Absolute Increase In Serum Creatinine Research Articles

Contrast-induced nephropathy after computed tomography.

Contrast induced nephropathy is the third most prevalent preventable cause of acute kidney injury in hospitalized patients. It defined as an absolute increase in serum creatinine ≥ 0.5 mg/dL and relative ≥ 25% increase. We studied the risk factors to intravenous injection contrast nephropathy after computed tomography. We studied 400 patients prospectively. The incidence of contrast induced nephropathy, with an absolute or a relative increase were 4.0% and 13.9%, respectively. Diabetes and cardiac failure were independent risk factors for CIN a relative increase de serum creatinine (O.R.: 3.5 [95% CI: 1.92-6.36], p < 0.01, 2.61 [95% CI: 1.14-6.03%], p < 0.05, respectively). We showed association between uses of intravenous injection contrast after computed tomography with acute injury renal, notably with diabetes and heart failure.

The Importance of Contrast Volume/Glomerular Filtration Rate Ratio in Contrast-Induced Nephropathy Patients after Transcatheter Aortic Valve Implantation

Background/Aim: Transcatheter aortic valve implantation (TAVI) is a method which is increasingly applied in severe aortic stenosis treatment. The development of contrast-induced nephropathy (CIN) after TAVI increases morbidity and mortality rates. Within the scope of this study, the importance of the contrast medium volume to glomerular filtration rate (CV/GFR) ratio in determining the development of CIN and the amount of CV that could be applied was evaluated. Methods: Seventy-two patients (aged 78.6 ± 11.6 years; 38 females) who underwent aortic valve replacement with the TAVI method between June 2013 and August 2014 were included in the study. CIN was defined as an absolute increase in serum creatinine of >0.5 mg/dl or a relative increase of >25% within 48-72 h after TAVI. CIN+ and CIN- patients were classified into two groups. The χ² test, t test, Mann-Whitney U test, ROC analysis, and univariate and multivariate regression analyses were applied for statistical analyses. Results: CIN was detected in 16 patients (22%) in our study. Baseline creatinine, baseline GFR, the Mehran risk score, CV, and the CV/GFR ratio were determined as the predictive factors of CIN development. A CV/GFR ratio of 3.9 was specified to predict CIN development with 71% sensitivity and 80% specificity. Conclusion: After TAVI, CIN may develop due to various reasons. In patients to whom TAVI was applied, the CV/GFR ratio may be a guideline helping to prevent the development of renal pathologies. The amount of contrast medium that can be given to a patient can be calculated in terms of baseline GFR.

ASSA14-12-04 Comparison of the efficacy of rosuvastatin versus atorvastatin in preventing contrast induced nephropathy in patients with chronic kidney disease undergoing percutaneous coronary intervention

<h3>Objectives</h3> We prospectively compared the preventive effects of rosuvastatin and atorvastatin on contrast-induced nephropathy (CIN) in patients with chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI). <h3>Methods</h3> We enrolled 1078 consecutive patients with CKD undergoing elective PCI. Patients in Group 1 (n = 273) received rosuvastatin (10 mg), and those in group 2 (n = 805) received atorvastatin (20 mg). The primary end-point was the development of CIN, defined as an absolute increase in serum creatinine ≥0.5 mg/dL, or an increase ≥25% from baseline within 48–72 h after contrast medium exposure. <h3>Results</h3> CIN was observed in 58 (5.4%) patients. The incidence of CIN was similar in patients pretreated with either rosuvastatin or atorvastatin (5.9% vs 5.2%, p = 0.684). The same results were also observed when using other definitions of CIN. Clinical and procedural characteristics did not show significant differences between the two groups (p &gt; 0.05). Additionally, there were no significant inter-group differences with respect to in-hospital mortality rates (0.4% vs 1.5%, p = 0.141), or other in-hospital complications. Multivariate logistic regression analysis revealed that rosuvastatin and atorvastatin demonstrated similar efficacies for preventing CIN, after adjusting for potential confounding risk factors (odds ratio = 1.17, 95% confidence interval, 0.62–2.20, p = 0.623). A Kaplan–Meier survival analysis showed that patients taking either rosuvastatin or atorvastatin had similar incidences of all-cause mortality (9.4% vs 7.1%, respectively; p = 0.290) and major adverse cardiovascular events (29.32% vs 23.14%, respectively; p = 0.135) during follow-up. <h3>Conclusions</h3> Rosuvastatin and atorvastatin have similar efficacies for preventing CIN in patients with CKD undergoing PCI.

Clinical impact of acute kidney injury on short- and long-term outcomes after transcatheter aortic valve implantation with the CoreValve prosthesis

BackgroundAcute kidney injury (AKI) after cardiac surgery is associated with increased mortality, but few data exist on the occurrence and clinical impact of AKI associated with transcatheter aortic valve implantation (TAVI). The objective of this study was to determine the incidence and prognosis of AKI after percutaneous implantation of the CoreValve® (Medtronic, Minneapolis, MN, USA) prosthesis. MethodsA total of 357 patients with severe aortic stenosis and 9 patients with pure native aortic regurgitation were treated with the CoreValve prosthesis. AKI was defined according to Valve Academic Research Consortium criteria as the absolute increase in serum creatinine ≥0.3mg/dl at 72h post percutaneous procedure. ResultsAKI was identified in 58 patients (15.8%), none of whom required renal replacement therapy. In patients with AKI, the mortality at 30 days was 13.5% compared with 1.6% of patients without AKI, [odds ratio (OR)=12.2 (95% CI 3.53–41.9); p<0.001] and total mortality after a mean of 26.2±17 months was 29.3% vs. 14.9% [OR=2.36 (95% CI 1.23–4.51), p=0.008]. In the multivariate analysis, AKI was an independent predictor of cumulative total mortality [hazard ratio=2.151, (95% CI from 1.169 to 3.957), p=0.014]. ConclusionsThe deterioration of renal function in patients undergoing TAVI with the CoreValve prosthesis is a serious and frequent complication. The occurrence of AKI was associated with increased early mortality and was also a predictor of worse outcomes in follow-up.

Worsening of renal function during 1 year after hospital discharge is a strong and independent predictor of all-cause mortality in acute decompensated heart failure.

BackgroundRenal impairment is a common comorbidity and the strongest risk factor for poor prognosis in acute decompensated heart failure (ADHF). In clinical practice, renal function is labile during episodes of ADHF, and often worsens after discharge. The significance of worsening of renal function (WRF) after discharge has not been investigated as extensively as baseline renal function at admission or WRF during hospitalization.Methods and ResultsAmong 611 consecutive patients with ADHF emergently admitted to our hospital, 233 patients with 3 measurements of serum creatinine (SCr) level measurements (on admission, at discharge, and 1 year after discharge) were included in the present study. Patients were divided into 2 groups according to the presence or absence of WRF at 1 year after discharge (1y‐WRF), defined as an absolute increase in SCr >0.3 mg/dL (>26.5 μmol/L) plus a ≥25% increase in SCr at 1 year after discharge compared to the SCr value at discharge. All‐cause and cardiovascular mortality were assessed as adverse outcomes. During a mean follow‐up of 35.4 months, 1y‐WRF occurred in 48 of 233 patients. There were 66 deaths from all causes. All‐cause and cardiovascular mortality were significantly higher in patients with 1y‐WRF (log‐rank P<0.0001 and P<0.0001, respectively) according to Kaplan–Meier analysis. In a multivariate Cox proportional hazards model, 1y‐WRF was a strong and independent predictor of all‐cause and cardiovascular mortality. Hemoglobin and B‐type natriuretic peptide at discharge, as well as left ventricular ejection fraction <50%, were independent predictors of 1y‐WRF.ConclusionsIn patients with ADHF, 1y‐WRF is a strong predictor of all‐cause and cardiovascular mortality.

Additional value of the red blood cell distribution width to the Mehran risk score for predicting contrast-induced acute kidney injury in patients with ST-elevation acute myocardial infarction

BackgroundContrast-induced acute kidney injury (CI-AKI) after percutaneous coronary intervention in patients with ST-elevation myocardial infarction (STEMI) is a common complication associated with worse outcome. Considering the prognostic predictive value of the red cell distribution width (RDW), we aimed to measure the usefulness of RDW for predicting CI-AKI. MethodsAll consecutive STEMI patients without hemodialysis from June 2011 to September 2013 admitted to St. Luke's International Hospital were enrolled. We performed primary percutaneous coronary intervention in all patients. CI-AKI was defined as a >25% increase or an absolute increase in serum creatinine of 0.5mg/dl within 3 days after percutaneous coronary intervention. The potential additional predictive value of RDW with the Mehran risk score (MRS) on admission was estimated. ResultsA total of 102 patients (78.4% males) were analyzed – 10 of the 102 (10%) STEMI patients developed CI-AKI. Multivariate analysis showed that RDW was an independent variable predicting CI-AKI in these patients [odds ratio, 2.029; 95% confidence interval (95% CI), 1.029–3.999; p=0.041]. The areas under the receiver operating characteristic curves for MRS only, RDW only, and the combined model (MRS and RDW) for the prediction of CI-AKI were 0.806 (95% CI, 0.696–0.917), 0.719 (95% CI, 0.536–0.902), and 0.846 (95% CI, 0.744–0.949), respectively. ConclusionWe showed the potential predictive ability of RDW, only if used with MRS, for CI-AKI in STEMI patients. Further evaluation of RDW for predicting CI-AKI in patients with STEMI is needed.

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.

Predictive value of GRACE risk scores for contrast-induced acute kidney injury in patients with ST-segment elevation myocardial infarction before undergoing primary percutaneous coronary intervention

Contrast-induced acute kidney injury (CI-AKI) is a well-known serious complication of percutaneous coronary intervention (PCI) and may cause increased morbidity and mortality. We aim to identify the predictive value of Global Registry for Acute Coronary Events (GRACE) risk scores for CI-AKI in patients with ST-segment elevation myocardial infarction (STEMI) before primary PCI, allowing pre-procedural decisions regarding prevention therapy for CI-AKI. We enrolled 251 consecutive patients with STEMI undergoing primary PCI. Receiver operating characteristic curves were used to identify the optimal sensitivity for the observed range of GRACE risk scores. CI-AKI was defined as any of the following: absolute increase in serum creatinine (SCr) of ≥ 0.3 or ≥ 0.5 mg/dL within 48-72 h after contrast exposure, or a percentage increase in SCr level of ≥ 50 %. Forty-three patients (17.1 %) developed CI-AKI0.3, 22 (8.8 %) CI-AKI0.5, and 19 (7.6 %) CI-AKI50. The GRACE quartiles were as follows: Q1 (<136), Q2 (136-159), Q3 (159-180), and Q4 (>180). Patients with high GRACE risk scores had higher risk for CI-AKI0.3, 0.5, and 50 (6.6, 6.6, 23.4, 31.7 %, respectively, p < 0.001; 1.6, 1.6, 9.4, 22.2 %, respectively, p < 0.001; and 3.3, 3.2, 9.4, 14.3 %, respectively, p = 0.009). ROC showed that a GRACE risk score >160 was a fair discriminator for CI-AKI0.3, 0.5, and 50 (C statistic = 0.723, 0.788, 0.668, respectively). After adjusting for potential confounding predictors, GRACE risk score >160 remained significantly associated with CI-AKI0.3 or 0.5 (OR 3.84; 95 % CI 1.61-9.17; p = 0.002, or OR 5.54; 95 % CI 1.42-21.66; p = 0.014), and high-sensitivity C-reactive protein (Hs-CRP) >15.5 mg/L was a highly significant predictor of CI-AKI0.3, 0.5, and CI-AKI50. GRACE risk score (>160) and post-procedural Hs-CRP >15.5 mg/L are independent and significant predictors of CI-AKI in patients with STEMI before primary PCI.

Risk Factors for Hemodialysis and Mortality in Patients With Contrast-Induced Nephropathy

The purpose of this study was to identify risk factors for renal failure requiring hemodialysis and mortality in patients who developed contrast-induced nephropathy (CIN) after cardiac catheterization. Out of 13,742 patients who received cardiac catheterization at Westchester Medical Center/New York Medical College from 2005 to 2008, 268 patients (2%) with a discharge diagnosis of renal failure were screened for CIN. CIN was defined as either a >25% increase of the serum creatinine or an absolute increase in serum creatinine of 0.5 mg/dL within the first 48 hours of the procedure. Chart reviews were performed on 80 patients (1%) who met the criteria for CIN. The 80 patients in the study included 46 men and 34 women, mean age 69 ± 14 years. Of the 80 patients, 18 patients (23%) died, and 22 patients (28%) developed renal failure requiring hemodialysis. Stepwise logistic regression analysis showed that independent risk factors for mortality were the use of calcium channel blockers [odds ratio = 0.0025, 95% confidence interval (CI), 0.0001-0.1210, P < 0.01], catecholamine use (odds ratio = 71.2177, 95% CI, 4.2153-1203, P < 0.01), circulatory failure with lactic acidosis (odds ratio = 32.1405, 95% CI, 2.6331-392, P < 0.01), and renal failure requiring hemodialysis (odds ratio = 17.0376, 95% CI, 1.2344-235, P < 0.05). Significant independent risk factors for renal failure requiring hemodialysis were smoking (odds ratio = 0.06, 95% CI, 0.0045-0.8080, P < 0.05), N-acetylcysteine use (odds ratio = 0.08, 95% CI, 0.0148-0.4179, P < 0.01), anemia (odds ratio = 11.32, 95% CI, 2.57-50, P < 0.01), and circulatory failure with lactic acidosis (odds ratio = 9.76, 95% CI, 2.37-40, P < 0.01). Our data showed that risk factors for mortality in patients with CIN were catecholamine use, circulatory failure with lactic acidosis, and renal failure requiring hemodialysis. Risk factor for reducing mortality in patients with CIN was calcium channel blocker use. Significant risk factors for renal failure requiring hemodialysis were anemia, and circulatory failure with lactic acidosis. Risk factors for reducing renal failure requiring hemodialysis were N-acetylcysteine use and smoking.

Clinical impact of acute Kidney injury after Transcatheter Aortic Valve Implantation (TAVI) with the corevalve prosthesis in patients with aortic stenosis

Acute Kidney Injury (AKI) after cardiac surgery is associated with increased mortality, but very few data exist on the ocurrence of AKI associated with Transcatheter Aortic Valve Implantation (TAVI). The objective of this study was to determine the incidence, predictors and prognosis of AKI after percutaneous implantation of the CoreValve aortic valve prosthesis. Methods: Between April 2008 and January 2011, 230 patients with severe aortic stenosis were treated with the CoreValve aortic valve prosthesis. The AKI was defined according to Valve set by the Academic Research Consortium, as the absolute increase in serum creatinine ≥0.3 mg/dl or an increase of over 50% at 72 hours a percutaneous procedure. Were excluded from analysis 7 patients, in 5 patients were unsuccessful procedural and 2 patients had chronic renal failure on dialysis. Results: Of the 223 patients treated with TAVI, 53 patients (23.8%) had chronic renal failure. AKI was identified in 37 patients (16.6%) and none reqired renal replacement therapy. After implantation there was a slight improvement in renal function, baseline serum creatinine decreased from 1.29±0.5 mg/dl to 1.22 mg/dl, P = 0.023 and Glomerular Filtration Rate (GFR) increased from 49.6±22 to 52±23, P = 0.015. There were no differences in the amount of contrast received (197±67 for patients with AKI vs. 180±72 cc for patients without AKI, P = 0.580). In patients with AKI, the mortality at 30 days was 13.5% compared to 1.6% of patients without AKI, P = 0.001 and late mortality after a mean of 16.7±11 months was 18.8% in those patients with AKI compared to 8.2% in those witout AKI, P = 0.068. In the multivariate analysis AKI was an independent predictor of cumulative total mortality (HR = 3.516, 95% CI from 1.098 to 11.255, P = 0.034). The factors associated with development of AKI were males and the presence of stroke prior the procedure. Conclusions: The deterioration of renal function in patients undergoing TAVI with the CoreValve prosthesis is a serious and frequent complication. The occurrence of AKI was associated with increase early mortality and also was a predictor of worse outcomes in the long-term follow-up.

Contrast induced nephropathy: a new predictive model based on pre procedural glycemia and glomerular filtration rate

Aims: The risk of contrast induced nephropathy (CIN) is predicted by the already proposed formula of the ratio of contrast volume to glomerular filtration rate (GFR). Recent data from literature undescore that the incidence of CIN is significantly influenced by admission glycemia. Therefore, our aim was to identify a predictive model of CIN based on the quantity of contrast used during pPCI, known independent predictors of CIN, and pre procedural glycemia. Methods and results: 679 STEMI patients treated with primary PCI (pPCI) were enrolled in our prospective study. CIN was defined as an absolute serum creatinine increase ≥0.3 mg/dl after procedure. Admission hyperglycemia was defined as glucose levels >198 mg/dl. Medium volume of contrast (CV) we used ranged from 30 to 700 ml. We observed a significant increase in the incidence of CIN with the increase of the CV/GFR ratio which was in turn influenced by admission hyperglycemia. We therefore created a model of CIN prediction based on CV, GFR and admission glycemia. This model results from the product of admission glycemia and CV/GFR × 100. We then confronted our model with previously proposed models for prediction of CIN in pPCI patients (model 1: CV/GFR >3.7; model 2: CV/{[5 × weigth (kg)]/serum creatinin (mg/dl)} >1) obtaining better AUC with ROC analisys (AUC 0.72 vs 0.63, p<0.001 with model 1, AUC 0.72 vs 0,59, p<0.001 with model 2). At multivariate analisys a value of 4.2 was the best indipendent predictor of CIN. Conclusions: Our CIN risk model based on CV and admission glycemia was more accurate than the existing models. This model can be useful before pPCI to identify the safe quantity of contrast to use, and after pPCi to identify the subgroup of patients at higher risk of CIN.

Admission hyperglycemia and contrast induced nephropathy

Aims: Admission hyperglycemia is a frequent condition in ST elevation myocardial infarction (STEMI) associated with an increased risk of contrast induced nephropathy (CIN)after primary percutaneous coronary intervention (pPCI). We evaluate the possible different role of acute and chronic hyperglycemia on CIN and the impact of its early spontaneous or pharmacologic normalization. Methods and results: 679 STEMI patients treated with pPCI were enrolled in our prospective study. CIN was defined as an absolute serum creatinine increase ≥0.3 mg/dl after procedure. Admission hyperglycemia was defined as glucose levels >198 mg/dl: acute or chronic increase was identified respectivelyin patients with a glycated haemoglobin A1c ≤7% and >7%.In hyperglicemic patients, a decrease of fasting glucose levels <140 mg/dl in second day was considered for early normalization. Admission hyperglycemia (17%) was an independent predictor for CIN incidence, but at subgroup analysis its prognostic impact emerged only in non diabetic patients. Similarly, only in this subgroup its rapid normalization was associated to a lower incidence of CIN and to a better outcome. Actually, CIN incidence was significantly higher in patients with acute hyperglycemia than in those with chronic hyperglycemia (34.5% vs 16.9%, p=0.03), irrespective of diabetes mellitus. Conclusions: Admission hyperglycemia relates to an increase risk of CIN, especially when it occurs acutely. A condition ofglycemic levels ≥198 mg/dl and glycated haemoglobin A1c ≤7%, identifies patients at higher risk, in whom a rapid glycemic control could become a further strategy of CIN prevention.

Age, glomerular filtration rate, ejection fraction, and the AGEF score predict contrast‐induced nephropathy in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention

In patients undergoing primary percutaneous coronary interventions (PCI) for ST-segment elevation myocardial infarction (STEMI), the occurrence of Contrast-Induced Nephropathy (CIN) has a pronounced impact both on morbidity and mortality. We investigated the variables associated with CIN development in 481 consecutive patients with STEMI undergoing primary PCI and evaluated the predictive value of a 3-variable clinical risk score (the AGEF score) based on age, left ventricular ejection fraction (EF), and estimated glomerular filtration rate (eGFR). CIN was defined as an absolute increase in serum creatinine ≥0.5 mg/dL or an increase ≥25% from baseline within 72 hr. AGEF score was calculated by adding 1 point to the Age/EF(%) ratio if the eGFR was <60 mL/min per 1.73 m(2) . Overall, the incidence of CIN was 5.2%. In-hospital mortality was higher in patients with CIN than in those without (16% Vs 1.3%, P = 0.001). At multivariate analysis age (OR 1.06, P = 0.042), eGFR (OR 0.95, P = 0.001), EF (OR 0.94, P = 0.007) and post-procedural TIMI flow grade (OR 0.43, P = 0.045) were independent predictors of CIN. AGEF score was an accurate (OR 5.19, P < 0.001, AUC 0.88) and calibrated (Hosmer-Lemeshow χ(2) = 10.25, P = 0.25) predictor of CIN. Advanced age, depressed EF, and reduced eGFR are independent predictors of CIN development after primary PCI for STEMI. The preprocedural individual patient risk can be clinically assessed with the calculation of the AGEF score, which is based on such readily available parameters.

The association between atherosclerotic renal artery stenosis and acute kidney injury in patients undergoing cardiac surgery.

BackgroundAtherosclerotic renal artery stenosis (ARAS) and coronary artery disease (CAD) commonly co-exist. Some patients with unidentified ARAS may undergo cardiac surgery. While acute kidney injury (AKI) is a frequent and serious complication of cardiac surgery, we aim to evaluate the influence of ARAS on the occurrence of postoperative AKI in patients with normal or near-normal baseline renal function following cardiac surgery.MethodsA total of 212 consecutive patients undergoing aortography after coronary angiography and cardiac surgery were retrospectively studied for their preoperative and intraoperative conditions. AKI was defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl (≥26.4 µmol/l) or a percentage increase in creatinine of more than or equal to 50% (1.5-fold from baseline) after cardiac surgery. A propensity score-adjusted logistic regression models was used in estimating the effect of ARAS on the risk of postoperative AKI.ResultsARAS (≥50%) was observed in 50 (23.6%) patients, and 83 (39.2%) developed AKI after cardiac surgery. A correlation existed between renal artery patency and preoperative–to–postoperative %ΔCr in patients with ARAS (r = 0.297, P<0.0001). The propensity score-adjusted regression model showed the occurrence of postoperative AKI in patients with ARAS was significantly higher than those without ARAS (OR 2.858, 95% CI 1.260–6.480, P = 0.011).ConclusionARAS is associated with postoperative AKI in patients with normal or near-normal baseline renal function after cardiac surgery.

Response to Letter Regarding Article, “Ischemic Preconditioning for Prevention of Contrast Medium–Induced Nephropathy: Randomized Pilot RenPro-Trial (Renal Protection Trial)”

We thank the authors for their interest in our study on the impact of remote ischemic preconditioning on contrast medium–induced acute kidney injury (CI-AKI).1 The incidence of CI-AKI varies substantially among several studies because of the lack of a uniform definition of CI-AKI.2 Rates of CI-AKI may be as high as 50% or even higher, depending on the presence of risk factors such as chronic renal insufficiency and diabetes mellitus. Although the definition of CI-AKI varies across the trials, the most commonly used definition includes an absolute increase in serum creatinine of 0.5 mg/dL or a 25% relative increase in …

Recovery from AKI and Short- and Long-Term Outcomes after Lung Transplantation

Patients with AKI after lung transplantation are at increased risk for CKD and death. Whether patients who completely recover from AKI have improved long-term outcome compared with patients who do not completely recover remains unknown. This study retrospectively evaluated data on 657 patients who underwent lung transplantation from 1997 to 2009. Outcomes analyzed were the incidence of renal recovery after AKI and the association of this recovery with short- and long-term mortality. AKI was defined by an absolute increase in serum creatinine of ≥0.3 mg/dl or a percent increase in serum creatinine of ≥50% from baseline at any time during the first 2 weeks after transplantation. Four hundred twenty-four (65%) patients experienced AKI in the first 2 weeks after transplantation. Of these patients, complete renal recovery occurred in 142 (33%) patients. The incidence of in-hospital complications was similar between patients who recovered renal function and patients without recovery. At 1 year, the cumulative incidence of CKD was 14% and 22% (P=0.10) and patient survival rate was 81% and 76% (P=0.20) in patients with complete recovery from AKI and patients without recovery, respectively. Patients with completely recovered AKI had similar risk-adjusted long-term mortality compared with patients who did not recover (hazard ratio [95% confidence interval]=1.42 [1.15-2.05] versus 1.53 [1.01-2.00]). Patients who recover completely from early AKI after lung transplantation have a similar risk for CKD and long-term mortality compared with patients who do not recover.

Blood Transfusion and the Risk of Acute Kidney Injury After Transcatheter Aortic Valve Implantation

Blood transfusion is associated with acute kidney injury (AKI) after transcatheter aortic valve implantation (TAVI). We sought to elucidate in more detail the relation between blood transfusion and AKI and its effects on short- and long-term mortality. Nine hundred ninety-five patients with aortic stenosis underwent TAVI with the Medtronic CoreValve or the Edwards Valve in 7 centers. AKI was defined by the Valve Academic Research Consortium (absolute increase in serum creatinine ≥0.3 mg/dL [≥26.4 μmol/L] or ≥50% increase ≤72 hours). Logistic and Cox regression was used for predictor and survival analysis. AKI occurred in 20.7% (n=206). The number of units of blood transfusion ≤24 hours was the strongest predictor of AKI (≥5 units, OR, 4.81 [1.45-15.95], 3-4 units, OR, 3.05 [1.24-7.53], 1-2 units, OR, 1.47 [0.98-2.22]) followed by peripheral vascular disease (OR, 1.48 [1.05-2.10]), history of heart failure (OR, 1.43 [1.01-2.03]), leucocyte count ≤72 hours after TAVI (OR, 1.05 [1.02-1.09]) and European System for Cardiac Operative Risk Evaluation (EuroSCORE; OR, 1.02 [1.00-1.03]). Potential triggers of blood transfusion such as baseline anemia, bleeding-vascular complications, and perioperative blood loss were not identified as predictors. AKI and life-threatening bleeding were independent predictors of 30-day mortality (OR, 3.15 [1.56-6.38], OR, 6.65 [2.28-19.44], respectively), whereas transfusion (≥3 units), baseline anemia, and AKI predicted mortality beyond 30 days. AKI occurred in 21% of the patients after TAVI. The number of blood transfusions but not the indication of transfusion predicted AKI. AKI was a predictor of both short- and long-term mortality, whereas blood transfusion predicted long-term mortality. These findings indicate that outcome of TAVI may be improved by more restrictive use of blood transfusions.

Efficacy of Ascorbic Acid, N‐Acetylcysteine, or Combination of Both on Top of Saline Hydration versus Saline Hydration Alone on Prevention of Contrast‐Induced Nephropathy: A Prospective Randomized Study

Antioxidant drugs such as N-acetylcysteine (NAC) and ascorbic acid have been evaluated in interventional studies to prevent contrast-induced nephropathy (CIN), however, there are limited data on comparing either or both, with background of standard intravenous saline hydration versus the standard intravenous saline hydration alone in preventing CIN. We conducted a single-center randomized trial among patients undergoing coronary angiography or percutaneous coronary intervention who had serum creatinine ≥ 1.3 mg/dL or were on diabetes mellitus medication. Eligible patients were randomly assigned to one of the following 4 groups: (1) NAC, (2) ascorbic acid, (3) combination of both drugs, and (4) control group. Additionally, all the groups received the standard intravenous saline hydration. Creatinine was measured 4-5 days after procedure. A total of 243 patients were randomized; 62 to NAC, 57 to ascorbic acid, 58 to both drugs, and 66 to placebo. The development of 0.5 mg/dL absolute increase of serum creatinine, 25% relative decrease of creatinine clearance, or either (CIN) were measured in the ascorbic acid group (3.6% for all), NAC group (6.8%, 3.4%, 8.5%, respectively), combined group (5.5%, 5.5%, 9.1%, respectively), and control group (6.2%, 6.2%, 7.7%, respectively). None of these differences were significant (P = 0.896 for serum creatinine, P = 0.863 for creatinine clearance, and P = 0.684 for CIN). In a cohort of patients at risk of developing CIN, we could not detect any significant benefit of the use of ascorbic acid, NAC, or a combination of both drugs over the standard hydration regimen in preventing CIN.

Elevated Uric Acid Increases the Risk for Acute Kidney Injury

BackgroundUric acid has been proposed to play a role in acute kidney injury. We therefore investigated the potential influence of preoperative serum uric acid (SUA) on acute kidney injury in patients undergoing cardiovascular (CV) surgery. The primary aims were to investigate the incidence of acute kidney injury, peak serum creatinine (SCr) concentrations, hospital length of stay, and days on mechanical ventilation. MethodsRetrospective study included patients who underwent CV surgery and had preoperative SUA available. Acute kidney injury was defined as an absolute increase in SCr ≥0.3 mg/dL from baseline within 48 hours after surgery. Univariate and multivariate logistic regression analysis was performed to determine the odds ratio for acute kidney injury. ResultsThere were 190 patients included for analysis. SUA were divided into deciles. The incidences of acute kidney injury were higher with higher deciles of SUA. When the incidences of acute kidney injury were plotted against all available values of SUA at increments of 0.5 mg/dL, a J-shaped curve emerged demonstrating higher incidences of acute kidney injury associated with both hypo- and hyperuricemia. In the univariate analysis, SUA ≥5.5 mg/dL was associated with a 4-fold (odds ratio [OR] 4.4; 95% confidence interval [CI], 2.4-8.2), SUA ≥6 mg/dL with a 6-fold (OR 5.9; 95% CI, 3.2-11.3), SUA ≥6.5 mg/dL with an 8-fold (OR 7.9; 95% CI, 3.9-15.8), and SUA ≥7 mg/dL with a 40-fold (OR 39.1; 95% CI, 11.6-131.8) increased risk for acute kidney injury. In the multivariate analysis, SUA ≥7 mg/dL also was associated with a 35-fold (OR 35.4; 95% CI, 9.7-128.7) increased risk for acute kidney injury. The 48-hour postoperative and hospital-stay mean peak SCr levels also were higher in the SUA ≥5.5 mg/dL group compared with the SUA <5 mg/dL group. SUA ≥7 mg/dL was associated with increased length of hospital stay (SUA <7 mg/dL, 18.5±1.8 days vs SUA ≥7 mg/dL, 32.0±6.8 days, P = 0.058) and a longer duration of mechanical ventilation support (SUA <7 mg/dL, 2.4±0.4 days vs SUA ≥7 mg/dL, 20.4±4.5 days, P = 0.001). ConclusionPreoperative SUA was associated with increased incidence and risk for acute kidney injury, higher postoperative SCr values, and longer hospital length of stay and duration of mechanical ventilation support in patients undergoing cardiac surgery. A J-shaped relationship appears to exist between SUA and acute kidney injury.

Primary focal segmental glomerulosclerosis in nephrotic patients: common complications and risk factors

Focal segmental glomerulosclerosis (FSGS) presents a range of potentially serious complications, including acute kidney injury (AKI), infection and thromboembolism. This study aimed to find out the incidence rates and risk factors for these complications in FSGS patients. Patients with biopsy-proven primary FSGS and nephrotic-range proteinuria were included in this study. A short-term (16-week) follow-up was performed to observe the aforementioned complications. Clinical characteristics of patients were recorded upon enrollment. AKI was diagnosed as an absolute increase in serum creatinine of ≥0.3 mg/dL or a percentage increase of ≥50% within 48 hours; infection, by a combination of clinical manifestations, laboratory tests and imaging examinations; and thromboembolism, by imaging methods. Risk factors for complications were evaluated by logistic regression model. The study population included 90 FSGS patients (63 males, mean age 28.9 ± 12.9 years). The incidences of AKI, infection and thromboembolism were 44.4%, 25.6% and 12.2%, respectively. Patients with AKI were more likely to be male, with lower serum albumin, greater proteinuria and more severe acute tubulointerstitial damage. Patients with infection had higher proteinuria and lower serum albumin, globulin and IgG. Circulating endothelial cells (CECs) and von Willebrand factor were higher in patients with thromboembolism. Logistic regression showed that increased urine retinol-binding protein, decreased serum albumin and IgG, and increased CECs and hemoglobin were independent risk factors for AKI, infection and thromboembolism, respectively. AKI, infection and thromboembolism are common among FSGS patients. Awareness of risk factors and prevention of these complications are important for the prognosis of these patients.