Tubular cell calcium concentration and content rise following acute renal injury induced by ischemic and toxic insults. Since calcium plays a critical role in many cell functions and the proximal tubule appears to be a major site of injury in acute renal failure, it is possible that cell calcium overload plays a direct role in the pathogenesis of acute renal failure. Tubular cell calcium overload has been associated with altered function at the level of the plasma membrane, mitochondria, endoplasmic reticulum and cytoskeleton. While there is evidence to support a role for calcium in acute renal injury, the importance of cell calcium overload needs to be further explored. Furthermore, alterations in extracellular calcium and mineral metabolism may be involved in some aspects of acute renal failure and recovery. Calcium channel blockers and other interventions designed to modulate calcium changes may have a role in the treatment of acute renal failure.