1. ¹Department of Internal Medicine, University of Arkansas for Medical Sciences, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA
2. ²Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA

Correspondence: Peter M. Price, Department of Internal Medicine, University of Arkansas for Medical Sciences, VA Medical Center, Research Section, 4300 West 7th Street, Route 151, Little Rock, Arkansas 72205, USA. E-mail: PricePeterM@uams.edu

Received 12 March 2009; Revised 23 April 2009; Accepted 28 April 2009; Published online 17 June 2009.

Abstract

Acute kidney injury (AKI) activates pathways of cell death and cell proliferation. Although seemingly discrete and unrelated mechanisms, these pathways can now be shown to be connected and even to be controlled by similar pathways. The dependence of the severity of renal-cell injury on cell cycle pathways can be used to control and perhaps to prevent acute kidney injury. This review is written to address the correlation between cellular life and death in kidney tubules, especially in acute kidney injury.