Peng Ran

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

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.

Development of contrast-induced acute kidney injury after elective contrast media exposure in patients with type 2 diabetes mellitus: effect of albuminuria.

Background The influence of albuminuria and urinary pH on the development of contrast-induced acute kidney disease (CI-AKI) in patients with type 2 diabetes mellitus (T2DM) after elective coronary angiography (CAG) or percutaneous coronary intervention (PCI) is unknown. Methods CI-AKI was defined as an increase in serum creatinine >26.4 µmol/L or ≥50% of baseline value within 48 hours after contrast media exposure. Demographics, traditional risk factors, clinical outcomes and CI-AKI incidence were compared between groups. Univariate analysis and multivariate logistic regression were performed to assess risk factors of CI-AKI. Results We observed 597 patients with T2DM after CAG or PCI. Patients were divided into 3 groups based on early morning urinary albumin: negative group (urine dipstick negative, n = 483), trace group (urine dipstick trace, n = 60), and positive group (urine dipstick ≥1+, n = 54). CI-AKI occurred in 33 (5.5%) patients, including 19 (3.9%) in the negativealbuminuria group, 4 (6.7%) in the trace group, and 10 (18.5%) in the positive group (p< 0.001), respectively. After adjusting for potential confounding risk factors, positive albuminuria (OR = 3.8, 95% CI: 1.5 to 9.2, p = 0.004) and urinary pH<6 (OR = 2.4, 95% CI: 1.1 to 5.1, p = 0.020) remained significantly associated with CI-AKI. Conclusion Preprocedural albuminuria and urinary pH <6 are independent risk factors of CI-AKI in patients with T2DM undergoing elective cardiac catheterization, and may be used to identify patients at high risk of post-procedural CI-AKI.

Atorvastatin protects against contrast-induced nephropathy via anti-apoptosis by the upregulation of Hsp27 in vivo and in vitro

Contrast-induced nephropathy (CIN) is an iatrogenic acute renal failure occurring following the intravascular injection of iodinated radiographic contrast medium. However, the regulatory mechanisms for CIN remain to be fully elucidated. The present study aimed to investigate whether atorvastatin protects against CIN via anti-apoptotic effects by the upregulation of Hsp27 in vivo and in vitro. To determine whether atorvastatin attenuated CIN, the inflammatory response and apoptosis in vivo and in vitro, a rat model of iopamidol-induced CIN was used, and human embryonic proximal tubule (HK2) cell damage was assessed. The rats were assigned into four groups (n=10 per group), as follows: Control rats; rats+atorvastatin; rats + iopamidol; rats+iopamidol+atorvastatin. In vitro, the HK2 cells were treated with iopamidol in the presence or absence of atorvastatin, heat shock protein (Hsp)27 small interfering (si)RNA or pcDNA3.1-Hsp27. The renal tissues were examined histopathologically and collected for western blot analysis. The results showed that atorvastatin ameliorated the apoptosis and deterioration of renal function (P<0.05). Furthermore, atorvastatin reduced the iopamidol-induced activity of B cell lymphoma-2 (Bcl-2)-associated X protein (Bax)/caspase-3 and increased the expression of Bcl-2 in vivo and in vitro. Notably, following treatment with Hsp27 siRNA or pcDNA3.1-Hsp27, it was found that iopamidol enhanced or weakened the upregulation of Bax/caspase-3 and downregulation of Bcl-2 in the HK2 cells, respectively. The results of the present study suggested that atorvastatin protected against contrast-induced renal tubular cell apoptosis through the upregulation of Hsp27 in vivo and in vitro.

LDL cholesterol as a novel risk factor for contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention

BACKGROUND Low density lipoprotein cholesterol (LDL-C) is associated with endothelial dysfunction, inflammation and increased vasoconstriction, which are involved in the development of contrast-induced acute kidney injury (CI-AKI). However, whether LDL-C is an independent risk factor of CI-AKI in patients undergoing percutaneous coronary intervention (PCI) is unknown. METHODS We prospectively enrolled 3236 consecutive patients undergoing PCI between January 2010 and September 2012. Multivariate logistic regression analysis was used to determine whether LDL-C is an independent risk factor of CI-AKI. CI-AKI was defined as an absolute increase in serum creatinine of ≥ 0.5 mg/dL or ≥ 25% over the baseline value within 48-72 h after contrast exposure. RESULTS CI-AKI was observed in 338 patients (10.4%). Patients with CI-AKI had a significantly higher rate of in hospital mortality (4.4% vs. 0.5%, p < 0.001), and significantly higher rates of other in hospital complications compared with those without CI-AKI. The LDL-C quartiles were as follows: Q1 (<2.04 mmol/L), Q2 (2.04-2.61 mmol/L), Q3 (2.61-3.21 mmol/L) and Q4 (>3.21 mmol/L). Patients with high baseline LDL-C levels were more likely to develop CI-AKI and composite end points including all-cause mortality, renal replacement therapy, non-fatal myocardial infarction, acute heart failure, target vessel revascularization or cerebrovascular accident during the observation period of hospitalization (8.9%, 9.9%, 10.5%, 12.6%, p = 0.001, and 5.0%, 5.2%, 6.1%, 8.1%, respectively; p = 0.007). Univariate logistic analysis showed that LDL-C levels (increment 1 mmol/L) were significantly associated with CI-AKI (odds ratio = 1.25, 95% confidence interval (CI), 1.11-1.39, p < 0.001). Furthermore, LDL-C remained a significant risk factor of CI-AKI (odds ratio = 1.23, 95% CI, 1.04-1.45, p = 0.014), even after adjusting for potential confounding risk factors. CONCLUSIONS Measurement of plasma LDL-C concentrations in patients undergoing PCI may be helpful to identify those who are at risk of CI-AKI and poor in hospital outcomes.

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

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).

Preprocedural N-terminal pro-brain natriuretic peptide (NT-proBNP) is similar to the Mehran contrast-induced nephropathy (CIN) score in predicting CIN following elective coronary angiography.

Background N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) has been associated with important risk factors for contrast‐induced nephropathy (CIN). However, few studies have investigated the predictive value of NT‐proBNP itself. This study investigated whether levels of preprocedural NT‐proBNP could predict CIN after elective coronary angiography as effectively as the Mehran CIN score. Methods and Results We retrospectively observed 2248 patients who underwent elective coronary angiography. The predictive value of preprocedural NT‐proBNP for CIN was assessed by receiver operating characteristic and multivariable logistic regression analysis. The 50 patients (2.2%) who developed CIN had higher Mehran risk scores (9.5±5.1 versus 4.8±3.8), and higher preprocedural levels of NT‐proBNP (5320±7423 versus 1078±2548 pg/mL, P<0.001). Receiver operating characteristic analysis revealed that NT‐proBNP was not significantly different from the Mehran CIN score in predicting CIN (C=0.7657 versus C=0.7729, P=0.8431). An NT‐proBNP cutoff value of 682 pg/mL predicted CIN with 78% sensitivity and 70% specificity. Multivariable analysis suggested that, after adjustment for other risk factors, NT‐proBNP >682 pg/mL was significantly associated with CIN (odds ratio: 4.007, 95% CI: 1.950 to 8.234; P<0.001) and risk of death (hazard ratio: 2.53; 95% CI: 1.49 to 4.30; P=0.0006). Conclusions Preprocedural NT‐proBNP >682 pg/mL was significantly associated with the risk of CIN and death. NT‐proBNP, like the Mehran CIN score, may be another useful and rapid screening tool for CIN and death risk assessment, identifying subjects who need therapeutic measures to prevent CIN.

Relationship Between the Urine Flow Rate and Risk of Contrast-Induced Nephropathy After Emergent Percutaneous Coronary Intervention.

AbstractA low urine flow rate is a marker of acute kidney injury. However, it is unclear whether a high urine flow rate is associated with a reduced risk of contrast-induced nephropathy (CIN) in high-risk patients.We conducted this study to evaluate the predictive value of the urine flow rate for the risk of CIN following emergent percutaneous coronary intervention (PCI).We prospectively examined 308 patients undergoing emergent PCI who provided consent. The predictive value of the 24-hour postprocedural urine flow rate, adjusted by weight (UR/W, mL/kg/h) and divided into quartiles, for the risk of CIN was assessed using multivariate logistic regression analysis.The cumulative incidence of CIN was 24.4%. In particular, CIN was observed in 29.5%, 19.5%, 16.7%, and 32.0% of cases in the UR/W quartile (Q)-1 (⩽0.94 mL/kg/h), Q2 (0.94–1.30 mL/kg/h), Q3 (1.30–1.71 mL/kg/h), and Q4 (≥1.71 mL/kg/h), respectively. Moreover, in-hospital death was noted in 7.7%, 3.9%, 5.1%, and 5.3% of patients in Q1, Q2, Q3, and Q4, respectively. After adjusting for potential confounding predictors, multivariate analysis indicated that compared with the moderate urine flow rate quartiles (Q2 + Q3), a high urine flow rate (Q4) (odds ratio [OR], 2.69; 95% confidence interval [CI], 1.27–5.68; P = 0.010) and low urine flow rate (Q1) (OR, 2.23; 95% CI, 1.03–4.82; P = 0.041) were significantly associated with an increased risk of CIN. Moreover, a moderate urine flow rate (0.94–1.71 mL/kg/h) was significantly associated with a decreased risk of mortality.Our data suggest that higher and lower urine flow rates were significantly associated with an increased risk of CIN after emergent PCI, and a moderate urine flow rate (0.94–1.71 mL/kg/h) may be associated with a decreased risk of CIN with a good long-term prognosis after emergent PCI.

Preprocedural High-Sensitivity C-Reactive Protein Predicts Contrast-Induced Nephropathy and Long-Term Outcome After Coronary Angiography:

We investigated whether high-sensitivity C-reactive protein (hsCRP) levels were associated with contrast-induced nephropathy (CIN) and long-term mortality after coronary angiography (CAG). Patients (N = 2133) undergoing CAG with preprocedural hsCRP were consecutively enrolled. High-sensitivity C-reactive protein was measured before angiography. Median follow-up was 2.3 years. The overall incidence of CIN was 2.77% (59 of 2133). There was a positive trend of hsCRP quartiles (Q) with rates of CIN: 0.9% for Q1 (<1.6 mg/L), 0.9% for Q2 (1.6-3.9 mg/L), 2.4% for Q3 (4.0-11.3mg/L), and 6.8% for Q4 (>11.3 mg/L; P < .05). The receiver operating characteristic (ROC) analysis showed that the cutoff point of hsCRP was 7.3 mg/L for predicting CIN with a 72.7% sensitivity and a 67.0% specificity (area under the curve [AUC] = 0.742, 95% confidence interval [CI] 0.672-0.810; P < .05). The predictive value of hsCRP was similar to the Mehran score for CIN (AUChsCRP = 0.742 vs AUCMehran = 0.801; P = .228). After adjustment for other potential risk factors, hsCRP >7.3 mg/L still was an independent predictor of CIN (odds ratio [OR] = 2.83, 95% CI: 1.44-5.58; P = .003). Furthermore, hsCRP >7.3 mg/L was associated with higher mortality (OR = 2.04, 95% CI: 1.30-3.19; P = .002).