Contrast-induced acute kidney injury in interventional cardiology: Emerging evidence and unifying mechanisms of protection by remote ischemic conditioning

Abstract

Contrast-induced acute kidney injury (CI-AKI) is a common complication of many diagnostic and therapeutic cardiovascular procedures. It is associated with longer in-hospital stay, more complicated hospitalization course, and higher in-hospital morbidity and mortality. With increasing use of contrast media in various diagnostic and interventional procedures, the prevalence of CI-AKI is expected to rise. Although pre-hydration with intravenous normal saline is recommended in patients with elevated risk of CI-AKI, this approach is often not feasible in many clinical settings. Remote ischemic conditioning (RIC), elicited by application of one or more, brief, non-injurious episodes of ischemia and reperfusion of a limb, is a promising therapy for preventing or attenuating the deleterious effects of contrast media on the kidney. Although the mechanisms of protection by RIC have not been completely defined, complex humoral, neural, and inflammatory pathways have been hypothesized to be in play. Given that RIC is non-invasive and cheap, it is attractive from clinical and economic perspective as a therapy to protect the kidney from CI-AKI. In this succinct review, we highlight the unifying mechanisms of CI-AKI and provide an overview of proposed biological mechanisms of renal protection by RIC. Emerging pre-clinical and clinical evidence in interventional cardiology are also discussed.

Limb remote ischemic conditioning of the recipient protects the liver in a rat model of arterialized orthotopic liver transplantation

“…The effects of remote ischemic conditioning have been investigated in IR scenarios of different organs (e.g. myocardium [ 23 , 24 ], brain [ 25 ], kidney [ 26 , 27 ], and by our group on liver [ 10 , 12 ]) in multiple experimental and clinical studies over the past years [ 9 ]. However, available and consistent datasets from well-designed and comprehensive experimental studies, which would demonstrate the effects of this approach in liver transplantation are rare ( Table 1 .)…”

Effect of remote ischemic Pre-conditioning on primary percutaneous coronary intervention outcomes: a randomized clinical trial

“…The exact mechanism behind the renal protection of RIPC is not clearly understood. However, it has been reported that RIPC can develop its effect on kidneys in two different ways; generating nitric oxide/nitrate and release of damage associate proteins, and inducing cell cycle arrest in kidneys (33). Nitric oxide generation and vasodilatation can prevent renal vasoconstriction, while damaged associate proteins will further prevent cell death and therefore prevent renal injury (33).…”

“…However, it has been reported that RIPC can develop its effect on kidneys in two different ways; generating nitric oxide/nitrate and release of damage associate proteins, and inducing cell cycle arrest in kidneys (33). Nitric oxide generation and vasodilatation can prevent renal vasoconstriction, while damaged associate proteins will further prevent cell death and therefore prevent renal injury (33). Moreover, recent metaanalyses about the efficacy of RIPC has demonstrated that this intervention can reduce the incidence of AKI and MI in patients undergoing PCI (34,35).…”

Nicorandil for the prevention of contrast‐induced nephropathy: A meta‐analysis of randomized controlled trials

“…With the more and more common application of invasive diagnostic and treatment procedures, contrast‐induced nephropathy (CIN) has become an important cause of acute renal failure in current clinical practice . Generally, CIN is defined as a relative increment of serum creatinine (SCr) of more than 25% or an absolute increment of SCr of more than 0.5 mg (or 44.2 μmol/L) as compared with its baseline level within 48 or 72 hours after contrast exposure .…”