| Literature DB >> 26538634 |
Mark de Caestecker1, Ben D Humphreys2, Kathleen D Liu3, William H Fissell4, Jorge Cerda5, Thomas D Nolin6, David Askenazi7, Girish Mour6, Frank E Harrell8, Nick Pullen9, Mark D Okusa10, Sarah Faubel11.
Abstract
Despite extensive research, no therapeutic interventions have been shown to prevent AKI, accelerate recovery of AKI, or reduce progression of AKI to CKD in patients. This failure in translation has led investigators to speculate that the animal models being used do not predict therapeutic responses in humans. Although this issue continues to be debated, an important concern that has not been addressed is whether improvements in preclinical study design can be identified that might also increase the likelihood of translating basic AKI research into clinical practice using the current models. In this review, we have taken an evidence-based approach to identify common weaknesses in study design and reporting in preclinical AKI research that may contribute to the poor translatability of the findings. We focused on use of N-acetylcysteine or sodium bicarbonate for the prevention of contrast-induced AKI and use of erythropoietin for the prevention of AKI, two therapeutic approaches that have been extensively studied in clinical trials. On the basis of our findings, we identified five areas for improvement in preclinical study design and reporting. These suggested and preliminary guidelines may help improve the quality of preclinical research for AKI drug development.Entities:
Keywords: acute kidney injury; preclinical research; reproducibility
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Year: 2015 PMID: 26538634 PMCID: PMC4657852 DOI: 10.1681/ASN.2015070832
Source DB: PubMed Journal: J Am Soc Nephrol ISSN: 1046-6673 Impact factor: 10.121