Prevention of contrast nephropathy by BP cuff inflation

Prevention of contrast nephropathy by BP cuff inflation: ischemic preconditioning with intermittent inflation

Prevention of contrast nephropathy by BP cuff inflation: Contrast induced acute kidney injury (CI-AKI or contrast nephropathy) occurs in a small group of individuals undergoing coronary angiography and percutaneous revascularization. One of the possible mechanisms is thought to be ischemic kidney injury. It is well known that ischemic preconditioning can reduce the damage due to ischemia. Similarly ischemic preconditioning at a distance (by inducing ischemia in a different vascular territory) has also been found to have a similar benefit. Fikret Er and colleagues [Ischemic Preconditioning for Prevention of Contrast-Medium-Induced Nephropathy: Randomized Pilot RenPro-Trial (Renal Protection Trial). Circulation. 2012 Jul 17;126(3):296-303] checked whether this could principle could be applied to prevent contrast induced acute kidney injury. Their study had 100 patients with either a serum creatinine value more than 1.4 mg/dL and/or an estimated glomerular filtration rate less than 60 mL/min/1.73 square meter body surface area, who were undergoing elective coronary angiography. Half of them were randomized to standard care and the rest of them to ischemic preconditioning with intermittent inflation (50 mm Hg above the individual’s systolic pressure) and deflation of a arm blood pressure cuff for four cycles of five minutes each. Angiography was done within forty five minutes of the last inflation.

Contrast induced acute kidney injury was defined as 25 percent or more elevation from baseline serum creatinine or 0.5 mg/dL or more absolute elevation of serum creatinine within two days of contrast exposure. While forty percent of those in the control group had evidence of contrast induced acute kidney injury, only twelve percent had it in the remote ischemic preconditioning group (P=0.002). Remote ischemic preconditioning was not associated with any major adverse events. It may be noted that both patient groups were at high risk of developing contrast induced acute kidney injury as assessed by Mehran risk score. If the results from this study are replicated in larger studies, it should be a path breaking discovery, benefitting many high risk patients for prevention of contrast nephropathy to a great extent.

A second extended trial (RenPro-II-Trial) has been designed by the same group to test the effects of ischemic preconditioning on cardiovascular mortality and morbidity. We can look out for good message from the second trial as well.