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.

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.

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.

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.

Contrast Volume to Cystatin C-Based Glomerular Filtration Ratio Predicts the Risk of Contrast-Induced Nephropathy After Cardiac Catheterization.

Cystatin C is considered to be a better alternative to creatinine for estimating glomerular filtration rate (GFR). The aim of this study was to investigate whether a contrast volume to estimated GFR based on cystatin C (V/eGFRcys) is a better predictor of contrast-induced nephropathy (CIN). We enrolled 1195 consecutive patients undergoing elective cardiac catheterization. Receiver-operating characteristic (ROC) curves were used to identify the optimal cutoff value of V/eGFRcys for detecting CIN. Multivariate regression models were used to evaluate whether V/eGFRcys is an independent risk factor for CIN. A total of 19 (1.6%) patients developed CIN. There was a significant association between a higher V/eGFRcys ratio and CIN risk ( P = .008). A ROC curve analysis indicated that a V/eGFRcys ratio of 2.29 was a fair discriminator for CIN. After adjusting for other known CIN risk factors, V/eGFRcys ratios >2.29 remained significantly associated with CIN (odds ratio = 2.93, 95% confidence interval: 1.02-8.44, P = .047). In conclusion, a V/eGFRcys >2.29 was a significant and independent predictor of CIN after cardiac catheterization.

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).

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

A 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.