Acute kidney injury 2016: diagnosis and diagnostic workup

Marlies Ostermann, Michael Joannidis, Marlies Ostermann, Michael Joannidis

Abstract

Acute kidney injury (AKI) is common and is associated with serious short- and long-term complications. Early diagnosis and identification of the underlying aetiology are essential to guide management. In this review, we outline the current definition of AKI and the potential pitfalls, and summarise the existing and future tools to investigate AKI in critically ill patients.

Figures

Fig. 1
Fig. 1
Generation and clearance of creatinine. Arg arginine, Glyc glycine
Fig. 2
Fig. 2
Biomarkers of AKI. α-GST α glutathione S-transferase, AAP alanine aminopeptidase, ALP alkaline phosphatase, γ-GT γ-glutamyl transpeptidase, п GST п glutathione S-transferase, HGF hepatocyte growth fator, IGFBP-7 insulin like growth factor binding protein 7, IL-18 interleukin 18, KIM-1 kidney injury molecule-1, L-FAB liver fatty acid-binding protein, NAG N-acetyl-β-d-glucosaminidase, NGAL neutrophil gelatinase-associated lipocalin, RBP retinol binding protein, TIMP2 tissue inhibitor metalloproteinase 2
Fig. 3
Fig. 3
Diagnosis of AKI based on functional and damage markers. The combination of functional and damage biomarkers allows the clinician to diagnose AKI earlier and to differentiate the disease process better. It is recognised that the process is dynamic and that patients may move from one phase to another. Reproduced with permission from http://www.adqi.org/
Fig. 4
Fig. 4
Diagnostic work up. AKI acute kidney injury, ANCA anti-neutrophil cytoplasmic antibody, ANA anti-nuclear antibody, Anti-ds-DNA anti-double stranded DNA, anti-GBM anti-glomerular basement membrane, C3 complement component 3, C4 complement component 4, CK creatine kinase, CK-MB creatine kinase MB fraction, ENA extractable nuclear antigen, HIV human immunodeficiency virus, HUS haemolytic uraemic syndrome, LDH lactate dehydrogenase, NT-proBNP N-terminal pro-brain natriuretic peptide, TTP thrombotic thrombocytopenic purpura

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