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Renal oxygenation and haemodynamics in acute kidney injury and chronic kidney disease
Author(s) -
Singh Prabhleen,
Ricksten SvenErik,
Bragadottir Gudrun,
Redfors Bengt,
Nordquist Lina
Publication year - 2013
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12036
Subject(s) - medicine , kidney disease , acute kidney injury , sepsis , nitric oxide , kidney , hypoxia (environmental) , renal replacement therapy , atrial natriuretic peptide , fibrosis , cardiology , oxygen , chemistry , organic chemistry
SummaryAcute 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.