Relation of Contrast-Induced Nephropathy to Long-Term Mortality After Percutaneous Coronary Intervention

Abe, Mitsuru; Morimoto, Takeshi; Akao, Masaharu; Furukawa, Yutaka; Nakagawa, Yoshihisa; Shizuta, Satoshi; Ehara, Natsuhiko; Taniguchi, Ryoji; Doi, Takahiro; Nishiyama, Kei; Ozasa, Neiko; Saito, Naritatsu; Hoshino, Kozo; Mitsuoka, Hirokazu; Toma, Masanao; Tamura, Toshihiro; Haruna, Yoshisumi; Kita, Toru; Kimura, Takeshi

doi:10.1016/j.amjcard.2014.05.009

Cited by 94 publications

(75 citation statements)

References 19 publications

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“…29 In addition, the combined CIN (increase of ≥25% or absolute 0.5 mg/dL creatinine levels) was not significantly correlated with longterm mortality in patients without CKD (≥60 mL/min per 1.73 m 2 ). 30 Therefore, we used the definition of an increase of 0.5 mg/dL in patients with relative preserved renal function. The overall risk level of the studied group was low, as reflected by the high baseline creatinine clearance (mean, 71.89 mL/min) and the low Mehran score for the overall incidence of CIN (2.6%).…”

Section: Discussionmentioning

confidence: 99%

Safe Limits of Contrast Vary With Hydration Volume for Prevention of Contrast-Induced Nephropathy After Coronary Angiography Among Patients With a Relatively Low Risk of Contrast-Induced Nephropathy

Liu

Chen

Tan

et al. 2015

Circ: Cardiovascular Interventions

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Background-Few studies have investigated the safe limits of contrast to prevent contrast-induced nephropathy (CIN) based on hydration data. We aimed to investigate the relative safe maximum contrast volume adjusted for hydration volume in a population with a relatively low risk of CIN. Methods and Results-The ratios of contrast volume-to-creatinine clearance (V/CrCl) and hydration volume to body weight (HV/W) were determined in patients undergoing cardiac catheterization. Receiver-operator characteristic curve analysis based on the maximum Youden index was used to identify the optimal cutoff for V/CrCl in all patients and in HV/W subgroups. Eighty-six of 3273 (2.6%) patients with mean CrCl 71.89±27.02 mL/min developed CIN. Receiver-operator characteristic curve analysis indicated that a V/CrCl ratio of 2.44 was a fair discriminator for CIN in all patients (sensitivity, 73.3%; specificity, 70.4%). After adjustment for other confounders, V/CrCl >2.44 continued to be significantly associated with CIN (adjusted odds ratio, 4.12; P<0.001) and the risk of death (adjusted hazard ratio, 2.62; P<0.001). The mean HV/W was 12.18±7.40. We divided the patients into 2 groups (HV/W ≤12 and >12 mL/kg). The best cutoff value for V/CrCl was 1.87 (sensitivity, 67.9%; specificity, 64.4%; adjusted odds ratio, 3.24; P=0.011) in the insufficient hydration subgroup (HV/W, ≤12 mL/kg; CIN, 1.32%) and 2.93 (sensitivity, 69.0%; specificity, 65.0%; adjusted odds ratio, 3.04; P=0.004) in the sufficient hydration subgroup (HV/W, >12 mL/kg; CIN, 5.00%). Conclusions-The V/CrCl ratio adjusted for HV/W may be a more reliable predictor of CIN and even long-term outcomes after cardiac catheterization. We also found a higher best cutoff value for V/CrCl to predict CIN in patients with a relatively sufficient hydration status, which may be beneficial during decision-making about contrast dose limits in relatively low-risk patients with different hydration statuses. (Circ Cardiovasc Interv. 2015;8:e001859.

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Section: Discussionmentioning

confidence: 99%

Safe Limits of Contrast Vary With Hydration Volume for Prevention of Contrast-Induced Nephropathy After Coronary Angiography Among Patients With a Relatively Low Risk of Contrast-Induced Nephropathy

Liu

Chen

Tan

et al. 2015

Circ: Cardiovascular Interventions

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“…Maioli, et al 15) found that persistent renal damage occurred in 18.6% of CIN patients, and death was probably more common in patients with persistent renal damage than in patients with transient renal damage or in those without CIN at 5 years. Another study 16) stated that CIN was significantly correlated with long-term mortality in the entire cohort and in patients with chronic kidney disease (CKD) but not in patients without CKD. A study 17) on AMI patients undergoing PCI showed that patients with transient renal dysfunction had a lower two-year event rate of death or dialysis compared with those with persistent renal dysfunction, but a higher event rate compared with those without CIN.…”

Section: )mentioning

confidence: 99%

Pre-Procedural Risk Score of Contrast-Induced Nephropathy in Elderly Patients Undergoing Elective Coronary Angiography

Lian

Liu

et al. 2017

Int. Heart J.

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SummaryTo establish a scoring model to predict the risk of contrast-induced nephropathy (CIN) in elderly patients undergoing elective coronary angiography (CAG).A total of 1286 patients aged > 65 years who had undergone elective CAG between August 2009 and February 2013 were enrolled in this study. They were randomly (3:2) assigned to a development (n = 756) or validation dataset (n = 530). Independent predictors of CIN were identified by using logistic regression and were assigned a weighted integer, which was used to establish a score model. CIN incidence in the development set was 6.3%. The risk score model contained 3 variables (with the weighted integer): age > 75 years (1.5), creatinine clearance (CrCl) < 60 mL/minute (1), and congestive heart failure (CHF) (1.5). CIN incidence was 3.1%, 9.1%, and 29.0% in the low-risk group (≤ 1), moderate risk group (1 -3), and high-risk group (≥ 3), respectively. The risk model demonstrated good prediction value in the development (c-statistic = 0.727) and validation (c-statistic = 0.695) datasets. Compared to the non-CIN group, the CIN group had a significantly higher rate of inhospital major adverse cardiac events (P < 0.01).The risk score model with 3 variables, namely age > 75 years, CrCl < 60 mL/minute, and CHF, is a clinical prediction tool for CIN in elderly patients before elective CAG. CIN is one of the independent risk factors of major adverse cardiac events (MACE). (Int Heart J 2017; 58: 197-204)

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“…CIAKI is the third most common cause of acute renal failure in hospitalized patients [1], accounting for up to 12% of all cases of acute renal failure [2, 3]. CIAKI is also associated with replacement therapy, prolonged hospitalization, increased medical cost and increased mortality [4, 5]. The factors contributed to the pathophysiology of CIAKI are still under controversy, but primarily involve the tubular toxicity, microvascular alteration, oxidative stress, inflammation and tubular obstruction [4, 6-8].…”

Section: Introductionmentioning

confidence: 99%

Involvement of S100A8/A9-TLR4-NLRP3 Inflammasome Pathway in Contrast-Induced Acute Kidney Injury

Tan

Zheng

Huang

et al. 2017

Cell Physiol Biochem

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Background: Contrast-induced acute kidney injury (CIAKI) is a common cause of hospital-acquired acute kidney injury (AKI). S100A8/A9-TLR4-NLRP3 inflammasome pathway triggers inflammation, apoptosis and tissue injury in several AKI models. Nevertheless, the underlying mechanism of S100A8/A9-TLR4-NLRP3 inflammasome pathway in CIKAI is not clear. We aimed to investigate the possible role of S100A8/A9-TLR4-NLRP3 inflammasome in the pathophysiology of CIAKI. Methods: We treated male rats and NRK-52E cells by iopromide to establish in vivo and in vitro models of CIAKI. We collected serum and urine samples to detect renal function. We obtained kidney tissue for histological analysis and detection of protein concentration. We used inhibitor of TLR4 and NLRP3-siRNA to further testify their role in CIAKI in NRK-52E cells. Results: Iopromide caused elevation of SCr, BUN and NGAL level, decrease of endogenous creatinine clearance, morphological injury and tubular apoptosis, enhanced IL-1β and IL-18 expression, and increased expression of S100A8/A9, TLR4 and NLRP3 inflammsome. In NRK-52E cells, iopromide caused enhanced apoptotic rates and ROS generation, which could be ameliorated by inhibitor of TLR4 and NLRP3-siRNA. Moreover, inhibition of TLR4 dampened NLRP3 expression. Conclusion: S100A8/A9-TLR4-NLRP3 inflammasome pathway represented a key mechanism of CI-AKI, which provided a potential therapeutic target.

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Relation of Contrast-Induced Nephropathy to Long-Term Mortality After Percutaneous Coronary Intervention

Cited by 94 publications

References 19 publications

Safe Limits of Contrast Vary With Hydration Volume for Prevention of Contrast-Induced Nephropathy After Coronary Angiography Among Patients With a Relatively Low Risk of Contrast-Induced Nephropathy

Safe Limits of Contrast Vary With Hydration Volume for Prevention of Contrast-Induced Nephropathy After Coronary Angiography Among Patients With a Relatively Low Risk of Contrast-Induced Nephropathy

Pre-Procedural Risk Score of Contrast-Induced Nephropathy in Elderly Patients Undergoing Elective Coronary Angiography

Involvement of S100A8/A9-TLR4-NLRP3 Inflammasome Pathway in Contrast-Induced Acute Kidney Injury

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