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Review
. 2021 Aug;47(8):835-850.
doi: 10.1007/s00134-021-06454-7. Epub 2021 Jul 2.

Acute kidney injury in the critically ill: an updated review on pathophysiology and management

Affiliations
Review

Acute kidney injury in the critically ill: an updated review on pathophysiology and management

Peter Pickkers et al. Intensive Care Med. 2021 Aug.

Abstract

Acute kidney injury (AKI) is now recognized as a heterogeneous syndrome that not only affects acute morbidity and mortality, but also a patient's long-term prognosis. In this narrative review, an update on various aspects of AKI in critically ill patients will be provided. Focus will be on prediction and early detection of AKI (e.g., the role of biomarkers to identify high-risk patients and the use of machine learning to predict AKI), aspects of pathophysiology and progress in the recognition of different phenotypes of AKI, as well as an update on nephrotoxicity and organ cross-talk. In addition, prevention of AKI (focusing on fluid management, kidney perfusion pressure, and the choice of vasopressor) and supportive treatment of AKI is discussed. Finally, post-AKI risk of long-term sequelae including incident or progression of chronic kidney disease, cardiovascular events and mortality, will be addressed.

Keywords: Acute kidney injury; Biomarkers; Blood pressure management; Diagnosis; Fluid therapy; Heterogeneity; Long-term consequences; Machine learning; Nephrotoxicity; Organ cross-talk; Pathophysiology; Phenotypes; Vasopressor.

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Conflict of interest statement

PP declares having received speaker fees from Baxter and consultancy fees from AM-Pharma. MD declares having received speaker fees from Astelas, Gilead-Kite and MSD along with a grant from MSD outside the scope of this manuscript. EH declares speaker fees from Alexion and Sopachem (paid to the university), travel grant from AM-Pharma. MJ has received honoraria and research support from Baxter Healthcare Corp, AM-Pharma, CLS Behring, Fresenius, and Astute Medical. ML declares no conflict of interest. MO declares speaker fees from Fresenius and Biomerieux, research funding from Baxter, Biomerieux and LaJolla Pharma and consultancy fee from NxStage. JRP has received grant and/or research support from bioMérieux, consulting fees from Medibeacon Inc., Beckton Dickinson Inc and Jafron Biomedical Co Ltd and speaker’s honoraria from Nikkiso Europe GmbH, Baxter, Braun Medical Ltd, Fresenius Medical Care and Fresenius-Kabi UK. AS has received a grant from the Leenaards foundation, speaker honoraria from Fresenius Medical Care and consulting honoraria from B Braun Melsungen AG. MS has no conflict of interest to declare.

Figures

Fig. 1
Fig. 1
Different phases of AKI development and progression and associated diagnostic tests. AKI acute kidney injury, TIMP tissue inhibitor of metalloproteinases, IGFBP  insulin-like growth factor-binding protein, NGAL  neutrophil gelatinase-associated lipocalin, UO urine output
Fig. 2
Fig. 2
Following the development of AKI, several scenarios are possible that may lead to recovery of renal function or to more prolonged dysfunction. Acute kidney disease (AKD) is assessed between 7 and 90 days after AKI. In patients that do not improve, chronic kidney disease (CKD) is established after day 90. Biomarkers of renal injury and function may be able to refine the prediction of rapid recovery (i.e., transient AKI) or transition to more persistent impairment of renal function and several therapeutic interventions may be able to modulate the progression of the disease course
Fig. 3
Fig. 3
Simplified overview of AKI pathophysiology illustrating the heterogeneity in etiology, presentation, pathology, progression and outcomes and how investigations may help us understand underlying AKI phenotypes at various stages in illness. Green indicates functional/reversible processes; red indicates acute and chronic tissue injury. Yellow boxes indicate etiological factors in AKI pathogenesis, blue boxes diagnostic tests indicative of underlying pathophysiological processes

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