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Introduction: We aimed to evaluate the frequency of contrast induced nephropathy (CIN), its relationship with accepted risk factors and long‐term renal outcomes in patients who underwent coronary angiography (CAG). Methods: All patients who underwent CAG between April 2020 and April 2021 were retrospectively evaluated. CIN was defined as characteristic increase in serum creatinine after CAG. Results: CIN developed in 50 (5.4%) of 934 patients. The CIN rate was found to be statistically significantly higher in patients with diabetes, hypertension, heart failure and those using diuretics. Pre‐procedural hemoglobin, albumin and GFR were found to be independent risk factors for CIN. After discharge, the urea and creatinine values of the patients who developed CIN were significantly higher than those who did not. Conclusion: We concluded that in order to reduce the development of CIN, hemoglobin and albumin levels should be evaluated with renal functions before the procedure and they should be kept within normal limits. [ABSTRACT FROM AUTHOR]

Contrast-induced acute kidney injury (CI-AKI) is an important complication following the use of iodinated contrast media. Bilirubin has a protective effect but may also aggravate CI-AKI. The purpose of this systematic review was to assess whether bilirubin is a risk factor for CI-AKI. We searched the databases PubMed, Embase, Web of Science, Cochrane Library, Scopus, Ovid Medline, CNKI (China National Knowledge Infrastructure), VPCS (Vip Paper Check System), Wanfang, and CBM (Chinese BioMedical Literature Database) from the initial date to May 6, 2023. We summarized the results by directly combining the effect-size odds ratio (OR) and 95% confidence interval (CI) and identified sources of heterogeneity through subgroup analysis, sensitivity analysis, and meta-regression analysis. A total of 10 studies (14 data sets) were included: 7 retrospective studies (10 data sets) and 3 prospective studies (4 data sets), involving 12776 participants. The incidence of CI-AKI of 16% (95% CI: 14-19%). Total bilirubin was positively associated with the occurrence of CI-AKI (OR = 1.80; 95% CI: 1.36-2.38). Both low and high bilirubin concentrations were risk factors for CI-AKI. The incidence of CI-AKI was higher in the low bilirubin group than in the high bilirubin group. [ABSTRACT FROM AUTHOR]

BACKGROUND: Endoluminal interventions have become one of the main options for the treatment of arteriosclerosis obliterans (ASO). OBJECTIVE: To explore the effect of hydration therapy and nursing intervention on the prevention of contrast-induced nephropathy (CIN) after interventional treatment of lower extremity ASO. METHODS: A convenience sampling method was used to select 94 patients who received ASO treatment in our hospital from March 2019 to May 2021 as the study subjects. All patients underwent endovascular interventional therapy and were randomly divided into two groups by the random number table method, with odd numbers entering the observation group (n = 47) and even numbers entering the control group (n = 47). The control group received routine nursing intervention, while the observation group underwent hydration therapy and had a corresponding nursing intervention scheme. The clinical efficacy of the two groups and the incidence of contrast-induced nephropathy after interventional therapy were compared, and an evaluation of satisfaction within the two groups was performed via a questionnaire. RESULTS: The total effective rate of patients in the observation group was higher after hydration treatment (97.87% vs 87.23%, p < 0.05). The blood urea nitrogen, creatinine, and β 2 microglobulin levels in the observation group were significantly lower than those in the control group after the intervention (p < 0.05). Patients in the observation group had higher nursing satisfaction after using preventive measures of hydration therapy combined with nursing interventions (100% vs 89.36%, p < 0.05). CONCLUSION: Hydration therapy and nursing intervention can effectively prevent CIN after interventional treatment of lower extremity ASO. After interventional therapy, patients had better clinical outcomes, lower biochemical indexes and improved satisfaction evaluations. The therapy is worthy of clinical promotion and application. [ABSTRACT FROM AUTHOR]

Contrast-related acute renal failure is a multifactorial condition that involves oxidative stress, inflammation, and direct tubular toxicity. Risk factors for contrast-induced nephropathy comprise pre-existing kidney dysfunction, diabetes mellitus, advanced age, congestive heart failure, hypotension, anemia, and volume depletion. Preventive measures include identifying high-risk patients and implementing preventive measures such as adequate hydration, minimizing contrast use, and avoiding using contrast media in patients with pre-existing renal dysfunction. The systemic inflammation score is a promising tool for predicting contrast-associated acute kidney injury (CAAKI) in patients undergoing contrast-enhanced imaging procedures. Further studies are needed to validate the use of SIS in clinical practice and to better understand the underlying mechanisms of inflammation in (CA-AKI). [ABSTRACT FROM AUTHOR]

Introduction: Contrast nephropathy is a result of contrast media given through intravascular routes. Nitric oxide gene polymorphisms may alter the hemodynamic stability resulting in medullary ischemia Nitric oxide gene polymorphisms may have an enhancing role in contrast media related renal injury. The aim of this study was to investigate the role of eNOS intron 4a/b, T786C, and G894T gene polymorphisms on contrast‐nephropathy risk. Methods: Ninety‐four chronic kidney disease patients with contrast nephropathy and 120 chronic kidney disease patients without contrast nephropathy were included. DNA isolation was performed and specific regions of DNA for eNOS G894T, T786C, and intron 4a/b genes were amplified by polymerase chain reaction technique. Results: TT polymorphism of T786C gene and GG polymorphism of G894T gene were detected to be possibly protective from contrast induced nephropathy. Conclusion: Endothelial nitric oxide synthase G894T gene polymorphisms, older age, and presence of diabetes mellitus may influence contrast nephropathy development. [ABSTRACT FROM AUTHOR]

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Onco-nephrology has been a growing field within the adult nephrology scope of practice. Even though pediatric nephrologists have been increasingly involved in the care of children with different forms of malignancy, there has not been an emphasis on developing special expertise in this area. The fast pace of discovery in this field, including the development of new therapy protocols with their own kidney side effects and the introduction of the CD19-targeted chimeric antigen receptor T cell (CAR-T) therapy, has introduced new challenges for general pediatric nephrologists because of the unique effects of these treatments on the kidney. Moreover, with the improved outcomes in children receiving cancer therapy come an increased number of survivors at risk for chronic kidney disease related to both their cancer diagnosis and therapy. Therefore, it is time for pediatric onco-nephrology to take its spot on the expanding subspecialties map in pediatric nephrology. [ABSTRACT FROM AUTHOR]

Aim: Contrast-induced acute kidney injury (AKI) may be seen after contrast agent exposure which is known as nephrotoxic. It is fact that, patients with AKI have an increased risk after contrast exposure compared to patients with normal renal function values. However, the incidence of contrast nephropathy after contrast exposure with AKI is not clear. In this study, we planned to investigate the incidence of contrast nephropathy in patients undergoing coronary angiography with AKI and whether there is an increased risk compared to the control group. Materials and Methods: The study was planned as a retrospective study and we investigated the clinical outcome of patients who underwent isoosmolar contrast angiography in the arterial phase with acute kidney injury between January 2014 and December 2017. Results: The number of AKI patients included in the study was 280 and the control group consisted of 478 participants. There was no statistically significant difference between two groups. (3.2% (n: 9) of patients with AKI contrast nephropathy vs 6.5% (n: 31) of patients with normal kidney function and contrast nephropathy) (p> 0.05). On the other hand, there was statistically significant difference between two groups according to diabetes mellitus (patients with contrast nephropathy 26 (65%) had diabetes vs 14 (35%) participants had no diabetes). This difference was statistically significant (p <0.05). Conclusion: In this study, in patients who underwent emergency angiography with a preliminary diagnosis of acute coronary syndrome in the emergency department, we did not find an increased risk of acute renal injury and contrast-enhanced nephropathy compared to the patient population with normal kidney function. [ABSTRACT FROM AUTHOR]

Hospitalized patients who have established kidney disease and those who have acute kidney injury in the hospital, along with patients with electrolyte disturbances tend to be some of the most complex to care for. Through working closely in nephrology consultation in the hospital with patients and providers, in both private and academic settings, we have come to encounter certain common presentations and recurrent themes that are worthy of emphasis, and of which a good understanding can translate into improved patient care. For the provider who works closely with such patients, many of these aspects are important to recognize and understand. In this review, we present 10 questions that address some of the highly relevant aspects of nephrology for the provider in the hospital. Through a MEDLINE database search, we reviewed the most pertinent studies as we then go through the explanation of management decisions in an evidence-based methodology with an up-to-date approach based on the current literature on the subject. [ABSTRACT FROM AUTHOR]

Background and aims: Contrast-induced renal impairment endangers the patients' health and imposes a financial burden on families and the health care system. Therefore, this study was conducted to examine the rate of nephropathy in patients admitted to Mofid Children's Hospital in 2018 and 2019. Methods: In this cross-sectional study serum creatinine was measured at baseline and 48-72 hours after CT-scan an increase of more than 25% in serum creatinine was considered CIN. Paired sample t-test was used to assess the change in the Cr. The research data were analyzed using SPSS-25 software and the significance level in all tests was set at P = 0.001. Results: In this study, 180 children underwent contrast-enhanced CT-scan with a mean age of 5.72 years, of whom 81 (45%) were girls and 99 (55%) were boys. The mean baseline creatinine was 0.633 ± 0.137 mg / dl, which increased significantly to 0.675± 0.164 mg / dl 48-72 hours after the first measurement. The chance of developing ARF in ciprofloxacin users was 4.86 times higher than patients who did not use this drug. Conclusion: In children underwent CT scan, the incidence of ARF is 17.2%. Ciprofloxacin increases the risk of acute kidney problems by 4.8 times. [ABSTRACT FROM AUTHOR]

Introduction: During the recent years, several studies have investigated that hyperuricemia is associated with greater incidence of contrast induced nephropathy (CIN). Most of them are in acute conditions like primary percutaneous coronary interventions. This study aimed to assess the relationship between high serum uric acid and incidence of acute kidney injury in patients undergoing elective angiography and angioplasty. Methods: This prospective study was conducted on 211 patients who were admitted to hospital for elective coronary angiography or angioplasty. The researchers measured serum creatinine and uric acid on admission and repeated creatinine measurement in 48 hours and seven days after the procedure. According to serum uric acid, the patients were divided into two groups; group 1 with normal uric acid and group 2 with hyperuricemia which was defined as uric acid more than 6 mg/dL in women and 7 mg/dL in men. CIN is defined as an increased creatinine level of more than 0.5 mg/dL or 25% from the baseline in 48 hours after the intervention. Results: In total, 211 patients with mean age of 60.58 years were enrolled in the study. Of these, 87 (41.2%) patients were in the high uric acid group and 124 (58.8%) were in the normal uric acid group. CIN was occurred in 16 patients (7.5%). Seven out of 16 (8.04%) were in the high uric acid and nine (7.2%) were in the normal uric acid group. There were no significant differences between the two groups (P =0.831). Conclusion: The frequency of CIN development was not different in the patients with hyperuricemia. [ABSTRACT FROM AUTHOR]

Introduction: Despite high rates of morbidity and mortality in patients with contrast-induced nephropathy (CIN), there is no consensus regarding prevention of this well-known complication of contrast media use. One agent that has been widely used in this regard is N-acetyl cysteine (NAC). Nevertheless, its efficacy is still controversial. The aim of this study was to assess the efficacy of NAC, both in the oral and intravenous forms, for the prevention of CIN. Methods: This study is a double-blind randomized placebo controlled clinical trial. We randomized 434 adult patients with chronic kidney disease (constant serum creatinine ≥1.5 mg/dL) who were candidates for coronary angiography/plasty. The patients were categorized into three groups. One group received 1,200 mg NAC intravenously half an hour before the procedure and oral placebo starting 3 days before angiography. The second group received oral NAC 600 mg twice daily for 3 days, starting the day before the intervention and intravenous placebo half an hour before intervention. The third group received both oral and intravenous placebo. CIN was defined as a 25% relative increase in serum creatinine from baseline value, 48 h after use of contrast medium. Results: Of the 434 patients, 149 received intravenous NAC, 145 received oral NAC, and the remaining 140 received placebo. The incidence of CIN in the three groups was 6.1%, 7.6%, and 10.8%, respectively (p = 0.34). Conclusion: In patients with chronic kidney disease, neither intravenous nor oral NAC is superior to placebo for preventing CIN. [ABSTRACT FROM AUTHOR]

Introduction Contrast-induced acute kidney injury (CI-AKI) is a serious complication of angiographic procedures with significant morbidity and mortality. We aimed to find the incidence, risk factors and outcomes of CI-AKI in patients who have undergone coronary angiography/angioplasty in a referral hospital in Nepal. Methods It was a descriptive observational study of consenting consecutive patients above 18 years undergoing coronary angiography/angioplasty at Manmohan Cardiothoracic Vascular and Transplant Centre, Nepal from July 2015 to September 2017. CI AKI was defined as an elevation of serum creatinine of >25% or ≥0.5 mg/dl (44 μmol/L) from baseline within 48 hour of exposure to contrast. Statistical analysis was performed using SPSS 18 software. Statistical analysis was completed using Student's t-test, chi-square test and multivariable logistic regression analysis. Results Out of 240 patients, 156 (65%) were male, mean age was 60.36±11.29 years. Eighteen patients (7.5%) developed CI-AKI. Incidence of CI-AKI was 20% in patients with chronic kidney disease (CKD), 5.4% in diabetics, 13.6% in patients >70 years, 12.79 % in patients with anaemia and 12.3% in patients with prior contrast exposure. Multivariate logistic regression analysis found smoking and history of prior contrast exposure to be independent predictors for development of CI-AKI. Among patients with CI-AKI, one (5.88%) required dialysis and one (5.88%) died. Conclusion Incidence of CI-AKI after coronary angiography/angioplasty was 7.5%. Patients with prior contrast exposure and smoking were at significantly increased risk of CI-AKI; higher trend of CI-AKI was seen in patients with CKD, diabetes, elderly and anaemia. [ABSTRACT FROM AUTHOR]

Background and objectives: Contrast-induced nephropathy (CIN) is a relatively common complication following primary coronary angiography (CAG) or percutaneous coronary intervention (PCI), especially in at-risk patients. The goal of this study is to evaluate the role of pre-procedural serum osmolarity as a risk factor for CIN in patients undergoing elective CAG for stable coronary artery disease (CAD). Materials and methods: A total of 356 stable CAD patients scheduled to undergo CAG or PCI were included in this two-center study. Serum osmolarity was calculated on admission. CIN was defined according to the KDIGO criteria. Results: There were 45 (12.6%) patients who developed CIN 48–72 h after CAG or PCI. CIN patients had a higher prevalence of diabetes (51.1% in those with CIN vs 24.4% in those without CIN, p < 0.001), higher serum glucose (129 mg/dL in those with CIN vs 108 mg/dL in those without CIN, p < 0.001), blood urea nitrogen (22.4 mg/dL in those with CIN vs 19.0 mg/dL in those without CIN, p = 0.01) and serum osmolarity (294.2 mOsm in those with CIN vs 290.1 mOsm in those without CIN, p < 0.001) levels, had received a higher dose of contrast (250 mL in those with CIN vs 200 mL in those without CIN, p = 0.03) but had lower hemoglobin (12.9 g/dL in those with CIN vs 13.6 g/dL in those without CIN, p = 0.04) level. In multivariate analysis, serum osmolarity [odds ratio (OR) 1.11; 95% confidence interval (CI) 1.04–1.18 for each mOsm/L increase; p = 0.001], diabetes (OR 2.43, 95% CI 1.26–4.71; p = 0.01), C-reactive protein (OR 1.04, 95% CI 1.01–1.08 for each mg/dL increase; p = 0.02) and contrast volume (OR 34.66, 95% CI 1.25–962.22 for each L increase; p = 0.04) remained as independent predictors of CIN. Serum sodium, glucose and blood urea nitrogen contributed to the excess serum osmolarity of CIN patients. Conclusion: Serum osmolarity is a cheap and widely available marker that can reliably predict CIN after CAG or PCI. Future research should focus on determining a clinically optimal cutoff for serum osmolarity that would warrant preventive interventions. Furthermore, later research may investigate the role of serum osmolarity not only as a risk factor but also as a pathogenetic mechanism underlying CIN. [ABSTRACT FROM AUTHOR]

Background: Hyperuricemia may cause acute kidney injury by activating inflammatory, pro-oxidative and vasoconstrictive pathways. In addition, radiocontrast causes an acute uricosuria, potentially leading to crystal formation. We therefore aimed to investigate the effect of urine acidity and urine uric acid level on the development of contrast-induced nephropathy (CIN) in patients undergoing elective coronary angiography. Methods: We enrolled 175 patients who underwent elective coronary angiography. CIN was defined as a >25% increase in the serum creatinine levels relative to basal values 48–72 h after contrast use. Prior to coronary angiography and 48–72 h later, serum uric acid, urea, creatinine, bicarbonate levels, and spot uric acid to creatinine ratio (UACR) were measured. Results: Of the 175 subjects included, 29 (16.6%) developed CIN. Those who developed CIN had a higher prevalence of diabetes, higher UACR (0.60 vs. 0.44, p = 0.014), higher contrast volume, and lower serum sodium level. With univariate analysis of a logistic regression model, the risk of CIN was found to be associated with diabetes (p = 0.0016, OR = 3.8 [95% CI: 1.7–8.7]), urine UACR (p = 0.0027, OR = 9.6 [95% CI: 2.2–42.2]), serum sodium (p = 0.0079, OR = 0.8 [95% CI: 0.77–0.96]), and contrast volume (p = 0.0385, OR = 1.8 [95% CI: 1.03–3.09]). In a multiple logistic regression model with stepwise method of selection, diabetes (p = 0.0120, OR = 3.2 [95% CI: 1.3–8.1]) and UACR (p = 0.0163, OR = 6.9 [95% CI: 1.4–33.4]) were the 2 risk factors finally identified. Conclusions: We have demonstrated that higher urine UACR is associated with the development of CIN in patients undergoing elective coronary angiography. [ABSTRACT FROM AUTHOR]

Background: Contrast-induced acute kidney injury (CIAKI) following coronary angiography is frequently observed in the general population. End-stage liver disease (ESLD) patients are at a particularly increased risk for development of CIAKI following coronary angiography due to preexisting renal hypoperfusion. Methods: We performed a retrospective study of 544 consecutive cardiac catheterizations in ESLD patients from December 2003 to May 2013 to calculate the incidence of CIAKI post-coronary angiography and to identify risk factors for CIAKI. CIAKI was defined as a serum creatinine increase of either ≥ 25% or ≥ 0.5 mg/dL from baseline within 72 hours. Multivariable and Cox regression analysis was performed for development of CIAKI and all-cause mortality, respectively. Results: Overall, 179 cases of coronary angiography were included in the final analysis. CIAKI occurred in 23% of patients. All-cause mortality was 52% in the CIAKI group and 37% in the non-CIAKI group, with a mean follow-up of 2.2 ± 3.8 years. Multivariable analysis identified intensive care unit admission (OR 2.72, CI 1.05–7.01, p < 0.05) and baseline estimated glomerular filtration rate (OR 1.02, CI 1.002–1.035, p < 0.05) as independent predictors of CIAKI. Cox regression analysis identified pre-angiography beta-blocker use (HR 2.13, CI 1.04–4.38, p < 0.05), international normalized ratio (HR 1.37, CI 1.05–1.78, p < 0.05) and Mehran risk score (HR 1.13, CI 1.02–1.25, p < 0.05) as independent predictors of all-cause mortality. Conclusions: CIAKI in ESLD patients undergoing coronary angiography occurs at a moderately elevated rate when compared to the general population. [ABSTRACT FROM AUTHOR]

Purpose: Contrast-induced acute kidney injury is a prominent complication following cardiac catheterization, though the risk has progressively decreased in recent times with appropriate risk stratification and use of safer contrast agents. Despite data supporting further lowering of risk with the iso-osmolar agent, iodixanol, uptake has lagged, perhaps due to increased upfront cost of this agent. We undertook an economic analysis to estimate the cost-effectiveness of a strategy utilizing iodixanol compared to using a low-osmolar contrast agent.Methods: We created a Markov model to evaluate the two strategies, and included a differential relative risk of contrast-induced acute kidney injury, based on a systematic review of the literature. Downstream clinical events, including need for dialysis and mortality, were modeled using data from existing published literature. A third-party payer perspective was utilized for the analysis and presentation of the primary economic analysis.Results: The strategy of using iodixanol dominated in both the low-risk and high-risk base case analyses. However, the difference was quite small in the low-risk scenario (lifetime cost: C$678,034 vs. C$678,059 and life expectancy: 19.80 vs. 19.72 years). The difference was more marked (life expectancy 15.65 vs. 14.15 years and cost C$680,989 vs. C$682,023) in the high-risk case analysis. This was robust across most of the variables tested in sensitivity analyses.Conclusion: The use of iodixanol, compared with low-osmolar contrast agents, for cardiac catheterization, results in a small benefit clinical outcomes, and in a savings in direct healthcare costs. Overall, our analysis supports the use of iodixanol for cardiac catheterization, especially in patients at high risk of acute kidney injury. [ABSTRACT FROM AUTHOR]

Background: Contrast-induced acute kidney injury (CI-AKI) is defined as worsening of renal function after the administration of iodinated contrast material. In patients with cardiovascular disease, kidney disease, and/or diabetes, renin-angiotensin system blockers, non-steroidal anti-inflammatory drugs, diuretics, and metformin can increase the risk of CI-AKI when undergoing contrast imaging. Despite CI-AKI being the leading iatrogenic cause of acute kidney injury, there is a lack of sufficient scientific evidence supporting which drugs should be stopped, when they should be stopped, and when they should be resumed. The purpose of this systematic review is to assess (1) the effect of withholding medication before contrast procedures on the risk of CI-AKI and other clinical outcomes and (2) the incidence of adverse events occurring after withholding these drugs prior to contrast procedures. This protocol has been registered with PROSPERO, https://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42016033178. Methods: An information specialist will assist in searching MEDLINE, Embase, and the Cochrane Library databases to identify randomized controlled trials, observational studies, case reports, and case series. Relevant abstracts from professional society meetings and web-based registries of clinical trials will also be included. Studies included will compare patients aged ≥ 18 years instructed to continue taking the drugs of interest and those advised to stop taking them before undergoing contrast procedures. If these drugs are not withheld prior to contrast procedures, the studies must compare patients who are administered these drugs and those who are not before undergoing contrast procedures. Two reviewers will independently screen the titles and abstracts of the studies obtained from the search using pre-defined inclusion criteria and will then extract data from the full texts of selected studies. The quality of the studies will be assessed by two independent reviewers using the Cochrane Risk of Bias 2.0 tool for randomized trials and the Newcastle-Ottawa Scale for observational studies. Discussion: This systematic review will provide a synthesis of current evidence on the discontinuation of drugs prior to contrast procedures and its effect on CI-AKI and other clinical outcomes. These findings will provide clinicians with guidelines and serve as a strong research base for future studies in this field. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) is the most common cause of secondary hypertension. More than half of the patients have uncontrolled hypertension (≥140/90mmHg on three or more antihypertensive agents at optimum doses). Renal sympathetic denervation (RSDN) has been shown to reduce blood pressure (BP) in patients with resistant hypertension. Although patients with CKD have high sympathetic drive, all major clinical trials have excluded patients with estimated glomerular filtration rates (eGFRs)<45 mL/min/1.73m2 for risk of contrast-induced nephropathy. Methods: In this pilot study, carbon dioxide (CO2) was used as the sole contrast agent to carry out renal angiography and RSDN in patients with moderate to severe CKD (eGFR 15-44 mL/min/1.73m2) and uncontrolled hypertension. Results: Eleven patients (eight males) underwent RSDN. The median age was 57 years [interquartile range (IQR) 49-66]. The median number of antihypertensives being taken at baseline was 4 (IQR 3-4). No statistically significant difference was observed in serum creatinine in the serial follow-ups until at 6 months[median difference 0.25 mg/dL (IQR 0.09-0.53); P±0.008]. There was a non-significant reduction in median clinic BP from baseline to 6 months [-14mmHg (IQR -24-5)] and a significant increase in daytime ambulatory systolic BP [7mmHg (IQR -2-12); P±0.045]. A trend towards a serial reduction in albuminuria was observed. Procedure-related complications included a groin haematoma (n±1) and reported flank (n±1) and groin pain (n±1). Conclusions: This pilot study shows that CO2 renal angiography can be used to perform RSDN in patients with significant renal impairment and may lead to associated improvements in clinic BP and albuminuria. [ABSTRACT FROM AUTHOR]

Objective: Discontinuation of metformin treatment in patients scheduled for elective coronary angiography (CAG) is controversial because of post-procedural risks including acute contrast-induced nephropathy (CIN) and lactic acidosis (LA). This study aims to discuss the safety of continuing metformin treatment in patients undergoing elective CAG with normal or mildly impaired renal functions. Methods: Our study was designed as a single-centered, randomized, and observational study including 268 patients undergoing elective CAG with an estimated glomerular filtration rate of >60 mL/min/1.73 m2. Of these patients, 134 continued metformin treatment during angiography, whereas 134 discontinued it 24 h before the procedure. CIN was defined as either a 25% relative increase in serum creatinine levels from the baseline or a 0.5 mg/dL increase in the absolute value that measured 48 h after CAG. Logistic regression analysis was performed to identify independent predictors of CIN and LA after CAG. Results: Both groups were comparable in terms of demographics and laboratory values. CIN at 48 h was 8% (11/134) in the metformin continued group and 6% (8/134) in the metformin discontinued group (p=0.265). Patients in neither of the groups developed metformin-induced LA. Based on multiple regression analysis, the ejection fraction [p=0.029, OR: 0.760; 95% CI (0.590–0.970)] and contrast volume [p=0.016, OR: 0.022 95% CI (0.010–0.490)] were independent predictors of CIN. Conclusion: Patients scheduled for elective CAG with normal or mildly impaired renal functions and preserved left ventricular ejection fraction (>40%) may safely continue metformin treatment. [ABSTRACT FROM AUTHOR]

Background: The aim of this study is to evaluate the risk of contrast induced nephropathy (CIN) in diabetic patients with critical limb ischemia (CLI) and foot ulcers (FUs) treated by percutaneous transluminal angioplasty of lower limbs.Methods: The study group was composed of 145 diabetic patients who underwent a limb salvage protocol because of CLI and FUs between 2012 and 2015. All patients received a prophylactic strategy against the administration of contrast medium. Serum creatinine (SCr) levels were evaluated the day of procedure and for 3 days after. CIN was considered in case of increase of 25% of SCr in comparison to baseline value or an absolute increase of at least 0.5 mg/dl without other interfering factors.Results: CIN occurred in 9% (14/145) of the cases. In the 1-year follow-up SCr returned to baseline values in 10 patients (71 %), 3 patients died (21%), and 1 patient had a major cardiovascular event (7%). No patients required dialysis. The risk was independent of chronic kidney disease stage. The rate of contrast nephropathy in each stage (X = 0.27) was as follows: 3/20 (15%) in stage 2; 3/66 (4.6%) in stage 3, 7/51 (13.7%) in stage 4; and 1/8 (12.5%) in stage 5. At the univariate analysis factors predicting this risk were anemia (HR 95% 2.5 [CI 1.8-4.2] P = .039) and heart failure (HR 95% 2.6 [CI 2.1-4.6] P = .038), while any significant variable was found at multivariate analysis.Conclusions: Peripheral percutaneous transluminal angioplasty in diabetic patients with CLI and FUs can be performed with a good safety factor and a low risk of contrast medium toxicity. [ABSTRACT FROM AUTHOR]

Contrast media administration can lead to acute deterioration in renal function particularly in patients with pre-existing chronic kidney disease. This prospective, randomized controlled open-label parallel group study was undertaken at Nizam's Institute of Medical Sciences, Hyderabad, from June to December 2015. A total of 95 patients were included, of which 35 received n-acetylcysteine (NAC) + normal saline (NS), 30 patients received aiiopurinoi (ALL) + NS, and 30 patients received placebo. In our study, the overall incidence of CIN was 24%. Incidence of CIN in NAC + NS, ALL + NS, and placebo group were 20%, 16%, and 36%, respectively. The major finding of this study was there was no significant difference between NAC and aiiopurinoi in the prevention of contrast nephropathy. However, only aiiopurinoi was superior to placebo. In our study, hyperuricemia and baseline serum creatinine were the only risk factors associated with CIN. [ABSTRACT FROM AUTHOR]

Contrast-induced acute kidney injury (CI-AKI) is a common cause of hospital-acquired acute kidney injury (AKI). We evaluated the evidence that uric acid (UA) plays a pathogenic role in CI-AKI. Ten studies were eligible for inclusion for meta-analysis. Hyperuricemia predicted risk for cases with AKI in prospective cohort studies. Higher levels of serum UA (SUA), as defined by the authors, were associated with a 2-fold increased risk to develop AKI (pooled odds ratio 2.03; 95% confidence interval [CI] 1.48-2.78). Significant heterogeneity was found in cohort studies (P = .001, I2 = 85.7%). In 2 clinical trials, lowering of SUA with saline hydration was significantly associated with reduced risk for AKI compared with saline hydration alone or saline hydration with N-acetyl cysteine. An analysis of 2 randomized controlled trials found that allopurinol with saline hydration had a significant protective effect on renal function (assessed by serum creatinine values) compared with hydration alone (mean difference: −0.52 mg/dL; 95% CI: −0.81 to −0.22). Hyperuricemia independently predicts CI-AKI. Two clinical trials suggest lowering SUA may prevent CI-AKI. The mechanism by which UA induces CI-AKI is likely related to acute uricosuria. [ABSTRACT FROM AUTHOR]

Aim:Contrast medium-induced nephropathy is one of the major complications of intravenous contrast medium use. But its pathogenesis is unclear. Epithelial mesenchymal transition (EMT) is defined as the transformation of the primer epithelial cells to mesenchymal cells. EMT in tubular cells might cause tubulointerstitial damage. In this study, we investigated whether or not EMT has a role in radiocontrast-induced nephropathy. Radiocontrast medium might be triggering reversible EMT via serum and glucocorticoid-regulated kinase 1 (SGK 1). We investigated the effect of different concentrations of the contrast agent iopromide on human proximal tubule cell (HK-2) culture by measuring the level of SGK1, snail family zinc finger 1 (SNAIL1), connective tissue growth factor (CTGF), and collagen type I alpha 1 (COL1A1). Methods:We conducted a scratch assay and qPCR. HK-2 cells were cultured in the petri dishes/flasks and starved with serum-free medium. The 40, 20, and 10 mg/mL doses of iopromide were administrated to cells. The scratches were photographed immediately and again at the 20th hour. The levels of gene expression of SGK1, SNAIL1, CTGF, and COL1A1 were measured using the real-time qPCR system at the end of the 24th hour. Results:Iopromide caused the breaking of intercellular connections, the disappearance of the cobblestone appearance of cells, and the migration of cells at the 20th hour in the scratch assay. It also increased the expression of SGK1, SNAIL1, CTGF, and COL1A1 genes. Conclusion:Our study concluded that certain important markers of EMT increase in different concentrations of the contrast agent. High osmolality might trigger EMT. The relationship between contrast agent and EMT has not been defined before. Furtherin vivoandin vitrostudies are required. [ABSTRACT FROM AUTHOR]

Background Multi-modal CT ( MMCT) to guide decision making for reperfusion treatment is increasingly used, but there remains a perceived risk of contrast-induced nephropathy ( CIN). At our center, MMCT is used empirically without waiting for serum-creatinine ( sCR) or renal profiling. Aims To determine the incidence of CIN, examine the risk factors predisposing to its development, and investigate its effects on clinical outcome in the acute stroke population. Methods An institution-wide protocol was implemented for acute stroke presentations to have MMCT (100-150 ml nonionic tri-iodinated contrast, perfusion CT and CT angiography) without waiting for serum-creatinine to minimize delays. Intravenous saline is routinely infused (80-125 ml/h) for at least 24-h after MMCT. Serial creatinine levels were measured at baseline, risk period, and follow-up. Renal profiles and clinical progress were reviewed up to 90 days. Results We analyzed 735 consecutive patients who had MMCT for the evaluation of acute ischemic or hemorrhagic stroke during the last five-years. A total of 623 patients met the inclusion criteria for analysis: 16 cases (2·6%) biochemically qualified as CIN; however, the risk period serum-creatinine for 15 of these cases was confounded by dehydration, urinary tract infection, or medications. None of the group had progression to chronic kidney disease or required dialysis. Conclusions The incidence of CIN is low when MMCT is used routinely to assess acute stroke patients. In this population, CIN was a biochemical phenomenon that did not have clinical manifestations, cause chronic kidney disease, require dialysis, or negatively impact on 90-day mRS outcomes. Renal profiling and waiting for a baseline serum-creatinine are an unnecessary delay to emergency reperfusion treatment. [ABSTRACT FROM AUTHOR]

Neutrophil-gelatinase-associated lipocalin (NGAL) is a biomarker of acute kidney injury. The aim of this study was to define a cut-off for NGAL in the early diagnosis of contrast-induced nephropathy (CIN) in patients with normal kidney function. We enrolled 121 patients with normal serum creatinine who underwent coronary angiography. NGAL was measured in urine before the procedure and 12 and 24 h afterward. CIN was defined as a 0.3 mg/dl increase in serum creatinine within 48 h after the procedure. Seven of 121 patients had CIN (5.8%). The NGAL levels in the 12- and 24-h urine samples of these patients were 30 (5-45) and 2 0 ng/ml, respectively, whereas those in patients without CIN were 15 (5-45) and 15 (10-51) ng/ml, respectively (P=0.8). In patients with CIN, the sensitivity and specificity of NGAL with a cut-off of 22.5 ng/ml were 71.4% and 57.9% in 12-h urine samples, with the negative predictive values (NPV) and positive predictive values (PPV) of 97.1% and 9.4%, respectively. In conclusion, we suggest that urine NGAL with cut-off point of 22.5 ng/ml has acceptable sensitivity and specificity for early diagnosis of CIN in patients with normal serum creatinine, but regarding NPV and PPV the best performance of this value is to rule out the CIN in patients at risk who received contrast media. [ABSTRACT FROM AUTHOR]

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Currently, the number of imaging and interventional procedures that use contrast agents (CAs) is gradually increasing. Contrast-induced nephropathy (CIN) is the most important CA-related complication. Oxidative stress plays a significant role in its pathophysiology. Lycopene (LPN) is a natural substance with strong antioxidant capacity. The present study aimed to investigate the potential preventive effects of LPN against CIN. In total, 28 male Wistar albino rats were divided into 4 groups with 7 rats in each group; the groups include normal control group, LPN only group at a dose of 4 mg/kg/day for 10 days, CIN group by administering 10 mg/kg furosemide IM + 10 mg/kg indomethacin IP + 10 ml/kg iomeprol IV following 24-h dehydration, and CIN + LPN group. There were statistically significant increase in urea, creatinine, and malondialdehyde levels (p < 0.001, for all) but a significant decrease in glutathione, superoxide dismutase, catalase, and glutathione peroxidase levels (p < 0.001, for all) in the CIN group compared with the control group. On histological examination, a significant increase of infiltrated inflammatory cells and necrotic degenerative changes were observed in the CIN group and the immunohistochemical examination revealed a significant increase in inflammation (inducible nitric oxide synthase), autophagy (LC3/B), and apoptosis (cleaved caspase 3) in the CIN group compared with the control group (p < 0.05, for all). Significant improvements in these unfavorable parameters were observed with CIN + LPN group compared with the CIN only group. In conclusion, the favorable effects of LPN as an anti-inflammatory, antiautophagic, and antiapoptotic agent in an experimental model of CIN have been demonstrated. [ABSTRACT FROM PUBLISHER]

Background: Oxidative stress and vasoconstriction appear to be important components of contrast nephropathy (CN) pathogenesis, and both carvedilol and nebivolol are known to have vasodilatory and antioxidant effects. Aims: This study aimed to investigate whether carvedilol and nebivolol play preventive roles against developing CN and to compare the effects of each. Materials and methods: Wistar albino rats were divided into control (C, n = 6), contrast material (CM, n = 6), carvedilol (CV, n = 7), carvedilol + contrast material (CV + CM, n = 7), nebivolol (N, n = 7), and nebivolol + contrast (N + CM, n = 7) groups. Following 3 days of dehydration, 6 mL/kg diatrizoate was administered to each rat. Carvedilol was given at a dose of 2 mg/kg and nebivolol at a dose of 1 mg/kg by way of oral gavage. After scarification, total antioxidant capacity (TAC), malondialdehyde (MDA), and superoxide dismutase (SOD) were studied in renal tissue. Histopathological findings were graded as mild (+), moderate (++), and severe (+++). Results and discussion: Most of the histopathological findings and MDA levels were significantly higher in the CM group than that in the C, CVCM, and NVCM groups, whereas there was no significant difference between the C, CVCM and NVCM groups. TAC level in the CM group was significantly lower than in all other groups. There was no difference in SOD among groups. Conclusions: Carvedilol and nebivolol both prevent development of nephropathy related to CMs by decreasing oxidative stress. Neither is superior to the other. [ABSTRACT FROM AUTHOR]

Objective: There is still a group of patient that have unpredictable risk for the development of contrast nephropathy (CN). There is also an effort to find more effficient strategies to prevent CN. Carvedilol, metoprolol and nebivolol seem to have theoretical potentials for the prevention of CN. In this study, we aimed to investigate their effects on the prevention of CN. We also aimed to define the risk factors associated with the development of CN in our study group. Methods: In this prospective, cross-sectional study, the patients were divided into four groups according to whether they were taking 25 mg/day carvedilol (n:56), 5 mg/day nebivolol (n:60), 50 mg/day metoprolol (n:68) or none (n:63). We made analysis to determine the agents' efficiency on the prevention of CN. We also performed multiple logistic regression analysis including all groups to define the risk factors associated with CN. Results: The incidents of CN were the lowest in the carvedilol group (4%) while the worst performance occurred in those taking metoprolol (10%). The difference between the groups in terms of the development of CN did not reach statistical significance (p>0.05). Multiple logistic regression analysis showed age (p=0.003), higher triglyceride levels (p=0.011) and family history of coronary artery disease (p=0.038) to be the predictors of CN. Conclusion: In this study, we didn't find any relation between the development of CN and carvedilol, metoprolol or nebivolol usage. We found age, higher levels of triglyceride and family history of coronary artery disease to be risk factors for predicting CN. [ABSTRACT FROM AUTHOR]

Objectives : To evaluate the difference in the renal protective effects of allopurinol and n-acetyl cysteine along with saline hydration in patients of contrast induced nephropathy (CIN) post cardiac interventions. Background: CIN remains a common complication of cardiac procedures. Radio contrast agents can cause a reduction in renal function that may be related to oxidative stress underlining various patho-physiologies. Conflicting evidence suggests that administration of allopurinol, a xanthine oxidase inhibitor can prevent CIN. Materials and Methods: This is a study of 500 patients undergoing angiography and coronary revascularisation in patients showing significant coronary block. The angiography positive patients (275) were prospectively randomised to different treatment protocol to study for their reno-protective effect. The patients received either of the three drugs saline hydration (SH, 1ml/kg/hr), n-acetylcysteine (SH+NAC, 600 mg bd) or Allopurinol (SH+ALLP, 300 mg/day) 12 hours before and after administration of radio contrast agent. Levels of serum creatinine and blood urea of the 275 patients recorded at 24 hour interval were noted post angioplasty over a course of 5 days in patients receiving either omnipaque (125) or visipaque (150) contrast media. All the 500 patients were also assessed for development of any kind of adverse drug effects/reactions with the two contrast media. Results: CIN occurred in 56 of 500 the patients (10.6%) who underwent angiography and 49 of 275 patients (17.8%) who underwent angioplasty. In the omnipaque group CIN occurred in 16/40, 8/40, nil/45 in patients receiving SH, NAC plus SH and SH plus ALLP respectively. In the visipaque group CIN occurred in 15/50, 10/50, nil/50 in the three treatments groups respectively. Allopurinol maintained a consistent fall in the serum creatinine & blood urea levels from the baseline values from the end of the 1st day (p < .01 & .001) in both the category. Visipaque proved to be better dye than omnipaque with less adverse drug effects/ reactions. Conclusion: Prophylactic oral administration of allopurinol (300 mg/day) along with hydration is better than n-acetylcysteine and saline hydration alone for protection against CIN in patients undergoing coronary procedures. [ABSTRACT FROM AUTHOR]

Objective. To determine the risk in administering ß-blockers, contrast-induced nephropathy (CIN) and the trend in X-ray use, during coronary computed tomography angiography (CCTA). Methods. A total of 416 patients were referred for elective CCTA.To achieve a resting heart rate below 60 beats per minute, oral and/or intravenous β-blockers were administered. Using questionnaires, information on the adverse effects of β-blockers was collected from the patients. The levels of s-creatinine and estimated GFR (eGFR) were measured before and after contrast enhanced CCTA. Radiation exposure was compared with the exposure 3 years earlier. Results. There was no significant difference in the symptoms (dizziness, lipothymia and palpitations) between patients with and patients without β-blocker pretreatment. Compared to baseline values, the decrease in s-creatinine was not significant (75.2 vs. 74.6 μmol/L, p = 0.09), while the increase in eGFR was not significant (78 vs. 79 mL/min, p = 0.17). Also, subgroups of patients with hypertension, hypercholesterolemia, diabetes or pre-existing slight impairment in renal function did not develop CIN.The mean radiation exposure decreased from 17.5 to 6.7 mSv, p < 0.0001. Conclusions. In terms of the side effects of β-blockers and contrast media, there were no short term complications to CCTA. Furthermore, the radiation dose has been dramatically diminished over the last three years. [ABSTRACT FROM AUTHOR]

Contrast-induced nephropathy (CIN) refers to a decline in renal function following exposure to iodinated contrast media (CM). The present study was initiated to explore the role of known human risk factors (spontaneous hypertension, diabetes, protein-losing nephropathy) on CIN development in rodent models and to determine the effect of CM administration on kidney injury biomarkers in the face of preexisting kidney injury. Spontaneously hypertensive rats (hypertension), streptozotocin-treated Sprague Dawley rats (diabetes), and Dahl salt-sensitive rats (protein-losing nephropathy) were given single intravenous injections of the nonionic, low osmolar contrast medium, iohexol. Blood urea nitrogen (BUN), serum creatinine (sCr), and urinary biomarkers; albumin, lipocalin 2 (Lcn-2), osteopontin (Opn), kidney injury molecule 1 (Kim-1), renal papillary antigen 1 (Rpa-1), α-glutathione S-transferase (α-Gst), µ-glutathione S-transferase (µ-Gst), and beta-2 microglobulin (β2m) were measured in disease models and appropriate controls to determine the response of these biomarkers to CM administration. Each disease model produced elevated biomarkers of kidney injury without CM. Preexisting histopathology was exacerbated by CM but little or no significant increases in biomarkers were observed. When 1.5-fold or greater sCr increases from pre-CM were used to define true positives, receiver–operating characteristic curve analysis of biomarker performance showed sCr was the best predictor of CIN across disease models. β2m, Lcn-2, and BUN were the best predictors of histopathology defined kidney injury. [ABSTRACT FROM AUTHOR]

Background Contrast-induced acute kidney injury (CIAKI) has been linked to unfavorable consequences. In routine clinical practice, small increases in serum creatinine (SCr) following coronary angiography tend to be underestimated, especially in patients without chronic kidney disease (CKD). Methods We conducted a retrospective observational cohort study to analyze in-hospital and long-term outcomes of CIAKI following coronary angiography in patients with or without CKD (eGFR ≥ 60 mL/min/1.73 m2) from January 2008 through December 2009. CIAKI was defined as SCr either ≥ 25% or ≥ 0.5 mg/dL from baseline within 72 h after contrast exposure. Multivariable logistic regression for in-hospital mortality and Cox proportional hazards calculations for long-term mortality and requirement for dialysis were performed. Results A total of 1160 patients were included in the study. CIAKI occurred in 19% of CKD patients and in 18% of non-CKD patients. In CKD and non-CKD patients, CIAKI was more frequent in patients requiring mechanical ventilation or inotropes or in those given furosemide, and it was associated with adverse in-hospital (prolonged hospitalization, acute dialysis and mortality) and long-term (increased creatinine, initiation of dialysis and mortality) outcomes. In multivariable analysis, CKD patients had greater in-hospital mortality if they developed CIAKI (adjusted OR 8, 95% CI 1.9–34.5, P = 0.005), and non-CKD patients had greater long-term mortality if they developed CIAKI (adjusted HR 2.2, 95% CI 1.2–4.1, P = 0.016). Conclusions CIAKI following coronary angiography was associated with adverse in-hospital and long-term outcomes in both CKD and non-CKD patients. [ABSTRACT FROM AUTHOR]

Background: It has been shown that beta-glucan (BG), which has antioxidant and immunomodulatory effects, attenuats renal ischemia-reperfusion injury. We aimed to investigate whether BG might have a preventive role against the development of contrast-induced nephropathy and to compare its effect with nebivolol (Nb) and N-acetylcysteine (NAC). Methods: Thirty-six Wistar albino female rats were randomly divided into six groups ( n = 6 each): control, contrast media (CM), BG, BG + CM, Nb + CM, and NAC + CM. With the exception of control and CM groups, the others were given drugs orally once a day for 5 days. Kidney function parameters, inflammatory parameters, and serum and renal tissue oxidative stress markers were measured. Results: Increases of serum creatinine and blood urea nitrogen levels were significantly higher ( p < 0.05) in the CM group only. Absolute changes of serum creatinine levels in BG, BG + CM and Nb + CM groups were significantly lower than those in the CM group ( p < 0.05). Serum levels of advanced oxidation protein products and malondialdehyde were significantly less ( p < 0.05) in the BG group compared to the CM group. Histopathological lesions in the CM group were more advanced ( p < 0.05). No significant differences between the BG + CM, Nb + CM and NAC + CM groups were found with regard to histopathological findings. Conclusion: This study suggests that BG protects or ameliorates against contrast-induced nephropathy. Its beneficial effects may be similar to or greater than those of Nb or NAC. [ABSTRACT FROM AUTHOR]

Background and Aim: Previous studies have demonstrated that endogenous bone morphogenic protein-7 (BMP-7) level is reduced in acute kidney injury and administration of exogenous BMP-7 has a beneficial effect on kidney function. In spite of preventive management, contrast-induced nephropathy (CIN) is still the third cause of acute deterioration of kidney function in hospitalized patients. With this background in mind, we studied changes in serum BMP-7 in a group of patients with chronic kidney disease and contrast-induced nephropathy. Materials and Methods: We enrolled 45 consecutive adult patients with a baseline serum creatinine ≥1.4 mg/dl admitted for coronary angiography. We measured serum BMP-7 levels before and 48 h after coronary angiography. The primary end point was the development of CIN, defined as an increase in serum creatinine concentration by 0.25 mg/dl or 25% over the baseline value within 72 h from contrast exposure. Results: Overall, CIN occurred in 8 (17%) patients. The concentrations of serum BMP-7 were significantly decreased in the CIN group compared to baseline (488.6 ± 56.8 vs. 356.4 ± 24.8, P = 0.01); in contrast, the concentration of BMP-7 level did not change in patients without CIN (444.6 ± 54.6 vs. 440.0 ± 53.9, P = 0.09). Conclusion: BMP-7 level significantly decreases in patients who develop CIN after coronary angiography. Therefore, BMP-7 might be a diagnostic biomarker for CIN and a possibly promising agent for the treatment of CIN. [ABSTRACT FROM AUTHOR]

Peripheral arterial disease (PAD) is a common manifestation of atherosclerotic vascular disease and the incidence of infrapopliteal PAD continues to rise in the population. The historical experience with surgical and endovascular interventions for infrapopliteal stenosis was disappointing as operators experienced high rates of early technical failures and procedural complications, coupled with high rates of restenosis in this vascular territory when compared with more proximal vascular beds. While patients with infrapopliteal PAD may be asymptomatic, the majority would ultimately develop intermittent claudication or may also present with critical limb ischemia. In this article, we review the current literature, and discuss some of the technical aspects of endovascular therapy in this vascular bed. We also emphasize the importance of adjunctive evidence-based therapies such as antiplatelet agents, statins, and lifestyle modification such as smoking cessation in this particularly high-risk cohort to optimize clinical outcomes. [ABSTRACT FROM PUBLISHER]

Topics covered in this review include the relation of estimated glomerular filtration rate, proteinuria and outcome; sudden cardiac death; contrast-induced acute kidney injury (CI-AKI); imaging; clinical trials targeting cardiovascular disease in chronic kidney disease (CKD) patients; and treatment of ischemic heart disease and valvular disease. Several studies reinforce the importance of CKD in predicting mortality and make a case for redefining CKD to incorporate levels of proteinuria in the staging system. Another study provides support for using a combination of echocardiography and cardiac biomarkers for cardiac risk stratification in dialysis patients. Two studies reveal ongoing interest in and difficulty preventing CI-AKI. One study discusses chest ultrasound to detect pulmonary congestion and potentially guide ultrafiltration and volume removal in dialysis patients. Several clinical trials assess folic acid, statins and aspirin for prevention of future cardiovascular events in CKD patients. Finally, several studies compare the use of drug-eluting and bare metal stents in dialysis patients, discuss methods of surgical coronary artery revascularization in dialysis patients and describe testing allopurinol as a treatment for ischemic heart disease in non-renal patients. [ABSTRACT FROM AUTHOR]

Summary: Subjects with hypovolemia and/or dehydration and pre-existing renal failure are considered at highest risk for radiocontrast-medium-induced acute kidney injury (RCI-AKI), and this risk increases in the presence of glomerular filtration rate or creatinine clearance rates lower than 60mL/min (stage 3-5 chronic kidney disease according to the National Kidney Foundation). The authors critically review the evidence-based literature on RCI-AKI, its diagnosis, epidemiological aspects, predisposing conditions, and markers of risk, including advanced age. Procedures requiring the use of iodinated contrast media are increasingly performed in patients over 70 years of age, and there is no definitive consensus regarding the role of advanced age as a marker of risk for RCI-AKI. [Copyright &y& Elsevier]

Aim: The aim of this study is to investigate the efficacy and mechanism of action of intravenous (IV) bicarbonate in preventing radiocontrast nephropathy (RCN). Materials and methods: Twenty-eight Wistar rats were randomized into four groups including control (group 1), radiocontrast (group 2), bicarbonate (group 3), and radiocontrast plus bicarbonate (group 4). Once blood chemistry and arterial blood gases were examined and 24 h urine samples were collected, all rats were administered furosemide (2 mg/kg subcutaneous) and deprived of water for 24 h. Iothalamate sodium (6 mL/kg) was administered to group 2 and group 4. IV bicarbonate (8.4%) was administered to group 3 and group 4 (3 h before the administration of iothalamate). On the fourth day, 24 h urine was collected, and at the end of the day rats were sacrificed and blood chemistry and arterial blood gases were reexamined. Myeloperoxidase (MPO), nitric oxide (NO), total glutathione, and malondialdehyde were quantified on the renal tissue. H&E slides were examined. Results: Basal creatinine and creatinine clearance were similar between groups. There was no significant difference between creatinine and creatinine clearance by the end of the experiment. Glutathione level in group 2 was lower than in group 4. Histopathologically, there was no injury in the control group (group 1) whereas there was an intermediate-severe injury (71.4%) in the radiocontrast group (group 2). The percentage of intermediate-severe injury was significantly lower (71.4% vs. 28.6%, p = 0.02) in the radiocontrast plus bicarbonate group (group 4). Conclusions: Sodium bicarbonate attenuates the development of radiocontrast-induced tubular necrosis. [ABSTRACT FROM AUTHOR]

This study was done to investigate whether aminophylline reduces the incidence of contrast induced nephropathy (CIN) after coronary angioplasty. Sixty patients who had serum creatinine concentration of > 1.3 mg/dl randomly received 250 mg IV aminophylline or placebo 30 minutes before coronary angiography. Serum creatinine and blood urea nitrogen were determined immediately before (base line) and at 24 and 48 hours after administration of contrast medium. The primary end point was the incidence of CIN. The incidence of CIN was 20% in placebo group and 13.3% in aminophylline group; older age was significantly associated with CIN: In this study, we could not demonstrate the prophylactic effect of a single infusion of 250 mg aminophylline, 30 minutes before administration of contrast media. A larger trial that incorporates the evaluation of clinically relevant outcomes is required to more adequately assess the role for aminophylline in CIN prevention. [ABSTRACT FROM AUTHOR]

The article presents information on a study related to sodium bicarbonate therapy to prevent contrast media-induced acute kidney injury (CI-AKI). The researchers had made a comprehensive meta-analysis including a total of 18 trials focusing on separate analysis of papers both published and unpublished. It is reported that sodium bicarbonate-based hydration was found to be superior to normal saline in the prevention of CI-AKI in all recent meta-analyses.

Aim: Oxidative stress and ischaemia are suggested as possible mechanisms of contrast-induced nephropathy (CIN). Statins may offer renoprotection in both acute and chronic kidney diseases because of their antioxidant and anti-inflammatory properties. We investigated whether use of statins before non-emergent percutaneous coronary intervention (PCI) reduces the incidence of CIN. Methods: We retrospectively evaluated 540 consecutive adult patients who underwent non-emergent PCI over a 3 year period at a tertiary care centre. CIN was defined as 25% or 44 mmol/L increase from baseline creatinine at 48–72 h. In addition, we classified patients based on Mehran score for risk of development of CIN and analysed the effect of statins. Results: Three-hundred and fifty-three patients met inclusion criteria. Two-hundred and thirty-nine patients were taking statins before PCI and 114 were not. Baseline characteristics were similar for both groups. CIN occurred in 75 patients (21.2%). There was a higher incidence of CIN in patients on statins as compared with patients not on statins (24.7% vs 14%; 95% CI: 1.09–3.67; P = 0.02). However, propensity-based adjustment for receipt of statins revealed no significant differences in CIN between both groups (OR: 1.6; 95% CI: 0.87–3.22; P = 0.12). Multivariate logistic regression revealed Mehran score to be independently predictive of CIN. None of the patients who developed CIN required dialysis. Conclusions: Statin use before non-emergent PCI is not associated with reduction in CIN. Further randomized controlled trials based on proper risk adjustment for development of CIN are needed. [ABSTRACT FROM AUTHOR]

Background/Aims. Different serum and urinary biomarkers have been recently proposed to serve as markers of acute kidney injury. We tested the hypothesis whether NGAL and other biomarkers could represent an early biomarker of contrast nephropathy (CIN) in diabetic patients with normal serum creatinine undergoing cardiac catheterization in comparison with non-diabetic patients. Methods. Serum, urinary NGAL, cystatin C, urinary kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), and liver-type fatty acid binding protein (L-FABP) were evaluated before and 2, 4, 8, 24, and 48 hours after cardiac catheterization using commercially available kits. Results. In both groups we found a significant rise in serum NGAL after 2, 4, and 8 hours, and in urinary NGAL and IL-18 after 4, 8, and 24 hours after cardiac catheterization. Serum cystatin C increased significantly 8 hours, reaching peak 24 hours after cardiac catheterization in both groups, and then decreased after 48 hours. L-FABP and KIM-1 increase significantly after 24 and 48 hours after cardiac catheterization. Conclusions. CIN was similarly prevalent in both diabetic and non-diabetic patients undergoing cardiac catheterization. NGAL seems to be a potential early marker for nephrotoxicity and predictor of contrast nephropathy. It is particularly important in the upcoming setting of short-time hospitalizations for cardiac catheterization. [ABSTRACT FROM AUTHOR]

Introduction. Intravenous administration of saline and non-ionic isosmolar contrast media significantly reduces the incidence of contrast-induced nephropathy, one of the most common causes of acute renal failure. Results with oral N-acetylcysteine are conflicting. The aim of our study was to evaluate the prophylactic role of N-acetylcysteine in patients with stable chronic renal failure undergoing coronary and/or peripheral angiography and/or angioplasty. [ABSTRACT FROM PUBLISHER]

Contrast-induced nephropathy is well-known sequelae of iodinated contrast (diatrizoate meglumine). Carbon dioxide (CO2) can be used as an alternative contrast agent. The aim of this study was to compare the renal injury and the quality of images of aortogram using iodinated contrast versus CO2 using digital subtraction angiography (DSA). This prospective randomized study was done in 29 healthy dogs using DSA aortogram. Dogs were randomly assigned to receive iodinated contrast or CO2. 6-F pigtail catheter was introduced via femoral artery approach to perform aortogram under general anesthesia. Serum creatinine (S.Cr.) and urinary enzymes, namely: N-acetyl D-glucosaminidase (NAG), alanine aminopeptidase (AAP), and gamma glutamyl transferase (GGT), were measured before and 48 hours after aortogram. There was no change in S.Cr. in both the groups. Significantly more enzymuria was seen following iodinated contrast than CO2. Enzymuria pre and postaortogram following the iodinated contrast was GGT: 14.9 ± 5.92 vs. 26.2 ± 15.1 (P = 0.001), NAG: 1.63 ± 0.90 vs. 3.6 ± 2.14 (P = 0.0001), and AAP: 1.51 ± 0.75 vs. 3.38 2.41 (P = 0.001), and in the CO2 group was GGT: 15.5 ± 4.9 vs. 21.1 ± 9.04 (P = 0.02), NAG: 2.12 ± 1.06 vs. 3.82 3.27 (P = 0.08), and AAP: 1.28 ± 0.76 vs. 2.51 ± 1.72 (P = 0.03). More than 50% increase over the preprocedural value was significantly less following CO2. Images obtained with iodinated contrast were superior to those with CO2, however, the quality of image with CO2 was adequate for delineation of the renal artery and major branches. Both iodinated contrast and CO2 cause significant enzymuria. More severe enzymuria (>50% increase) was seen significantly less with the use of CO2. Quality of images is better with iodinated contrast. [ABSTRACT FROM AUTHOR]

The incidence of both acute kidney injury (AKI, previously referred to as acute renal failure) and chronic kidney disease (CKD) is reaching epidemic proportions. In both situations, early intervention can significantly improve the prognosis. However, the paucity of early, predictive, non-invasive biomarkers has impaired our ability to institute potentially effective therapies for these common clinical conditions in a timely manner. The current status of one of the most promising novel biomarkers, namely neutrophil gelatinase-associated lipocalin (NGAL), is presented in this review. The evidence for the role of NGAL measurements in a variety of clinical situations leading to AKI (cardiac surgery, kidney transplantation, contrast nephropathy, haemolytic uraemic syndrome and in the intensive care setting) or to CKD (lupus nephritis, glomerulonephritides, obstruction, dysplasia, polycystic kidney disease, IgA nephropathy) is explored. The emerging utility of standardized clinical platforms for reliable measurement of NGAL in plasma (Triage® NGAL Device; Biosite Incorporated) and urine (ARCHITECT® analyzer; Abbott Diagnostics) is also discussed. It will be important in future studies to validate the sensitivity and specificity of NGAL concentration measurements in clinical samples from large cohorts and from multiple clinical situations. Such studies will be facilitated by the anticipated widespread availability of standardized commercial tools in the near future. [ABSTRACT FROM AUTHOR]