Remote Ischemic Preconditioning To Reduce Contrast-Induced Nephropathy: A Randomized Controlled Trial.

BACKGROUND: Despite the increasing use of pre- and post-hydration protocols and low osmolar instead of high osmolar iodine containing contrast media, the incidence of contrast induced nephropathy (CIN) is still significant. There is evidence that contrast media cause ischemia reperfusion injury of the renal medulla. Remote ischemic preconditioning (RIPC) is a non-invasive, safe, and low cost method to reduce ischemia reperfusion injury. The aim of this study is to investigate whether RIPC, as an adjunct to standard preventive measures, reduces contrast induced acute kidney injury in patients at risk of CIN. METHODS: The RIPCIN study is a multicenter, single blinded, randomized controlled trial in which 76 patients at risk of CIN received standard hydration combined with RIPC or hydration with sham preconditioning. RIPC was applied by four cycles of 5 min ischemia and 5 min reperfusion of the forearm. The primary outcome measure was the change in serum creatinine from baseline to 48 to 72 hours after contrast administration. RESULTS: With regard to the primary endpoint, no significant effect of RIPC was found. CIN occurred in four patients (2 sham and 2 RIPC). A pre-defined subgroup analysis of patients with a Mehran risk score ≥11, showed a significantly reduced change in serum creatinine from baseline to 48 to 72 hours in patients allocated to the RIPC group (Δ creatinine -3.3 ± 9.8 µmol/L) compared with the sham group (Δ creatinine +17.8 ± 20.1 µmol/L). CONCLUSION: RIPC, as an adjunct to standard preventive measures, does not improve serum creatinine levels after contrast administration in patients at risk of CIN according to the Dutch guideline. However, the present data indicate that RIPC might have beneficial effects in patients at a high or very high risk of CIN (Mehran score ≥ 11). The RIPCIN study is registered at: http://www.controlled-trials.com/ISRCTN76496973.

Wall stress analysis in small asymptomatic, symptomatic and ruptured abdominal aortic aneurysms.

OBJECTIVES: To evaluate the potential of wall stress analysis for the identification of abdominal aortic aneurysm (AAA) at elevated risk of rupture in spite of small diameter. MATERIALS AND METHODS: Thirty patients with small AAA, 10 asymptomatic, 10 symptomatic and 10 ruptured, were included. Demographic data and results from physical examinations were recorded in a retrospective fashion. After CT-evaluation and the creation of a patient specific 3D model, wall stress was calculated using the finite element method. RESULTS: No differences were observed in diameter between asymptomatic, symptomatic or ruptured aneurysms (5.1+/-0.2 cm vs. 5.1+/-0.2 cm vs. 5.3+/-0.2 cm respectively; p=0.57). Peak aortic wall stress at maximal systolic blood pressure is significantly higher in ruptured than asymptomatic aneurysms (51.7+/-2.4 N/cm(2) vs. 39.7+/-3.3 N/cm(2) respectively; p=0.04). Wall stress analysis at uniform blood pressure, performed to correct for higher blood pressure in the symptomatic and rupture group did not result in significant differences in peak wall stress (asymptomatic 31.7+/-2.3 N/cm(2); symptomatic 30.5+/-1.3 N/cm(2); rupture 36.7+/-4.0 N/cm(2); p=0.26). CONCLUSIONS: Wall stress analysis at maximal systolic blood pressure is a promising technique to detect aneurysms at elevated aneurysm rupture risk. Since no significant differences were found at uniform blood pressure, the need for adequate blood pressure control in aneurysm patients is reiterated.