Clinical and translational research in acute kidney injury (AKI) requires well designed prospective studies as well as access to well characterized patients with longitudinal follow up coupled with biological samples enabling investigators to probe the underlying mechanisms and pathways contributing to outcomes.
The specific aims of the Resource for Clinical Studies of AKI (Core A) are to 1) provide core resources to support the design and conduct of clinical research In AKI, 2) provide a genomics resource to perform systematic genomic analyses and allow correlation with clinical phenotypic information, and 3) provide a biological sample repository linked to the clinical and genomics database for the characterization of patients for our investigator base. This core will specifically provide investigators access to patients with AKI through an established international network of collaborating investigators who are contributing to an ongoing registry of AKI in the ICU setting currently with over 1000 patients, access to biological samples including DNA from patients and healthy controls and protocols and tools for quantitative assessment of changes in kidney function. Since its inception the Core has been successful in supporting investigators for clinical and translational research. The Core has established a robust data management system and database of patients with AKI that Is flexible In accommodating the research objectives of individual investigators and collaborating centers;currently supporting 5 large multicenter projects including the AKI registry and an international prospective study for the genomics of drug-induced kidney injury. The genomics resource has facilitated the investigation of genetic determinants (both risk and outcome) of AKI, and identified novel genomic predictors of the longitudinal course in AKI. Over 14,000 biomarker assays incorporating more than 20 analytes have been performed to support both pediatric and adult AKI research. A biological sample repository has been established and has >2000 sequential samples from well-characterized patients with and without AKI. The Core has supported 143 projects for 52 investigators (including 4 pilot recipients and 45 non-core personnel), resulting in 57 publications. These rich resources will continue to enable interdisciplinary clinical investigation in AKI to advance our understanding of the natural history, pathophysiology and treatment of human AKI. Core A in conjunction with existing resources at UAB and UCSD and other cores within the O'Brien center will accelerate the translation of new investigative insights towards improving outcomes for patients with AKI.

Public Health Relevance

Acute kidney injury is associated with severe consequences Including death, prolonged hospitalization and can lead to chronic kidney disease. Core A of this Center provides investigators key resources required to study patients with acute kidney injury to enable a better understanding of the underlying mechanisms and determine best approaches to diagnose and manage this disease.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
5P30DK079337-07
Application #
8733665
Study Section
Special Emphasis Panel (ZDK1-GRB-6)
Project Start
Project End
Budget Start
2014-08-01
Budget End
2015-07-31
Support Year
7
Fiscal Year
2014
Total Cost
$307,567
Indirect Cost
Name
University of Alabama Birmingham
Department
Type
DUNS #
063690705
City
Birmingham
State
AL
Country
United States
Zip Code
35294
Guan, Z; Wang, F; Cui, X et al. (2018) Mechanisms of sphingosine-1-phosphate-mediated vasoconstriction of rat afferent arterioles. Acta Physiol (Oxf) 222:
Adedoyin, Oreoluwa; Boddu, Ravindra; Traylor, Amie et al. (2018) Heme oxygenase-1 mitigates ferroptosis in renal proximal tubule cells. Am J Physiol Renal Physiol 314:F702-F714
Layton, Anita T; Edwards, Aurélie; Vallon, Volker (2018) Renal potassium handling in rats with subtotal nephrectomy: modeling and analysis. Am J Physiol Renal Physiol 314:F643-F657
Li, Mao; Boddeda, Srinivasa Rao; Chen, Bo et al. (2018) NK cell and Th17 responses are differentially induced in murine cytomegalovirus infected renal allografts and vary according to recipient virus dose and strain. Am J Transplant 18:2647-2662
Fu, Yiling; Breljak, Davorka; Onishi, Akira et al. (2018) Organic anion transporter OAT3 enhances the glucosuric effect of the SGLT2 inhibitor empagliflozin. Am J Physiol Renal Physiol 315:F386-F394
Leaf, David E; Siew, Edward D; Eisenga, Michele F et al. (2018) Fibroblast Growth Factor 23 Associates with Death in Critically Ill Patients. Clin J Am Soc Nephrol 13:531-541
Bernard, Karen; Logsdon, Naomi J; Benavides, Gloria A et al. (2018) Glutaminolysis is required for transforming growth factor-?1-induced myofibroblast differentiation and activation. J Biol Chem 293:1218-1228
Singal, Ashwani K; Jackson, Bradford; Pereira, Glauber B et al. (2018) Biomarkers of Renal Injury in Cirrhosis: Association with Acute Kidney Injury and Recovery after Liver Transplantation. Nephron 138:1-12
Crotty Alexander, Laura E; Drummond, Christopher A; Hepokoski, Mark et al. (2018) Chronic inhalation of e-cigarette vapor containing nicotine disrupts airway barrier function and induces systemic inflammation and multiorgan fibrosis in mice. Am J Physiol Regul Integr Comp Physiol 314:R834-R847
Pang, Paul; Abbott, Molly; Abdi, Malyun et al. (2018) Pre-clinical model of severe glutathione peroxidase-3 deficiency and chronic kidney disease results in coronary artery thrombosis and depressed left ventricular function. Nephrol Dial Transplant 33:923-934

Showing the most recent 10 out of 404 publications