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Semin Nephrol. 2018 Jan;38(1):3-11. doi: 10.1016/j.semnephrol.2017.09.002.

Phenotyping of Acute Kidney Injury: Beyond Serum Creatinine.

Author information

1
Program of Applied Translational Research, Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, CT.
2
VA Connecticut Healthcare System, West Haven, CT. Electronic address: chirag.parikh@yale.edu.

Abstract

Acute kidney injury (AKI) is a common complication in hospitalized patients and is associated with adverse short- and long-term outcomes. AKI is diagnosed by serum creatinine (SCr)-based consensus definitions that capture an abrupt decrease in glomerular filtration rate associated with AKI. However, SCr-based AKI definitions lack sensitivity and specificity for diagnosing structural kidney injury. Moreover, AKI is a heterogeneous condition consisting of distinct phenotypes based on its etiology, prognosis, and molecular pathways, and that may potentially require different therapies. SCr-based AKI definitions provide no information on these AKI phenotypes. This review highlights traditional and novel tools that overcome the limitations of SCr-based AKI definitions to improve AKI phenotyping.

KEYWORDS:

AKI; IL-18; IL-6; KIM-1; L-FABP; NGAL; biomarkers; creatinine; cystatin C; furosemide; urinary casts; urine microscopy

PMID:
29291759
PMCID:
PMC5753429
DOI:
10.1016/j.semnephrol.2017.09.002
[Indexed for MEDLINE]
Free PMC Article

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