Abstract
Acute renal failure or acute kidney injury (AKI) is common in critically ill patients and carries significant morbidity and mortality. AKI has been used to describe the fullblown clinical picture of, predominantly, acute tubular necrosis following ischemic or nephrotoxic injury. Once risk factors for impending renal failure have been recognized, current clinical management is hardly able to beneficially affect the natural course, so that renal replacement therapy has to be instituted when hyperkalemia, overhydration, or other detrimental sequelae of AKI occur [1–3]. A better understanding of early mechanisms could help to design trials in the future to attenuate the development of AKI in high-risk patients. These mechanisms are, however, still poorly understood.
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Vaschetto, R., Plötz, F.B., Groeneveld, A.B.J. (2008). Role of Poly(ADP-Ribose) Polymerase in Acute Kidney Injury. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/978-0-387-77383-4_52
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DOI: https://doi.org/10.1007/978-0-387-77383-4_52
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