Journal
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
Volume 40, Issue 2, Pages 138-147Publisher
WILEY
DOI: 10.1111/1440-1681.12036
Keywords
acute kidney injury; chronic kidney disease; glomerular filtration rate; nitric oxide; oxygen consumption; oxygenation; renal blood flow
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Funding
- Swedish Research Council
- Jeansson Foundations
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [K08-DK084305]
- O'Brien Kidney Center for Acute Kidney Injury [P30DK079337]
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Acute kidney injury (AKI) is a major burden on health systems and may arise from multiple initiating insults, including ischaemia-reperfusion injury, cardiovascular surgery, radiocontrast administration and sepsis. Similarly, the incidence and prevalence of chronic kidney disease (CKD) continues to increase, with significant morbidity and mortality. Moreover, an increasing number of AKI patients survive to develop CKD and end-stage renal disease. Although the mechanisms for the development of AKI and progression to CKD remain poorly understood, initial impairment of oxygen balance likely constitutes a common pathway, causing renal tissue hypoxia and ATP starvation that, in turn, induce extracellular matrix production, collagen deposition and fibrosis. Thus, possible future strategies for one or both conditions may involve dopamine, loop diuretics, atrial natriuretic peptide and inhibitors of inducible nitric oxide synthase, substances that target kidney oxygen consumption and regulators of renal oxygenation, such as nitric oxide and heme oxygenase-1.
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