Remote ischemic preconditioning and renoprotection: from myth to a novel therapeutic option?

Abstract

There is currently no effective prophylactic regimen available to prevent contrast-induced AKI (CI-AKI), a frequent and life-threatening complication after cardiac catheterization. Therefore, novel treatment strategies are required to decrease CI-AKI incidence and to improve clinical outcomes in these patients. Remote ischemic preconditioning (rIPC), defined as transient brief episodes of ischemia at a remote site before a subsequent prolonged ischemia/reperfusion injury of the target organ, is an adaptational response that protects against ischemic and reperfusion insult. Indeed, several studies demonstrated the tissue-protective effects of rIPC in various target organs, including the kidneys. In this regard, rIPC may offer a novel noninvasive and virtually cost-free treatment strategy for decreasing CI-AKI incidence. This review evaluates the current experimental and clinical evidence for rIPC as a potential renoprotective strategy, and discusses the underlying mechanisms and key areas for future research.

Figure 1.

Mechanisms of rIPC. AP-1, activator protein-1; cGMP, cyclic guanosine monophosphate; CGRP, calcitonin gene-related peptide; COX2, cyclooxygenase 2; HIF-1α, hypoxia-inducible factor 1α; HSP, heat shock protein; iNOS, inducible nitric oxide synthase; JAK, Janus kinase; MEK, MAPK kinase; mPTP, mitochondrial permeability transition pore; Nrf2, nuclear factor (erythroid-derived 2)-like 2; STAT1/3, signal transducer and activator of transcription.