Renal ischemia is the most common cause of acute kidney injury (AKI) still associated with high mortality rates of about 50%
in the intensive care unit. Postischemic AKI is characterized by decreased glomerular filtration rate and high renal vascular resistance
with endothelial activation and dysfunction, a process of critical importance that is followed by a reduction in microvascular blood flow
mainly affecting the renal outer medulla. The pathophysiology of postischemic AKI remains incompletely understood, although it seems
to be a phenomenon of altered renal hemodynamics, linked critically to the production of high amounts of nitric oxide and free radicals.
On the other hand, and depending on the severity of renal ischemia, tubular epithelial cells undergo a varying degree of necrosis or apoptosis
with tubular obstruction followed by both, anatomical and functional recovery. The way in which vascular and tubular epithelium
recover determines the final status of the renal function, ranging from full recovery to chronic renal failure and ultimately to end-stage
renal disease. In this review we will revise the mechanisms responsible for these pathophysiologic alterations, including the role of heme
oxygenase system and sex differences in the susceptibility to ischemic acute renal failure, and we will also review the pre- and postconditioning
phenomena, in which brief episodes of ischemia before (pre-conditioning) or after (post-conditioning) the prolonged ischemia
have a protective effect on AKI after reperfusion. Interestingly, these protective responses can be elicited by ischemizing distant tissues
(remote conditioning). A better understanding of these mechanisms may help to improve the clinical outcome of those patients.