Effects of remote ischemic preconditioning on contrast induced nephropathy after percutaneous coronary intervention in patients with acute coronary syndrome

Abstract

Objective:The aim of this study was to explore the clinical effects of remote ischemic preconditioning (RIPC) on contrast-induced nephropathy after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS).Patients and Methods:The study was a single-center, prospective, randomized, controlled study. A total of 161 patients with ACS and the rate of estimate glomerular filtration (eGFR) 15 to 70 mL/min/1.73 m2 undergoing PCI were randomly assigned to RIPC group (induced by 4 times of 5-minute inflations of a blood pressure cuff to 200 mmHg around the upper arm, followed by 5-min intervals of reperfusion at 1 hour before PCI therapy) or control group (an uninflated cuff around the arm). Successful completion of the PCI eventually included 107 cases of patients, including 50 cases in the RIPC group and 57 cases in the control group. The level of serum creatinine (Scr), CystatinC (CysC), blood neutrophil gelatinase-associated lipocalin (NGAL), eGFR were measured in all patients at 6 am before the day of PCI, and 4-hour NGAL, 24-hour CysC, 72-hour Scr, and eGFR after PCI in the 2 groups. The incidence of major adverse events in the kidney (including the incidence of CIN, the need for dialysis, or renal replacement therapy after using contrast agent) and the composite endpoint of cardiovascular events were recorded at 6 months after PCI.Results:There were no statistically significant differences in baseline indicators between the 2 groups. Scr, CysC, and blood NGAL levels and the incidence of CIN in patients with RIPC group were significantly lower than those form the control group after PCI (P < .05), but there were no significant differences between the average value of eGFR and occurrence of Major cardiovascular events in the postoperative 6 months (P > .05).Conclusions:RIPC can reduce PCI-related CIN and protect renal function in patients with ACS. The benefits of these patients by RIPC may be related to the reduction of the NGAL and CysC.

The efficacy of remote ischemic conditioning in preventing contrast‐induced nephropathy among patients undergoing coronary angiography or intervention: An updated systematic review and meta‐analysis

“…In 2 out of 18 articles, patients were identified and randomized 1:1 with computer‐generated block randomization (Crimi et al, ; Yamanaka et al, ), while in the other studies, the randomization method was mentioned without a specific description. Eight studies reported completeness of follow‐up (Crimi et al, ; Deftereos et al, ; Elbadawi et al, ; Er et al, ; Hoole et al, ; Menting et al, ; Moretti et al, ; Zhou et al, ), and almost all of the studies included patients with similar baseline characteristics and provided details about the inclusion criteria and the intention‐to‐treat analysis. The literature quality scores are shown in Table .…”

“…We separated 18 studies into three groups according to the dose of CM administered: ≤100 ml group (low) 1 (Cao et al, ; Ferdinandy et al, ; Gholoobi et al, ; Igarashi et al, ), 100–200 ml group (medium) 1 (Balbir Singh et al, ; Bøtker et al, ; Er et al, ; Ferdinandy et al, ; Giricz et al, ; Han et al, ; Hausenloy et al, ; Hausenloy & Yellon, ; Hoole et al, ; Luo et al, ; Moretti et al, ; Narula et al, ; Sadat et al, ; Savaj et al, ; White et al, ; Xu et al, ; Yamanaka et al, ; Zagidullin et al, ; Zhou et al, , ), and >200 ml group (high) 2 (Deftereos et al, ; Sadat et al, ). RIC significantly decreased the incidence of CIN in all three groups (low group: OR = 0.29, 95% CI 0.14, 0.60, p < .05; medium group: OR = 0.47, 95% CI 0.34, 0.64; p < .05; and high group: OR = 0.47, 95% CI 0.26, 0.56; p < .05; Table ).…”

“…Although the mechanism of CIN in patients exposed to contrast medium has yet to be elucidated, renal ischemic injury and direct tubule toxicity in renal tubular cells have already been proposed (Igarashi et al, ; Zagidullin et al, ; Zhou et al, ). Another possible mechanism of injury is that CM elicits hypoxia of the renal medulla and leads to free radical production via postischemic oxidative stress in the renal tissue (Er et al, ; Savaj et al, ).…”

“…Based on the inclusion and exclusion criteria, 18 relevant studies were included. The study selection process is shown in Figure 1 (Balbir Singh et al, 2016;Cao, Wang, Zhang, Xia, & Yang, 2018;Crimi et al, 2013;Deftereos et al, 2013;Elbadawi et al, 2017;Er et al, 2012;Gholoobi, Sajjadi, Shabestari, Eshraghi, & Shamloo, 2015;Hoole et al, 2009;Igarashi, Iino, Watanabe, & Ito, 2013;Lavi et al, 2014;Luo et al, 2013;Menting et al, 2015;Moretti et al, 2018;Savaj, Savoj, Jebraili, & Sezavar, 2014;Xu et al, 2015;Yamanaka et al, 2015;Zagidullin et al, 2017;Zhou et al, 2018).…”

“…Our meta-analysis included 2,503 patients from 18 studies, of which 1,243 patients receiving RIC before or after surgery were assigned to the experimental group, and the remaining 1,260 patients were assigned to the control group. Two trials defined CIN as a relative increase of >25% from baseline (Crimi et al, 2013;Hoole et al, 2009); two trials used the definition of either an absolute increase in Scr > 0.5 mg/dl or 44.2 mmol/L or a relative increase of >25% from baseline within 16 hr after CM exposure (Luo et al, 2013;Xu et al, 2015), one trial used the same criteria as above within 24 hr after exposure (Lavi et al, 2014), three trials within 48 hr after exposure (Balbir Singh et al, 2016;Moretti et al, 2018;Zagidullin et al, 2017), three trials between 48 and 72 hr after exposure (Menting et al, 2015;Yamanaka et al, 2015;Zhou et al, 2018), one trial within 72 hr after exposure (Cao et al, 2018), and three trials within 96 hr after exposure (Deftereos et al, 2013;Elbadawi et al, 2017;Zagidullin et al, 2017); and two trials used the definition of an absolute increase in Scr of 0.3 mg/dl within 24 or 48 hr of exposure to the contrast agent (Gholoobi et al, 2015;Savaj et al, 2014). The mean CM dose ranged from 77.7 to 270 ml.…”