Remote ischemic preconditioning reduces contrast-induced acute kidney injury in patients with ST-elevation myocardial infarction: A randomized controlled trial

Yamanaka, Toshiaki; Kawai, Yusuke; Miyoshi, Toru; Mima, Tsutomu; Takagi, Kenji; Tsukuda, Saori; Kazatani, Yukio; Nakamura, Kazufumi; Ito, Hiroshi

doi:10.1016/j.ijcard.2014.10.135

Cited by 74 publications

(98 citation statements)

References 27 publications

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“…In the kidney, RIPC has been reported to attenuate post-ischemic injury. 4 Although RIPC reduces post-ischemic injury in many organs, its application requires foreknowledge of the ischemic event, which is difficult to anticipate in most circumstances, with the exception of surgery and transplantation. Recently, studies have attempted to circumvent this issue by modification of the reperfusion phase.…”

Section: Introductionmentioning

confidence: 99%

Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion

et al. 2016

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Purpose Renal ischemia/reperfusion (I/R) injury is a common clinical problem associated with significant mortality and morbidity. One newly described strategy to reduce this damage is remote perconditioning (RPEC), in which short-time ischemia of a limb during renal ischemia reduces the I/ R-induced kidney injury. This study aimed to assess whether RPEC confer protection through changes in pro-inflammatory mediators. Methods Rats were subjected to right nephrectomy and randomized into: sham (no intervention), I/R (subjected to 45-min left renal ischemia) and RPEC group (subjected to four cycles of 5-min I/R of the femoral artery administered during renal ischemia). After 24-h, blood, urine, and kidney samples were collected. Biochemical indicators of renal dysfunction were measured in the cases of Neutrophil gelatinase-associated lipocalin (NGAL), and N-acetyl-B-diglucosaminidase (NAG) activity. Inflammatory cytokines [interleukin (IL)-6 and tumor necrosis factor-alpha, TNF-a] expression in the renal tissues as well as Periodic acid-Schiff stained histological sections were evaluated. Results I/R resulted in renal dysfunction, as evidenced by higher renal NGAL expression and urinary NAG activities. This was accompanied by increased TNF-a and IL-6 expressions as well as histological changes in this group. However, RPEC improved renal histology and function compared with the I/R group. Furthermore, the RPEC group showed decreases in TNF-a and IL-6 expression. Conclusions These results suggest that RPEC reduces the dysfunction and injury associated with I/R of the kidney. This technique reduced the proinflammatory cytokine in the kidney. RPEC could be a promising strategy against I/R-induced acute kidney injury partly by down-regulation of inflammatory mediators. ARTICLE HISTORY

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Section: Introductionmentioning

confidence: 99%

Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion

et al. 2016

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“…Surprisingly, RIPC initially proved effective in reducing the rate of CI-AKI in patients undergoing elective CA 75 or PCI in the setting of STEMI. 76 Preliminary data concerning the use of RIPC in CI-AKI are promising but merit verification in high-volume randomized studies.…”

Section: Chronic Kidney Disease and Cardiac Interventionsmentioning

confidence: 99%

Contrast-induced acute kidney injury: the dark side of cardiac catheterization

Wybraniec¹,

Mizia-Stec²,

Wiȩcek³

2015

Polish Archives of Internal Medicine

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POLSKIE ARCHIWUM MEDYCYNY WEWNĘTRZNEJ 2015; 125 (12) 938the diagnostic criteria applied, comorbidities, and the type of procedure (coronary angiography [CA]; percutaneous coronary intervention [PCI]). CI-AKI is a challenge mainly for well-developed countries, in which excessive amounts of CM are used on a daily basis. When using the definition of CI-AKI as an increase of serum creatinine concentrations (SCr) by more than 25% relative to baseline and/or by more than 0.5 mg/dl at 48 hours after PCI, the rate of CI-AKI ranged from 3.3% according to the Mayo Clinic PCI registry 6 to 13.1% as stated by Mehran et al. 7 In the largest registry by Gurm et al, 8 based on 68 573 procedures, the rate of CI-AKI was 2.5%, defined as an absolute elevation in SCr by more than 0.5 mg/dl. Still, when only clinically relevant CI-AKI requiring dialysis was considered, the incidence decreased to a range from 0.8% to 1.7%. 9 This review sought to summarize the contemporary knowledge on pathophysiology, risk factors, diagnostic markers, and management of CI-AKI, with a special interest in CI-AKI as a result of cardiac catheterization. Accordingly, the Medline and EmBase databases were queried to Introduction Contrast-induced acute kidney injury (CI-AKI), previously known as contrast--induced nephropathy (CIN), represents a specific form of acute renal function impairment triggered by the use of iodinated contrast media (CM). As CI-AKI remains the subtype of acute kidney injury (AKI), it is recommended to use common definitions of AKI, such as the 2012 KDIGO criteria, 1 RIFLE classification (Risk, Injury, Failure, Loss of Function, End-Stage Renal Disease), 2 AKI Network criteria, 3 or the definition by Harjai 4 (Supplementary material online, Table S1).The rapid development of invasive cardiology triggered a massive increase in CM exposure. Since the implementation of the first CM in the 1950s, CI-AKI has emerged as the third most common subtype of hospital-acquired renal failure (reaching 11% of all cases), after renal hypoperfusion (42%) and postoperative AKI.5 Nearly half of all cases of CI-AKI occur after invasive cardiac procedures owing to CM-related nephrotoxicity and frequently present hemodynamic instability. 5The exact rate of CI-AKI in the setting of a cardiology department varies depending on ABSTRACTThe rapidly growing number of percutaneous coronary interventions has led to a considerable improvement in the outcome of patients with acute coronary syndromes, yet concurrently exposing patients to enormous volumes of contrast media with the inherent risk of renal function impairment. The issue of contrast-induced acute kidney injury (CI-AKI) is not only associated with direct sequelae such as prolonged hospital stay, but also with increased risk of chronic kidney disease, recurrent acute coronary syndromes, cerebral ischemia, and increased mortality rate. The ubiquitous application of contrast media warrants active search for reliable risk factors, diagnostic markers, preventive measures, and therapeutic modalities th...

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“…In an elegant randomized controlled trial involving STEMI patients (n=94) in Japan, Yamanaka et al showed that RIC applied before PCI significantly reduced CI-AKI (10% versus 36%) compared with PCI alone [55]. Recent analysis of data from National Cardiovascular Data Registry (NCDR) Acute Coronary Treatment and Intervention Outcomes Network Registry®-Get With the Guidelines ™ (ACTION Registry–GWTG) from two PCI-hospitals in the United States utilizing RIC during helicopter transport showed that STEMI patients who received RIC during inter-facility helicopter transport were less likely to have CI-AKI compared to patients who did not receive RIC (8.7% versus 18.5%; unadjusted OR=0.42, 95% CI 0.18– 0.94, p=0.036) [56].…”

Section: Overview Of Clinical Evidence Of Renal Protection By Remote mentioning

confidence: 99%

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

Atanda

Olafiranye

2017

Cardiovascular Revascularization Medicine

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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.

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Remote ischemic preconditioning reduces contrast-induced acute kidney injury in patients with ST-elevation myocardial infarction: A randomized controlled trial

Abstract: In patients with ST-elevation myocardial infarction, RIPC before percutaneous coronary intervention reduced the incidence of CI-AKI.

Cited by 74 publications

References 27 publications

Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion

Hind limb perconditioning renoprotection by modulation of inflammatory cytokines after renal ischemia/reperfusion

Contrast-induced acute kidney injury: the dark side of cardiac catheterization

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

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