Contrast-induced Acute Kidney Injury Patients Research Articles

Arginase2 mediates contrast-induced acute kidney injury via facilitating nitrosative stress in tubular cells

Contrast-induced acute kidney injury(CI-AKI) is the third cause of AKI. Although tubular injury has been regarded as an important pathophysiology of CI-AKI, the underlying mechanism remains elusive. Here, we found arginase2(ARG2) accumulated in the tubules of CI-AKI mice, and was upregulated in iohexol treated kidney tubular cells and in blood samples of CI-AKI mice and patients, accompanied by increased nitrosative stress and apoptosis. However, all of the above were reversed in ARG2 knockout mice, as evidenced by the ameliorated kidney dysfunction and the tubular injury, and decreased nitrosative stress and apoptosis. Mechanistically, HO-1 upregulation could alleviate iohexol or ARG2 overexpression mediated nitrosative stress. Silencing and overexpressing ARG2 was able to upregulate and downregulate HO-1 expression, respectively, while HO-1 siRNA had no effect on ARG2 expression, indicating that ARG2 might inhibit HO-1 expression at the transcriptional level, which facilitated nitrosative stress during CI-AKI. Additionally, CREB1, a transcription factor, bound to the promoter region of ARG2 and stimulated its transcription. Similar findings were yielded in cisplatin- or vancomycin-induced AKI models. Taken together, ARG2 is a crucial target of CI-AKI, and activating CREB1/ARG2/HO-1 axis can mediate tubular injury by promoting nitrosative stress, highlighting potential therapeutic strategy for treating CI-AKI.

Association of plasma free triiodothyronine levels with contrast-induced acute kidney injury and short-term survival in patients with acute myocardial infarction.

ObjectivePost-treatment contrast-induced acute kidney injury (CI-AKI) is associated with poor outcomes in patients with acute myocardial infarction (AMI). A lower free triiodothyronine (FT3) level predicts a poor prognosis of AMI patients. This study evaluated the effect of plasma FT3 level in predicting CI-AKI and short-term survival among AMI patients.MethodsCoronary arteriography or percutaneous coronary intervention was performed in patients with AMI. A 1:3 propensity score (PS) was used to match patients in the CI-AKI group and the non-CI-AKI group.ResultsOf 1480 patients enrolled in the study, 224 (15.1%) patients developed CI-AKI. The FT3 level was lower in CI-AKI patients than in non-CI-AKI patients (3.72 ± 0.88 pmol/L vs 4.01 ± 0.80 pmol/L, P < 0.001). Compared with those at the lowest quartile of FT3, the patients at quartiles 2–4 had a higher risk of CI-AKI respectively (P for trend = 0.005). The risk of CI-AKI increased by 17.7% as FT3 level decreased by one unit after PS-matching analysis (odds ratio: 0.823; 95% CI: 0.685–0.988, P = 0.036). After a median of 31 days of follow-up (interquartile range: 30–35 days), 78 patients died, including 72 cardiogenic deaths and 6 non-cardiogenic deaths, with more deaths in the CI-AKI group than in the non-CI-AKI group (53 vs 25, P < 0.001). Kaplan–Meier survival analysis showed that patients at a lower FT3 quartile achieved a worse survival before and after matching.ConclusionLower FT3 may increase the risk of CI-AKI and 1-month mortality in AMI patients.

Midkine as a novel biomarker for contrast-induced acute kidney injury

Contrast-induced acute kidney injury (CI-AKI) is an intrinsic kidney injury caused by contrast injection in susceptible individuals. Although the pathophysiological mechanisms by which contrast agents induce kidney injury have not been completely explained, direct and indirect effects, as well as hemodynamic perturbations, have been suggested. Renal effects develop immediately after contrast injection, and, theoretically, they could be detected early by using a sensitive biomarker. Recently, studies have been conducted to determine specific biomarkers to guide the early diagnosis of CI-AKI and thus improve the outcomes of these patients. Midkine (MK) is a heparin-binding growth factor that balances cell growth, survival, and migration. It has an antiapoptotic activity in nephrogenesis. Midkine has been investigated as an early biomarker for CI-AKI in patients undergoing percutaneous coronary intervention (PCI) for stable angina and was significantly higher in CI-AKI patients post PCU. However, more studies are needed to validate its efficacy in the early detection of CI-AKI.&#x0D; &#x0D; Keywords: Contrast-induced nephropathy, contrast-induced acute kidney injury, midkine, biomarker.

Midkine as an Early Biomarker of Contrast-induced Acute Kidney Injury in Chronic Kidney Disease Patients Undergoing Percutaneous Coronary Intervention for Acute Coronary Syndrome: A Single-center Prospective Study

Background: Contrast-induced acute kidney injury (CI-AKI), is an important complication of percutaneous coronary intervention (PCI). We aimed to study the role of serum midkine (MK) as an early biomarker of CI-AKI.&#x0D; Methods: We conducted a prospective observational cohort study. It includes 100 chronic kidney disease (CKD) patients with an estimated glomerular filtration rate (eGFR) &lt;60 ml/min/1.73m2. All patients were undergoing PCI for ACS. We measured serum midkine before, 2 and 24 hours after PCI. &#x0D; Results: The mean age of the patients was 70.32±3.62 years, 74% males. Twenty-seven patients developed CI-AKI. The CI-AKI group has a history of diabetes mellitus (DM) and/or dyslipidemia, history of diuretics, metformin and/or angiotensin-converting enzyme inhibitors/angiotensin-receptor blockers (ACEI/ARBs) use. The CI-AKI patients have low left ventricular ejection fraction (LVEF) (EF &lt; 45%) and low Creatinine Clearance (CrCl) before PCI. The CI-AKI received more contrast volume, had a longer duration of PCI and had high Mehran risk score after PCI. Comparison between the two studied groups regarding serum MK showed that there was a statistically significant difference regarding serum MK 2 hours after PCI. Receiver operating characteristic (ROC) curve analysis for serum MK showed that serum MK measured 2 hours after PCI was statistically significant to predict CI-AKI.&#x0D; Conclusion: An early Serum MK after PCI can be used as an early predictor of CI-AKI in ACS patients.

The association between neutrophil-to-lymphocyte ratio and contrast-induced acute kidney injury in patients with carotid artery stenting

Contrast-induced acute kidney injury (CI-AKI) is a life-threatening complication that leads to comorbidities and prolonged hospital stay lengths in the setting of peripheral interventions. The presence of some CI-AKI risk factors has already been investigated. In this study, we evaluated the predictors of CI-AKI after carotid artery stenting. A total of 389 patients with 50% to 99% carotid artery stenosis who underwent carotid artery stenting were included in this study. Patients were grouped according to CI-AKI status. CI-AKI developed in 26 (6.6%) patients. Age, baseline creatinine level, neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio were higher and estimated glomerular filtration rate, haemoglobin and lymphocyte count were lower in CI-AKI patients. In the multivariate regression analysis, the neutrophil-to-lymphocyte ratio triggered a 1.39- to 2.63-fold increase in the risk of CI-AKI onset (p < 0.001). The neutrophil-to-lymphocyte ratio may be a significant predictor of CI-AKI in patients with carotid artery stenting and higher neutrophil-to-lymphocyte ratio values may be independently associated with CI-AKI.

Incidence, Risk Factors, the Role of Plasma NGAL and Outcome of Contrast-Induced Acute Kidney Injury in Critically Ill Children.

To study the incidence of contrast-induced acute kidney injury (CI-AKI), evaluate its risk factors, study the role of plasma neutrophil gelatinase-associated lipocalin (NGAL) and evaluate the outcome of CI-AKI in critically ill children. In this prospective cohort study, children aged 1 mo to 12 y who underwent contrast computed tomography(CECT) for various medical indications were included. Patients without renal function test before contrast administration, children with chronic kidney disease, children admitted for less than 48h, and those with serum bilirubin more than 5mg per dL were excluded. Serum creatinine and estimated-Glomerular filtration rate (e-GFR) were measured at admission, immediately before, and at 6, 24, 48h after contrast. Plasma neutrophil gelatinase-associated lipocalin (NGAL) was measured before and 6h after contrast. The incidence of CI-AKI by p-RIFLE (Pediatric Risk, Injury, Failure, Loss, End Stage Renal Disease) criteria, its risk factors, the diagnostic role of NGAL in CI-AKI, and outcomes [30 d unfavorable outcome (death, readmission) and renal recovery] were studied. One hundred children were enrolled. The indications for CECT were brain (58%) and respiratory pathology (20%). Incidence of CI-AKI was 35% (95% CI 26.4% to 44.8%); 71% in 'Risk,' and 29% in the 'Injury' stage. After multivariate logistic regression, age younger than 2 y was independently associated with CI-AKI. There was no significant difference in NGAL before (ROC-AUC 0.38,95%CI 0.26 to 0.50) and 6h after CECT scan (AUC 0.41, 95%CI 0.29 to 0.54) to predict CI-AKI. There were 7% deaths but no readmission at 30 d. Among 33 CI-AKI patients who survived, the operational definition of renal recoverywas achieved in 51.5% (n = 17), complete renal recovery was achieved in 97% (n = 32), and partial renal recovery was achieved in 3% (n = 1) of patients at discharge, while none received renal supportive therapy. The incidence of contrast-induced acute kidney injury was 35% with age younger than two year being independently associated with CI-AKI. NGAL did not predict the CI-AKI.

Methods for Reducing Contrast Use and Avoiding Acute Kidney Injury During Endovascular Procedures.

Iodinated Contrast Media (CM) has a plethora of applications in routine non-invasive or percutaneous invasive imaging examinations and therapeutic interventions. Unfortunately, the use of CM is not without complications, with contrast-induced acute kidney injury (CI-AKI) being among the most severe. CI-AKI is a syndrome defined as a rapid development of renal impairment after a few days of CM endovascular injection, without the presence of any other underlying related pathologies. Although mostly transient and reversible, for a subgroup of patients with comorbidities related to renal failure, CI-AKI is directly leading to longer hospitalization, elevated rates of morbidity and mortality, as well as the increased cost of funding. Thus, a need for classification in accordance with clinical and peri-procedural criteria is emerged. This would be very useful for CI-AKI patients in order to predict the ones who would have the greatest advantage from the application of preventive strategies. This article provides a practical review of the recent evidence concerning CI-AKI incidence, diagnosis, and sheds light on prevention methods for reducing contrast use and avoiding AKI during endovascular procedures. In conclusion, despite the lack of a specific treatment protocol, cautious screening, assessment, identification of the high-risk patients, and thus the application of simple interventions -concerning modifiable risk factors- can significantly reduce CI-AKI risk.

PINK1-parkin pathway of mitophagy protects against contrast-induced acute kidney injury via decreasing mitochondrial ROS and NLRP3 inflammasome activation

Contrast-induced acute kidney injury (CI-AKI) occurs in more than 30% of patients after intravenous iodinated contrast media and causes serious complications, including renal failure and mortality. Recent research has demonstrated that routine antioxidant and alkaline therapy failed to show benefits in CI-AKI patients with high risk for renal complications. Mitophagy is a mechanism of selective autophagy, which controls mitochondrial quality and mitochondrial reactive oxygen species (ROS) through degradation of damaged mitochondria. The role of mitophagy and its regulation of apoptosis in CI-AKI are poorly understood. In this study, we demonstrated that mitophagy was induced in renal tubular epithelial cells (RTECs) during CI-AKI, both in vivo and in vitro. Meanwhile, contrast media–induced mitophagy was abolished when silencing PINK1 or PARK2 (Parkin), indicating a dominant role of the PINK1-Parkin pathway in mitophagy. Moreover, mitochondrial damage, mitochondrial ROS, RTEC apoptosis, and renal injury under contrast exposure were more severe in PINK1- or PARK2-deficient cells and mice than in wild-type groups. Functionally, PINK1-Parkin–mediated mitophagy prevented RTEC apoptosis and tissue damage in CI-AKI through reducing mitochondrial ROS and subsequent NLRP3 inflammasome activation. These results demonstrated that PINK1-Parkin–mediated mitophagy played a protective role in CI-AKI by reducing NLRP3 inflammasome activation.

Randomized trial of one-hour sodium bicarbonate vs standard periprocedural saline hydration in chronic kidney disease patients undergoing cardiovascular contrast procedures.

BackgroundGuidelines advise periprocedural saline hydration for prevention of contrast induced-acute kidney injury (CI-AKI). We analysed whether 1-hour sodium bicarbonate hydration administered solely prior to intra-arterial contrast exposure is non-inferior to standard periprocedural saline hydration in chronic kidney disease (CKD) patients undergoing elective cardiovascular diagnostic or interventional contrast procedures.MethodsWe performed an open-label multicentre non-inferiority trial between 2011–2014. Patients were randomized to 1 hour pre-procedure sodium bicarbonate hydration (250 ml 1.4%, N = 168) or 4–12 hours saline hydration (1000 ml 0.9%, N = 165) prior to and following contrast administration (2000 ml of saline total). Primary outcome was the relative serum creatinine increase (%) 48–96 hours post contrast exposure. Secondary outcomes were: incidence of CI-AKI (serum creatinine increase>25% or >44μmol/L), recovery of renal function, the need for dialysis, and hospital costs within two months follow-up.ResultsMean relative creatinine increase was 3.1% (95%CI 0.9 to 5.2%) in the bicarbonate and 1.1% (95%CI -1.2 to 3.5%) in the saline arm, mean difference 1.9% (95%CI -1.2 to 5.1%, p-non-inferiority <0.001). CI-AKI occurred in 11 (6.7%) patients randomized to sodium bicarbonate and 12 (7.5%) to saline (p = 0.79). Renal function did not fully recover in 40.0% and 44.4% of CI-AKI patients, respectively (p = 0.84). No patient required dialysis. Mean costs for preventive hydration and clinical preparation for the contrast procedure were $1158 for sodium bicarbonate vs. $1561 for saline (p < 0.001).ConclusionShort hydration with sodium bicarbonate prior to elective cardiovascular diagnostic or therapeutic contrast procedures is non-inferior to standard periprocedural saline hydration in CKD patients with respect to renal safety and results in considerable healthcare savings.Trial registrationNetherlands Trial Register (http://www.trialregister.nl/trialreg/index.asp), Nr NTR2699

Contrast-induced kidney injury: how does it affect long-term cardiac mortality?

Contrast-induced acute kidney injury (CIAKI) is a common complication after coronary angiography or percutaneous revascularization (PCI). This study aimed to investigate the association of CIAKI with long-term cardiovascular adverse events. In total, 980 patients undergoing coronary angiography/PCI were assessed in this prospective cohort study. The primary endpoint was major adverse cardiac and cerebrovascular events (MACCE) and cardiac death (CVD) during an 8-year follow-up. Glomerular filtration rate change during the follow-up was the secondary endpoint.CIAKI was defined as a serum creatinine increase at least 0.3 mg/dl in 48 h or at least 50% in 7 days. CIAKI was observed in 69 patients (7%). Chronic kidney disease [relative risk (RR) = 4, P < 0.01], reduced ejection fraction (RR = 2.88, P < 0.01), CIAKI risk score at least 4 (RR = 2.64, P = 0.02), and emergency coronary angiography/PCI (RR = 3.87, P < 0.01) increased CIAKI risk, whereas statins were protective (RR = 0.32, P < 0.01).Patients with CIAKI had higher rates of 8-year cardiovascular adverse events: 54 versus 15% MACCE (RR = 6.67, P < 0.01), 38 versus 4% CVD (RR = 15.73, P < 0.01). Among other factors, CIAKI was the strongest predictor of 8-year MACCE (RR = 3.16, P < 0.01) and CVD (RR = 7.34, P < 0.01).During the follow-up, glomerular filtration rate declined drastically in CIAKI patients: 70 versus 39% had chronic kidney disease stage worsening (P < 0.01) and 8 versus 0.3% started hemodialysis (P < 0.01). We found a strong correlation between CIAKI and poor long-term cardiac outcomes. Apparently showing up as a transient, functional impairment of kidney function, CIAKI implies an organic damage with structural modifications leading to significant kidney deterioration over time, responsible for an increased risk of long-term cardiac events. Statins significantly reduced CIAKI occurrence. A careful management of high-risk patients is needed to limit long-term complications of coronary angiography/PCI.

Prediction of contrast induced acute kidney injury using novel biomarkers following contrast coronary angiography.

Chronic kidney disease (CKD) is a risk factor for contrast induced acute kidney injury (CI-AKI). Contrast angiography in CKD patients is a common procedure. Creatinine is a delayed marker of CI-AKI and delays diagnosis which results in significant morbidity and mortality. Early diagnosis of CI-AKI requires validated novel biomarkers. A prospective observation study of 301 consecutive CKD patients undergoing coronary angiography was performed. Samples for plasma neutrophil gelatinase-associated lipocalin (NGAL), serum liver fatty acid-binding protein (L-FABP), serum kidney injury marker 1, serum interleukin 18 and serum creatinine were taken at 0, 1, 2, 4, 6 and 48 h post-contrast. Urinary NGAL and urinary cystatin C were collected at 0, 6 and 48 h. Incidence of major adverse clinical events (MACE) was recorded at 1 year. CI-AKI was defined as an absolute delta rise in creatinine of ≥26.5 µmol/l or a 50% relative rise from baseline at 48 h following contrast. CI-AKI occurred in 28 (9.3%) patients. Plasma NGAL was most predictive of CI-AKI at 6 h. L-FABP performed best at 4 h. A combination of Mehran score > 10, 4 h L-FABP and 6 h NGAL improved specificity to 96.7%. MACE was statistically higher at 1 year in CI-AKI patients (25.0 vs. 6.2% in non-CI-AKI patients). Mehran risk score, 4 h serum L-FAPB and 6 h plasma NGAL performed best at early CI-AKI prediction. CI-AKI patients were four times more likely to develop MACE and had a trebling of mortality risk at 1 year.

Randomised trial of no hydration vs. sodium bicarbonate hydration in patients with chronic kidney disease undergoing acute computed tomography–pulmonary angiography

Hydration to prevent contrast-induced acute kidney injury (CI-AKI) induces a diagnostic delay when performing computed tomography-pulmonary angiography (CTPA) in patients suspected of having acute pulmonary embolism. To analyze whether withholding hydration is non-inferior to sodium bicarbonate hydration before CTPA in patients with chronic kidney disease (CKD). We performed an open-label multicenter randomized trial between 2009 and 2013. One hundred thirty-nine CKD patients were randomized, of whom 138 were included in the intention-to-treat population: 67 were randomized to withholding hydration and 71 were randomized to 1-h 250mL 1.4% sodium bicarbonate hydration before CTPA. Primary outcome was the increase in serum creatinine 48-96h after CTPA. Secondary outcomes were the incidence of CI-AKI (creatinine increase >25%/>0.5mgdL(-1) ), recovery of renal function, and the need for dialysis within 2months after CTPA. Withholding hydration was considered non-inferior if the mean relative creatinine increase was ≤15% compared with sodium bicarbonate. Mean relative creatinine increase was -0.14% (interquartile range -15.1% to 12.0%) for withholding hydration and -0.32% (interquartile range -9.7% to 10.1%) for sodium bicarbonate (mean difference 0.19%, 95% confidence interval -5.88% to 6.25%, P-value non-inferiority <0.001). CI-AKI occurred in 11 patients (8.1%): 6 (9.2%) were randomized to withholding hydration and 5 (7.1%) to sodium bicarbonate (relative risk 1.29, 95% confidence interval 0.41-4.03). Renal function recovered in 80.0% of CI-AKI patients within each group (relative risk 1.00, 95% confidence interval 0.54-1.86). None of the CI-AKI patients developed a need for dialysis. Our results suggest that preventive hydration could be safely withheld in CKD patients undergoing CTPA for suspected acute pulmonary embolism. This will facilitate management of these patients and prevents delay in diagnosis as well as unnecessary start of anticoagulant treatment while receiving volume expansion.

A randomized comparison of 1-h sodium bicarbonate hydration versus standard peri-procedural saline hydration in patients with chronic kidney disease undergoing intravenous contrast-enhanced computerized tomography

Guidelines recommend saline hydration for prophylaxis of contrast-induced acute kidney injury (CI-AKI) in patients with chronic kidney disease (CKD) undergoing intravenous contrast media-enhanced CT (CE-CT). The safety and efficacy of a brief hydration protocol using sodium bicarbonate in this population is unknown. We analysed whether 1-h sodium bicarbonate hydration prior to CE-CT is non-inferior to saline hydration prior to and after CE-CT in CKD patients. We performed an open-label multicentre randomized trial. Patients were randomized to 250 mL of 1.4% sodium bicarbonate hydration prior to CE-CT or 1000 mL of 0.9% saline hydration prior to and, once again, after CE-CT. Primary outcome was the relative increase in serum creatinine 48-96 h post-CE-CT. Secondary outcomes were incidence of CI-AKI [serum creatinine increase >25%/>44 µmol/L (0.5 mg/dL)], recovery of renal function, the need for dialysis and 2-month hospital costs. Five hundred and seventy adult CKD patients undergoing CE-CT were randomized between 2010 and 2012, of whom 548 were included in the intention-to-treat population. Mean relative serum creatinine increase was 1.2% for sodium bicarbonate and 1.5% for saline (mean difference -0.3%; 95% confidence interval -2.7 to 2.1, P-value for non-inferiority <0.0001). CI-AKI occurred in 22 patients (4.1%); 8 (3.0%) randomized to sodium bicarbonate versus 14 (5.1%) to saline (P = 0.23). Renal function recovered in 75 and 69% of CI-AKI patients, respectively (P = 0.81). No patients developed a need for dialysis. Mean hydration costs per patient were €224 for the sodium bicarbonate and €683 for the saline regime (P < 0.001). Other healthcare costs were similar. Short hydration with sodium bicarbonate prior to CE-CT was non-inferior to peri-procedural saline hydration with respect to renal safety and may result in healthcare savings. [Netherlands Trial Register (http://www.trialregister.nl/trialreg/index.asp), Nr 2149, date of registration 23 December 2009.].

Contrast-induced acute kidney injury and clinical outcomes after intra-arterial and intravenous contrast administration: Risk comparison adjusted for patient characteristics by design

Direct comparisons between risk of contrast induced acute kidney injury (CI-AKI) after intra-arterial versus intravenous contrast administration are scarce. We estimated and compared the risk of CI-AKI and its clinical course after both modes of contrast administration in patients who underwent both. One hundred seventy patients who received both intra-arterial and intravenous contrast injections within one year between 2001 and 2010 were included. Primary outcome was occurrence of CI-AKI. Secondary outcomes were duration of hospital stay, the need for dialysis, recovery of renal function, and mortality. The risk of CI-AKI was 24/170 (14.0%, 95% CI 9.6-20.2) after intra-arterial contrast injection versus 20/170 (11.7%, 95% CI 7.7-17.5) after intravenous contrast administration, which led to a relative risk of 1.2 (95% CI 0.7-2.1). None of the patients had a need for dialysis. Median duration of hospital stay in CI-AKI patients was 15.0 days (2.5-97.5, percentile 1-92) after intra-arterial and 15.5 days (2.5-97.5, percentile 0-38) after intravenous contrast procedures. Renal function recovered after CI-AKI in 13/24 after intra-arterial and in 10/20 patients after intravenous contrast administration. Mortality risks in CI-AKI patients were slightly higher than in non-CI-AKI patients, hazard ratios 1.6 (95% CI 0.7-3.7) for intra-arterial and 1.7 (95% CI 0.7-4.4) for intravenous contrast administration, adjusted for confounders. The risk of CI-AKI, and its clinical course was similar after intra-arterial and intravenous contrast media administration, after adjustment by design for patient-related risk factors.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

Incidence of contrast-induced acute kidney injury associated with diagnostic or interventional coronary angiography

Contrast-induced acute kidney injury (CI-AKI) represents an important cause of hospital-acquired AKI. The aim of this study was to evaluate the incidence of CI-AKI after coronary angiography (CA) or percutaneous coronary intervention (PCI) and the role of patient-/procedure-related risk factors. For 11 months, patients undergoing CA or PCI were prospectively evaluated for CI-AKI, and factors possibly affecting CI-AKI were analyzed. Statistical analysis was completed using Student's t-test, chi-square or Fisher exact test, and multivariate logistic regression. Among 585 consecutive patients, incidence of CI-AKI was 5.1% (n=30) and renal replacement therapy was required in 10% of those (n=3). Incidence of CI-AKI was higher in patients with anemia or chronic kidney disease (CKD) associated with diabetes. Basal hemoglobin was significantly lower in CI-AKI patients while Mehran score, contrast medium (CM) volume, contrast ratio (CM volume / maximum contrast dose) and ratio glomerular filtration rate (CM volume / GFR) were significantly higher. Multivariate analysis selected a higher contrast ratio as a factor independently associated with a higher risk of CI-AKI which otherwise appeared to be lower with increasing basal hemoglobin. The incidence of CI-AKI after CA or PCI was higher in patients with CKD associated with diabetes. Lower levels of basal hemoglobin appeared to be related to a higher risk of CI-AKI, and contrast media volume, especially if exceeding the dose adjusted for renal function, was a strong modifiable risk factor for CI-AKI.

Renal Replacement Therapy for Prevention of Contrast-Induced Acute Kidney Injury: A Meta-Analysis of Randomized Controlled Trials

Background: Contrast-induced acute kidney injury (CI-AKI) is an important cause of acute renal injury. Several clinical trials using renal replacement therapy (RRT) for prevention of CI-AKI yielded conflicting results. We performed a meta-analysis to assess the efficacy of prophylactic RRT on CI-AKI. Methods: Randomized controlled trials on CI-AKI using RRT were identified without language restriction in Cochrane library, Pubmed and Embase. Data extracted from literature were analyzed with Review manager and Stata software. Results: Nine randomized controlled trials involving 751 patients were included. Heterogeneity was found across trials (p < 0.00001). A random effect model was used to combine the data. RRT reduced the risk of CI-AKI by 26% compared with the control group, but statistical significance was not reached (risk ratio (RR) 0.74, 95% CI 0.35–1.60, p = 0.45). Subgroup analysis of modality indicated that hemodialysis was ineffective in reducing the risk of CI-AKI (RR 1.21, 95% CI 0.63–2.32, p = 0.57), while CRRT decreased the incidence of CI-AKI (RR 0.22, 95% CI 0.07–0.64, p = 0.006). Subgroup analysis according to the CKD stage did not record heterogeneity across trials. RRT increased the odds of CI-AKI in CKD stage 3 patients (RR 1.53, 95% CI 0.07–0.64, p = 0.01), but decreased the occurrence of CI-AKI in patients with CKD stage higher than 3 (RR 0.74, 95% CI 0.35–1.60, p = 0.45). The pooled RR of the need for permanent dialysis demonstrated an insignificant trend towards benefit in patients treated with RRT (RR 0.61, 95% CI 0.26–1.40, p = 0.24). RRT reduced in-hospital mortality compared with control group (RR 0.33, 95% CI 0.14–0.77, p = 0.01). Conclusion: RRT fails to reduce the incidence of CI-AKI in CKD stage 3 patients, but may be beneficial in patients with more advanced renal function. CRRT is more effective than hemodialysis for prevention of CI-AKI. RRT is effective in reducing the in-hospital mortality of CI-AKI patients.