Adenosine Generation and Signaling during Acute Kidney Injury

Acute kidney injury (AKI) is among the leading causes of morbidity and mortality in hospitalized patients. Particularly in the perioperative period, the most common cause of AKI is renal ischemia. At present, therapeutic modalities to prevent or treat AKI are extremely limited and the search for nov...

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Bibliographic Details
Published in:Journal of the American Society of Nephrology 2011, Vol.22 (1), p.14-20
Main Authors: BAUERLE, Jessica D, GRENZ, Almut, KIM, Jae-Hwan, LEE, H. Thomas, ELTZSCHIG, Holger K
Format: Article
Language:English
Subjects:
Acute Kidney Injury - etiology
Acute Kidney Injury - metabolism
Acute Kidney Injury - physiopathology
Adenosine - metabolism
Animals
Biological and medical sciences
Humans
Ischemia - complications
Ischemia - metabolism
Ischemia - physiopathology
Kidney - blood supply
Kidney - metabolism
Kidneys
Medical sciences
Mice
Models, Animal
Nephrology. Urinary tract diseases
Receptors, Purinergic P1 - metabolism
Signal Transduction - physiology
Urinary system involvement in other diseases. Miscellaneous
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Summary:Acute kidney injury (AKI) is among the leading causes of morbidity and mortality in hospitalized patients. Particularly in the perioperative period, the most common cause of AKI is renal ischemia. At present, therapeutic modalities to prevent or treat AKI are extremely limited and the search for novel therapeutic interventions for ischemic AKI is an area of intense investigation. Recent studies implicate the endogenous signaling molecule, adenosine, in kidney protection from ischemia. As such, enzymatic production of adenosine from its precursor molecules ATP and AMP, and signaling events through adenosine receptors, play a critical role in attenuating renal inflammation and preserving kidney function during episodes of renal ischemia. Utilizing genetic mouse models with defects in adenosine generation or signaling provide strong evidence for the key role of extracellular adenosine in adapting renal tissues to limited oxygen availability and attenuating hypoxia-driven inflammation of the kidneys. Moreover, experimental therapeutics targeting individual adenosine receptors demonstrate strong prophylactic or therapeutic effects during murine AKI. If these experimental strategies can be translated into a clinical setting, adenosine receptor therapeutics may become an integral part in the prevention or treatment of AKI from renal ischemia.
ISSN:1046-6673
1533-3450
DOI:10.1681/asn.2009121217