New research supports the notion that pre-renal and intrinsic acute kidney injury are distinct molecular entities and hence different disease states despite similar increases in serum creatinine level. Pre-renal AKI induces protective molecular mechanisms whereas intrinsic AKI requires a 'second hit' that upregulates injury genes, and results in a persistent elevation of serum creatinine and kidney injury biomarkers.
This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
Euthyroid sick syndrome and its association with complications of type 1 diabetes mellitus onset
Pediatric Research Open Access 31 January 2023
-
Acute and chronic kidney complications in children with type 1 diabetes mellitus
Pediatric Nephrology Open Access 27 July 2022
Access options
Access Nature and 54 other Nature Portfolio journals
Get Nature+, our best-value online-access subscription
$29.99 / 30 days
cancel any time
Subscribe to this journal
Receive 12 print issues and online access
$209.00 per year
only $17.42 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
References
KDIGO. KDIGO clinical practice guideline for acute kidney injury. Kidney Int. Suppl. 2, 1–138 (2012).
Uchino, S., Bellomo, R., Bagshaw, S. M. & Goldsmith, D. Transient azotemia is associated with a high risk of death in hospitalized patients. Nephrol. Dial. Transplant. 25, 1833–1839 (2010).
Nickolas, T. L. et al. Diagnostic and prognostic stratification in the emergency department using urinary biomarkers of nephron damage: a multicenter prospective cohort study. J. Am. Coll. Cardiol. 59, 246–255 (2012).
Soto, K. et al. The risk of chronic kidney disease and mortality are increased after community-acquired acute kidney injury. Kidney Int. 90, 1090–1099 (2016).
Xu, K. et al. Unique transcriptional programs identify subtypes of AKI. J. Am. Soc. Nephrol. http://dx.doi.org/10.1681/ASN.2016090974 (2016).
Supavekin, S. et al. Differential gene expression following early ischemia/reperfusion. Kidney Int. 63, 1714–1724 (2003).
Devarajan, P. Genomic and proteomic characterization of acute kidney injury. Nephron 131, 85–91 (2015).
Haase-Fielitz, A., Haase, M. & Devarajan, P. Neutrophil gelatinase-associated lipocalin as a biomarker of acute kidney injury: a critical evaluation of current status. Ann. Clin. Biochem. 51, 335–351 (2014).
Murray, P. T. et al. ADQI10 workshop. Potential use of biomarkers in acute kidney injury: report and summary of recommendations from the 10th Acute Dialysis Quality Initiative consensus conference. Kidney Int. 85, 513–521 (2014).
Acknowledgements
P.D. has received funding from the NIH (grant number P50DK096418).
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Competing interests
P.D. is a co-inventor on patents (7776824 and 7977110) related to NGAL as a biomarker of kidney injury, and declares licensing agreements with BioPorto Diagnostics and Abbott Diagnostics.
PowerPoint slides
Rights and permissions
About this article
Cite this article
Devarajan, P. Acute kidney injury: still misunderstood and misdiagnosed. Nat Rev Nephrol 13, 137–138 (2017). https://doi.org/10.1038/nrneph.2017.9
Published:
Issue Date:
DOI: https://doi.org/10.1038/nrneph.2017.9
This article is cited by
-
Euthyroid sick syndrome and its association with complications of type 1 diabetes mellitus onset
Pediatric Research (2023)
-
Acute and chronic kidney complications in children with type 1 diabetes mellitus
Pediatric Nephrology (2023)
-
Subclinical AKI: ready for primetime in clinical practice?
Journal of Nephrology (2019)