A novel simple experimental model for low-osmolar contrast-induced acute kidney injury using different definitions based on the levels of serum creatinine and cystatin C.

BACKGROUND: It remained lack of a kind of contrast-induced acute kidney injury (CI-AKI) model which was widely used in clinical practice and comparable to CI-AKI in humans. METHODS: Fifty Sprague-Dawley rats were divided into five groups of 10 rats each: (1) sham group (normal saline [NS] + NS); (2) NS plus low osmolality contrast medium (CM15) (NS + CM15); (3) furosemide (FM) plus NS (FM + NS); (4) FM + CM10; and (5) FM + CM15.We measured the levels of serum creatinine (SCr), cystatin C (cys-C) and histopathological scores of kidney tissues. RESULTS: SCr level in the FM + CM15 group were significantly increased after CM exposure compared with baseline levels (32.9 ± 4.57 vs. 158.7 ± 14.48 µmol/L, p < 0.001). Minor changes were found about the SCr levels between the pre- and post-exposure CM or NS treatment in the other groups. Additionally, the cys-C levels after CM exposure were increased compared with pretreatment levels in the FM + CM15 group (0.08 ± 0.03 vs. 0.18 ± 0.05 mg/L, p < 0.001). Minor changes were noted in the FM + NS group before and after NS administration. Only rats in the FM + CM15 group developed CI-AKI with the definitions of SCr or cys-C. Comparing to the FM + NS group, the histopathological scores were significantly increased in the FM + CM15 group. CONCLUSIONS: A simple and reliable animal model for low osmolality contrast medium-induced AKI was established, which is similar to clinical CI-AKI based on different definitions for AKI.

MicroRNA expression profile by next-generation sequencing in a novel rat model of contrast-induced acute kidney injury.

BACKGROUND: MicroRNAs (miRNAs) are known to regulate most biological processes including contrast-induced acute kidney injury (CI-AKI). Few studies have investigated microRNA (miRNAs) expressions in a novel rat model of CI-AKI using nonionic low-osmolar iodic contrast medium Ultravist, and performed gene ontology (GO) categories analysis. METHODS: In this study, kidney tissues were collected from Sprague-Dawley rats at 24 h after contrast-exposure (CI-AKI) and saline-administration (control). MiRNAs microarray assays were used to detect miRNAs in the kidney tissue by next-generation sequencing. Real-time PCR was performed to verify the microarray assays results. All significant differently expressed miRNAs were analyzed by GO categories and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. RESULTS: Of the 173 detected miRNAs, 22 were down-regulated (miR-328a-5p, miR-31a-5p, miR-377-3p, et al.) and 19 were up-regulated (miR-3558-5p, miR-34c-3p, miR-384-5p, et al.) in the kidneys of CI-AKI rats according to log2 (fold change, control) >1, P<0.001 as significant differently expressed miRNAs, which included new differently expressed miRNAs, such as miRNA-1949 and miR-3558. The results showed that a large set of genes involved in essential biological processes were targeted by these miRNAs, such as dysfunction metabolic process, apoptotic process, and endoplasmic reticulum stress, in addition to genes implicated in signaling pathways involved in inflammation and dysfunctional metabolism, including AGE-RAGE signaling pathway and glycerophospholipid metabolism. CONCLUSIONS: The 41 miRNAs identified were differentially expressed in the kidneys of a novel rat model of CI-AKI, and thus possess the potential to serve as novel biological markers and new molecular targets for CI-AKI.

Safe Hydration to Prevent Contrast-Induced Acute Kidney Injury and Worsening Heart Failure in Patients with Renal Insufficiency and Heart Failure Undergoing Coronary Angiography or Percutaneous Coronary Intervention.

An optimal hydration volume (HV) that prevents contrast-induced acute kidney injury (CI-AKI) in patients with renal insufficiency and heart failure (HF) at a high risk of worsening HF (WHF) has not been determined. We aimed to determine a safe HV that prevents CI-AKI and WHF following coronary angiography (CAG) or percutaneous coronary intervention (PCI) in patients with renal insufficiency and HF. We recruited 1,307 patients with renal insufficiency and HF and investigated the relationships between the peri-procedural HV/weight (HV/W) ratio, and the risks of CI-AKI and WHF following CAG or PCI. Higher HV/W quartiles were associated with higher CI-AKI rates (Q1: 6.2%, Q2: 9.1%, Q3: 12.5%, and Q4: 18.7%; P < 0.001) and a greater likelihood of WHF (Q1: 2.2%, Q2: 2.7%, Q3: 4.9%, and Q4: 11.7%; P < 0.001). The multivariate analyses indicated that excessively high HV/W ratios were associated with moderately increased risks of CI-AKI (Q4 versus Q1: adjusted odds ratio [OR] 2.16, 95% confidence interval [CI] 1.17-4.00) and WHF (Q4 versus Q1: adjusted OR 3.09, 95% CI 1.21-7.88). The multivariate Cox regression analysis indicated that a higher HV/W ratio was associated with significantly increased long-term mortality (Q2 versus Q1: adjusted hazard ratio [HR] 2.36; Q3 versus Q1: adjusted HR 2.85; Q4 versus Q1: adjusted HR 2.94; all P < 0.05). In conclusion, an excessively high HV/W might be associated with a moderately increased risk of CI-AKI, WHF, and long-term mortality in patients with renal insufficiency and HF.

Optimal hydration volume among high-risk patients with advanced congestive heart failure undergoing coronary angiography.

We investigated the relationship between weight-adjusted hydration volumes and the risk of developing contrast-induced acute kidney injury (CI-AKI) and worsening heart failure (WHF) and explored the relative safety of optimal hydration volumes in patients with advanced congestive heart failure (CHF) undergoing coronary angiography (CAG) or percutaneous coronary intervention. We included 551 patients with advanced CHF (New York Heart Association class > 2 or history of pulmonary edema) undergoing CAG (follow-up period 2.62 ± 0.9 years). There was a significant association between hydration volume-to-weight ratio (HV/W) (quintile Q1, Q2, Q3, Q4, and Q5) and the incidence of CI-AKI (3.7%, 14.6%, 14.3%, 21.1%, and 31.5%, respectively) and WHF (3.6%, 5.4%, 8.3%, 13.6%, and 19.1%, respectively) (all P-trend < 0.001). Receiver operating curve analysis indicated that HV/W = 15 mL/kg and the mean HV/W (60.87% sensitivity and 64.96% specificity) were fair discriminators for CI-AKI (C-statistic 0.696). HV/W >15 mL/kg independently predicted CI-AKI (adjusted odds ratio [OR] 2.33; P = 0.016) and WHF (adjusted OR 2.13; P = 0.018). Moreover, both CI-AKI and WHF were independently associated with increased long-term mortality. Thus, for high-risk patients with advanced CHF undergoing CAG, HV/W > 15 mL/kg might be associated with an increased risk of developing CI-AKI and WHF. The potential benefits of a personalized limitation of hydration volume need further evaluation.

Correction: Predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury and mortality following coronary angiography or intervention.

[This corrects the article DOI: 10.18632/oncotarget.19034.].

Association of post-procedural early (within 24h) increases in serum creatinine with all-cause mortality after coronary angiography.

BACKGROUND: The majority of patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI) are discharged early, with only early (within 24h) serum creatinine (SCr) data available without evidence of clinical prognosis. We aimed to systemically evaluate the association between post-procedural early increase in SCr and all-cause mortality following CAG. METHODS: We performed a retrospective sub-study analysis within a prospective observational study including 3091 consecutive patients with baseline and post-procedural early (within 24h) SCr data. The degree (mild, moderate, or large) of absolute and relative increases in SCr from baseline. The mean follow-up time was 2.49years. RESULT: Moderate or large early increases in SCr were relatively rare (large increase: >1.0mg/dl [0.5%], >100% [0.4%]), whereas mild absolute and relative increases in SCr were more common (mild increase: 0.25 to 0.50mg/dl [4.5%], 25% to 50% [5.9%]). During the follow-up period, there were 136 post-procedural deaths (5.6%). After adjustment for confounders, mild absolute and relative increases in SCr were associated with increased mortality (hazard ratio [HR]: 1.9 and 1.8, respectively, both P<0.05). Moderate or large increases in SCr were associated with higher mortality, even higher than with pre-existing renal dysfunction (HR: 5.36 and 4.12 for moderate increase [0.5 to 1.0mg/dl] and estimated glomerular filtration rate<60ml/min). CONCLUSION: Post-procedural mild, moderate, or large early increase in SCr, is associated with significantly increased long-term mortality. Although moderate or large increase in SCr following CAG was relatively rare, the prognosis is more serious, and is worse than that of pre-existing renal dysfunction. CLINICAL TRIAL REGISTRATION: Predictive Value of Contrast Volume to Creatinine Clearance Ratio (PRECOMIN, ClinicalTrials.govNCT01400295).

miR­21 attenuates contrast­induced renal cell apoptosis by targeting PDCD4.

Contrast medium (CM) is widely used in cardiac catheterization; however, it may induce acute kidney injury or renal failure, although the underlying mechanism remains to be elucidated. MicroRNA­21 (miR­21) is involved in renal disease and has been indicated to regulate cellular apoptosis and fibrosis, although its role in CM­induced renal cell injury is unknown. The present study examined the expression and potential targets of miR­21 in human renal proximal tubular epithelial (HK­2) cells following CM treatment. CM induced renal cell apoptosis and decreased miR­21 expression. The expression level of the apoptosis regulator protein, B­cell lymphoma 2 (Bcl­2) was upregulated, whereas that of the apoptosis regulator, Bcl­2­associated X protein (Bax) was downregulated upon transfection of miR­21 mimics; miR­21 overexpression additionally directly inhibited the expression of programmed cell death protein 4 (PDCD4), as determined by a dual luciferase reporter assay, and PDCD4 silencing reduced the rate of HK­2 cell apoptosis. The results of the present study indicated that miR­21 protected renal cells against CM­induced apoptosis by regulating PDCD4 expression.

Association of left ventricular ejection fraction with contrast-induced nephropathy and mortality following coronary angiography or intervention in patients with heart failure.

BACKGROUND: Left ventricular ejection fraction (LVEF) is the most widely used parameter to evaluate the cardiac function in patients with heart failure (HF). However, the association between LVEF and contrast-induced nephropathy (CIN) is still controversial. Therefore, the aim of this study is to evaluate the association of LVEF with CIN and long-term mortality following coronary angiography (CAG) or intervention in patients with HF. METHODS: We analyzed 1,647 patients with HF (New York Heart Association [NYHA] or Killip class >1) undergoing CAG or intervention, including 207 (12.57%) patients with reduced LVEF (HFrEF), 238 (14.45%) with mid-range LVEF (HFmrEF) and 1,202 (72.98%) with preserved LVEF (HFpEF). CIN was defined as an absolute increase of ≥0.5 mg/dL or a relative increase of ≥25% from baseline serum creatinine within 48-72 h after contrast medium exposure. Multivariable logistic regression and Cox proportional hazards regression analyses were performed to identify the association between LVEF, CIN and long-term mortality, respectively. RESULTS: Overall, 225 patients (13.7%) developed CIN. Individuals with lower LVEF were more likely to develop CIN (HFrEF, HFmrEF and HFpEF: 18.4%, 21.8% and 11.2%, respectively; P<0.001), but without a significant trend after adjusting for the confounding factors (HFrEF vs HFpEF: odds ratio [OR] =1.01; HFmrEF vs HFpEF: OR =1.31; all P>0.05). However, advanced HF (NYHA class >2 or Killip class >1) was an independent predictor of CIN (adjusted OR =1.54, 95% confidence interval [CI], 1.07-2.22; P=0.019). During the mean follow-up of 2.3 years, reduced LVEF (HFrEF group) was significantly associated with increased mortality (HFrEF vs HFpEF: adjusted hazard ratio =2.88, 95% CI, 1.77-4.69; P<0.001). CONCLUSION: In patients with HF undergoing CAG or intervention, not worsened LVEF but advanced HF was associated with an increased risk of CIN. In addition, reduced LVEF was an independent predictor of long-term mortality following cardiac catheterization.

Comparing common doses (double-dose vs usual-dose) of atorvastatin for preventing contrast-induced acute kidney injury and mortality after coronary angiography.

High-dose atorvastatin pretreatment was proved reducing the risk of contrast-induced acute kidney injury (CI-AKI), especially in patients with high C-reactive protein (CRP) levels. We evaluated the effects of common atorvastatin doses (double vs usual) on the risk of CI-AKI and mortality.We recorded outcomes from 1319 patients who were administered periprocedural common doses of atorvastatin. The risks of CI-AKI and mortality between double-dose (40 mg/d) and usual-dose atorvastatin (20 mg/d) were compared using multivariable regression models in all patients or CRP tertile subgroups.Seventy-six (5.8%) patients developed CI-AKI. Double-dose atorvastatin compared with usual-dose did not further reduce the risk of CI-AKI (adjusted odds ratio [OR]: 2.28, 95% confidence interval [CI]: 0.92-5.62, P = .074), even for patients in the highest CRP tertile (>8.33 mg/L; adjusted OR: 3.76, 95% CI: 0.83-17.05, P = .086). Similar results were observed in reducing mortality in all patients (adjusted hazard ratio: 0.47, 95% CI: 0.10-2.18; P = .339) and in the highest CRP tertiles (P = .424). In the subgroup analysis, double-dose atorvastatin increased risk of CI-AKI in patients with creatinine clearance (CrCl) < 60 mL/min, anemia, contrast volume > 200 mL and > 2 stents implanted (P = .046, .009, .024, and .026, respectively).Daily periprocedural double-dose atorvastatin was not associated with a reduced risk of CI-AKI compared with usual-dose, and did not provide an improved long-term prognosis, even in patients with high CRP levels. However, it increased the risk of CI-AKI in patients with a high contrast volume/CrCl.

Safe Hydration Volume to Prevent Contrast-induced Acute Kidney Injury and Worsening Heart Failure in Patients With Heart Failure and Preserved Ejection Fraction After Cardiac Catheterization.

Few studies have investigated the efficacy and safety of hydration to prevent contrast-induced acute kidney injury (CI-AKI) and worsening heart failure (WHF) after cardiac catheterization in heart failure and preserved ejection fraction (HFpEF; HF and EF ≥50%) patients. We recruited 1206 patients with HFpEF undergoing cardiac catheterization with periprocedural hydration volume/weight (HV/W) ratio data and investigated the relationship between hydration volumes and risk of CI-AKI and WHF. Incidence of CI-AKI was not significantly reduced in individuals with higher HV/W [quartile (Q) 1, Q2, Q3, and Q4: 9.7%, 10.2%, 12.7%, and 12.2%, respectively; P = 0.219]. Multivariate analysis indicated that higher HV/W ratios were not associated with decreased CI-AKI risks [Q2 vs. Q1: odds ratio (OR), 0.95; Q3 vs. Q1: OR, 1.07; Q4 vs. Q1: OR, 0.92; all P > 0.05]. According to multivariate analysis, higher HV/W significantly increased the WHF risk (Q4 vs. Q1: adjusted OR, 8.13 and 95% confidence interval, 1.03-64.02; P = 0.047). CI-AKI and WHF were associated with a significantly increased risk of long-term mortality (mean follow-up, 2.33 years). For HFpEF patients, an excessively high hydration volume might not be associated with lower risk of CI-AKI but may increase the risk of postprocedure WHF.

Intensity of hydration changes the role of renin-angiotensin-aldosterone system blockers in contrast-induced nephropathy risk after coronary catheterisation in patients with chronic kidney disease.

OBJECTIVE: This study evaluated the potential effect of hydration intensity on the role of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) on contrast-induced nephropathy in patients with renal insufficiency. METHODS: All eligible patients were included and stratified according to hydration intensity defined as saline hydration volume to body weight tertiles: <10.21 mL/kg, 10.21 to <17.86 mL/kg, and ⩾17.86 mL/kg. RESULTS: In total, 84 (6.7%) of 1254 patients developed contrast-induced nephropathy: 6.2% in the ACEI/ARB group versus 10.8% in the non-ACEI/ARB group ( P=0.029), with an adjusted odds ratio (OR) of 0.89 (95% confidence interval (CI) 0.46-1.73, P=0.735). The incidence of contrast-induced nephropathy was lower in the ACEI/ARB group than in the non-ACEI/ARB group in the second tertile ( P=0.031), while not significantly different in the first ( P=0.701) and third ( P=0.254) tertiles. ACEIs/ARBs were independently associated with a lower contrast-induced nephropathy risk (OR 0.26, 95% CI 0.09-0.74, P=0.012) and long-term all-cause death (hazard ratio 0.461, 95% CI 0.282-0.755, P=0.002) only in the second hydration volume to body weight tertile. CONCLUSION: The effects of ACEIs/ARBs on contrast-induced nephropathy risk vary according to saline hydration intensity in chronic kidney disease patients, and may further reduce contrast-induced nephropathy risk in patients administered moderate saline hydration.

Association of lipoprotein(a) with long-term mortality following coronary angiography or percutaneous coronary intervention.

BACKGROUND: There is no consistent evidence to suggest the association of plasma lipoprotein(a) (Lp[a]) with long-term mortality in patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI). HYPOTHESIS: Level of Lp(a) is associated with long-term mortality following CAG or PCI. METHODS: We enrolled 1684 patients with plasma Lp(a) data undergoing CAG or PCI between April 2009 and December 2013. The patients were divided into 2 groups: a low-Lp(a) group (Lp[a] <16.0 mg/dL; n = 842) and a high-Lp(a) group (Lp[a] ≥16.0 mg/dL; n = 842). RESULTS: In-hospital mortality was not significantly different between the high and low Lp(a) groups (0.8% vs 0.5%, respectively; P = 0.364). During the median follow-up period of 1.95 years, the high-Lp(a) group had a higher long-term mortality than did the low-Lp(a) group (5.8% vs 2.5%, respectively; P = 0.003). After adjustment of confounders, multivariate Cox regression analysis revealed that a higher Lp(a) level was an independent predictor of long-term mortality (hazard ratio: 1.96, 95% confidence interval: 1.07-3.59, P = 0.029). CONCLUSIONS: Our data suggested that an elevated Lp(a) level was significantly associated with long-term mortality following CAG or PCI. However, additional larger multicenter studies will be required to investigate the predictive value of Lp(a) levels and evaluate the benefit of controlling Lp(a) levels for patients undergoing CAG or PCI.

Association of N-terminal pro-brain natriuretic peptide with contrast-induced acute kidney injury and long-term mortality in patients with heart failure and mid-range ejection fraction: An observation study.

The potential value of N-terminal pro-brain natriuretic peptide (NT-proBNP) for contrast-induced acute kidney injury (CI-AKI) in patients with heart failure and mid-range ejection fraction (HFmrEF) is unclear. We investigated whether NT-proBNP is associated with CI-AKI and long-term mortality following elective cardiac catheterization in patients with HFmrEF.A total of 174 consecutive patients with HFmrEF undergoing elective coronary angiography or intervention were enrolled. The primary endpoint was the development of CI-AKI, defined as an absolute increase of ≥0.3 mg/dL or ≥ 50% from baseline serum creatinine with 48 hours after contrast medium exposure. Receiver-operating characteristic curve analysis was conducted, and Youden index was used to determine the best cutoff NT-proBNP value. Multivariable logistic regression and Cox proportional hazards regression analyses were performed to identify the independent risk factors for CI-AKI and long-term mortality, respectively.The incidence of CI-AKI was 12.1%. Patients with CI-AKI had higher NT-proBNP values than those without (4373[1561.9-7470.5] vs 1303[625.2-2482.3], P = 0.003). Receiver-operating characteristic curve revealed that NT-proBNP was not significantly different from the Mehran risk score in predicting CI-AKI (area under the curve [AUC] = 0.723 vs 0.767, P = 0.516). The best cutoff NT-proBNP value for CI-AKI was 3299 pg/mL, with 70.6% sensitivity and 83.1% specificity. Multivariable analysis demonstrated that NT-proBNP ≥3299 pg/mL is significantly related to CI-AKI (odds ratio = 12.79; 95% confidence interval, 3.18-51.49; P < 0.001). Cox regression analysis showed that NT-proBNP ≥3299 pg/mL is associated with long-term mortality (adjusted hazard ratio = 11.91; 95%CI, 2.16-65.70; P = 0.004) during follow-up.In patients with HFmrEF, NT-proBNP ≥3299 pg/mL is associated with CI-AKI and long-term mortality following elective coronary angiography or intervention.

A novel risk score model for prediction of contrast-induced nephropathy after emergent percutaneous coronary intervention.

BACKGROUND: A few studies developed simple risk model for predicting CIN with poor prognosis after emergent PCI. The study aimed to develop and validate a novel tool for predicting the risk of contrast-induced nephropathy (CIN) in patients undergoing emergent percutaneous coronary intervention (PCI). METHODS: 692 consecutive patients undergoing emergent PCI between January 2010 and December 2013 were randomly (2:1) assigned to a development dataset (n=461) and a validation dataset (n=231). Multivariate logistic regression was applied to identify independent predictors of CIN, and established CIN predicting model, whose prognostic accuracy was assessed using the c-statistic for discrimination and the Hosmere Lemeshow test for calibration. RESULTS: The overall incidence of CIN was 55(7.9%). A total of 11 variables were analyzed, including age >75years old, baseline serum creatinine (SCr)>1.5mg/dl, hypotension and the use of intra-aortic balloon pump(IABP), which were identified to enter risk score model (Chen). The incidence of CIN was 32(6.9%) in the development dataset (in low risk (score=0), 1.0%, moderate risk (score:1-2), 13.4%, high risk (score≥3), 90.0%). Compared to the classical Mehran's and ACEF CIN risk score models, the risk score (Chen) across the subgroup of the study population exhibited similar discrimination and predictive ability on CIN (c-statistic:0.828, 0.776, 0.853, respectively), in-hospital mortality, 2, 3-years mortality (c-statistic:0.738.0.750, 0.845, respectively) in the validation population. CONCLUSIONS: Our data showed that this simple risk model exhibited good discrimination and predictive ability on CIN, similar to Mehran's and ACEF score, and even on long-term mortality after emergent PCI.

Predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury and mortality following coronary angiography or intervention.

OBJECTIVE: To investigate the predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury (CI-AKI) and all-cause mortality following coronary angiography or intervention. METHODS: We prospectively investigated 1042 consecutive patients with both baseline and early post-procedural cystatin C measurement undergoing coronary angiography or intervention. CI-AKI was defined as an increase ≥0.3 mg/dL or >50% in serum creatinine from baseline within 48 h post-procedure. Mean follow-up was 2.26 years. RESULTS: Overall, the patients had a CI-AKI incidence was 3.6% (38/1042), mean serum creatinine of 87 µmol/L. Compared with Mehran risk score, post-procedural early absolute increase (AUC: 0.584 vs. 0.706, P = 0.060) and relative increase (AUC: 0.585 vs. 0.706, P = 0.058) in cystatin C had poorer predictive value for CI-AKI. According to multivariate analysis, post-procedural significant early increase (≥0.3 mg/dL or ≥10%) in cystatin C developed in 231 patients (22.2%), was not independent predictor of CI-AKI (adjusted OR: 1.23, 95% CI, 0.56-2.69, P = 0.612), and long-term mortality (adjusted HR: 0.90; P = 0.838). CONCLUSIONS: Our data suggested post-procedural early increase (within 24 h) in cystatin C was not effective for predicting CI-AKI or all-cause mortality following coronary angiography or intervention among patients at relative low risk of CI-AKI, the negative finding of poor predictive value should be further evaluated in larger multicenter trials.

Could late measurement of serum creatinine be missed for patients without early increase in serum creatinine following coronary angiography?

Most patients are discharged early (within 24 hours) after coronary angiography (CAG) and may miss identification the late (24-48 hours) increase in serum creatinine (SCr), whose characteristics and prognosis have been less intensively investigated.We prospectively recruited 3065 consecutive patients with SCr measurement, including only1344 patients with twice SCr measurement (both early and late). The late contrast-induced acute kidney injury (CI-AKI) was defined as significantly increase in SCr (≥0.3 mg/dL or ≥50%) not in early phase, but only in late phase after the procedure, and the early CI-AKI experienced a significantly increase in early phase.Overall, CI-AKI developed in 134 patients (10%), and the incidence of late and early CI-AKI were 3.6% and 6.4%, respectively. There were no difference in age, renal, and heart function, contrast volume among patients with late and early CI-AKI. With mean follow-up period of 2.45 years, long-term mortality (3 years, 29.7% and 35.6%, respectively, P = .553) was similar for patients with late and early CI-AKI. Cox analysis showed that both late (adjusted HR 2.05; 95% CI, 1.02-4.15) and early (adjusted HR 2.68; 95% CI, 1.57-4.59) CI-AKI was significantly associated with long-term mortality (all P < .001).Only late increase in SCr, as late CI-AKI, accounted for about one-third of CI-AKI incidence and has similar good predictive value for long-term mortality with that of an early increase, early CI-AKI, among patients with SCr measured twice, supporting the importance of late repeating SCr measurement after CAG, even without an early significant increase in SCr.

Predictive Value of Neutrophil Gelatinase-Associated Lipocalin for Contrast-Induced Acute Kidney Injury After Cardiac Catheterization: A Meta-analysis.

BACKGROUND: Neutrophil gelatinase-associated lipocalin (NGAL) accumulates in cortical tubules in acute kidney injury (AKI) patients, with its levels associated with serum creatinine. However, the predictive value of NGAL level for contrast-induced acute kidney injury (CI-AKI) remains unclear. METHODS: A total of 1520 patients from 14 relevant studies retrieved from PUBMED, MEDLINE, EMBASE, Web of Science, ClinicalTrials.gov, Cochrane Library, and Google Scholar from the inception to November 2014 and 15 data sets were included. RESULTS: The pooled area under the curve of receiver operating characteristic analysis of NGAL for predicting CI-AKI was 0.93, and the diagnostic odds ratio, sensitivity, specificity, and median cutoff value were 42.54, 83.98%, 89.03%, and 52.4 ng/mL, respectively. Urine and serum/plasma NGAL levels performed similarly well in predicting CI-AKI, with somewhat better results obtained when the NGAL level was determined within 4 hours after exposure to contrast medium. CONCLUSIONS: Patient nationality and definition of CI-AKI were important factors that affected the efficiency of NGAL level in predicting CI-AKI. Urine and serum/plasma NGAL levels appear to be promising biomarkers for early detection of CI-AKI after percutaneous coronary intervention or coronary angiography.

Remote Ischemic Conditioning for Preventing Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Interventions/Coronary Angiography: A Meta-Analysis of Randomized Controlled Trials.

BACKGROUND: It is uncertain whether remote ischemic conditioning (RIC) has a protective effect on contrast-induced acute kidney injury (CI-AKI) after percutaneous coronary intervention (PCI)/coronary artery angiography (CAG). We performed a meta-analysis of randomized controlled trials (RCTs) to assess the effect of RIC on CI-AKI in such patients. METHODS: PubMed, MEDLINE, EMBASE, ClinicalTrials.gov, and the Cochrane Central Register of Controlled Trials databases were searched for RCTs that assessed the effect of RIC on CI-AKI in patients undergoing PCI/CAG. RESULTS: Ten RCTs with 1389 patients (RIC group, 757 and control, 632) were included. The RIC group significantly exerted a lower risk of CI-AKI compared to the controls (odds ratio [OR] = 0.52, 95% confidence interval [CI] = 0.34-0.77, P = .001), and they had the similar effect on major adverse cardiovascular events within 1 year (OR = 0.36, 95% CI = 0.20-0.66, P < .001). The RIC reduced the rates of death within 30 days, but this was not significant (OR = 0.16, 95% CI = 0.02-1.34, P = .091). The RIC was associated with a significantly lower incidence of CI-AKI in patients following elective PCI/CAG (OR = 0.54, 95% CI = 0.33-0.87, P = .011). The RIC before not after the intervention was effective in reducing the occurrence of CI-AKI (OR: 0.37 vs 1.05, P = .022). The RIC of the upper arm has statistically significant effect on protecting CI-AKI but not that of the lower limb (OR: 0.41 vs 1.41, P = .004). The effect of RIC on CI-AKI was similar between patients with a mean estimated glomerular filtration rate <60 mL/min/1.73 m(2) and those with mean rates ≥60 (OR: 0.23 vs 0.41, P = .333). CONCLUSION: The RIC reduced the incidence of CI-AKI in those receiving PCI/CAG. And RIC of the upper arm significantly reduced the risk of CI-AKI but not RIC of the lower limb in patients undergoing PCI/CAG.