EAJ, Kellum JA, Selby NM. et al. Global epidemiology and outcomes of acute kidney injury. Nat Rev Nephrol 2018; 14: 607-625 doi:10.1038/s41581-018-0052-0
• 6 Klein SJ, Brandtner AK, Peball M. et al. [Life after Acute Kidney Injury : Long-term consequences and implications for clinical practice]. Med Klin Intensivmed Notfmed 2017; 112: 597-604 doi:10.1007/s00063-017-0340-7
• 7 Walsh M, Devereaux PJ, Garg AX. et al. Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: toward an empirical definition of hypotension. Anesthesiology 2013; 119: 507-515 doi:10.1097/ALN.0b013e3182a10e26
• 8 Myles PS, Bellomo R, Corcoran T. et al. Restrictive versus Liberal Fluid Therapy for Major Abdominal Surgery. N Engl J Med 2018; 378: 2263-2274 doi:10.1056/NEJMoa1801601
• 9 Damman K, Navis G, Smilde TD. et al. Decreased cardiac output, venous congestion and the association with renal impairment in patients with cardiac dysfunction. Eur J Heart Fail 2007; 9: 872-878 doi:10.1016/j.ejheart.2007.05.010
• 10 Rabb H, Griffin MD, McKay DB. et al. Inflammation in AKI: Current Understanding, Key Questions, and Knowledge Gaps. J Am Soc Nephrol 2016; 27: 371-379 doi:10.1681/ASN.2015030261
• 11 Schwenger V, Kindgen-Milles D, Willam C. et al. [Extracorporeal renal replacement therapy in acute kidney injury: Recommendations from the renal section of the DGIIN, OGIAIN and DIVI]. Med Klin Intensivmed Notfmed 2018; 113: 370-376 doi:10.1007/s00063-018-0418-x
• 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 doi:10.1056/NEJMoa1312173
• 13 Zarbock A, John S, Jorres A. et al. [New KDIGO guidelines on acute kidney injury. Practical recommendations]. Anaesthesist 2014; 63: 578-588 doi:10.1007/s00101-014-2344-5
• 14 Meersch M, Schmidt C, Hoffmeier A. et al. Prevention of cardiac surgery-associated AKI by implementing the KDIGO guidelines in high risk patients identified by biomarkers: the PrevAKI randomized controlled trial. Intensive Care Med 2017; 43: 1551-1561 doi:10.1007/s00134-016-4670-3
• 15 Basile DP, Bonventre JV, Mehta R. et al. Progression after AKI: Understanding Maladaptive Repair Processes to Predict and Identify Therapeutic Treatments. J Am Soc Nephrol 2016; 27: 687-697 doi:10.1681/ASN.2015030309
• 16 Kashani K, Cheungpasitporn W, Ronco C. Biomarkers of acute kidney injury: the pathway from discovery to clinical adoption. Clin Chem Lab Med 2017; 55: 1074-1089 doi:10.1515/cclm-2016-0973
• 17 Kashani K, Al-Khafaji A, Ardiles T. et al. Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury. Crit Care 2013; 17: R25 doi:10.1186/cc12503
• 18 Koyner JL, Shaw AD, Chawla LS. et al. Tissue Inhibitor Metalloproteinase-2 (TIMP-2)IGF-Binding Protein-7 (IGFBP7) Levels Are Associated with Adverse Long-Term Outcomes in Patients with AKI. J Am Soc Nephrol 2015; 26: 1747-1754 doi:10.1681/ASN.2014060556
• 19 Ferguson TW, Komenda P, Tangri N. Cystatin C as a biomarker for estimating glomerular filtration rate. Curr Opin Nephrol Hypertens 2015; 24: 295-300 doi:10.1097/MNH.0000000000000115
• 20 Neyra JA, Hu MC, Minhajuddin A. et al. Kidney Tubular Damage and Functional Biomarkers in Acute Kidney Injury Following Cardiac Surgery. Kidney Int Rep 2019; 4: 1131-1142 doi:10.1016/j.ekir.2019.05.005
• 21 Hoste E, Bihorac A, Al-Khafaji A. et al. Identification and validation of biomarkers of persistent acute kidney injury: the RUBY study. Intensive Care Med 2020; 46: 943-953 doi:10.1007/s00134-019-05919-0
• 22 Brandenburger T, Salgado Somoza A, Devaux Y. et al. Noncoding RNAs in acute kidney injury. Kidney Int 2018; 94: 870-881 doi:10.1016/j.kint.2018.06.033