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Background: Contrast-induced acute kidney injury (CI-AKI) is a frequent complication of coronary interventions associated with an increased risk of mortality and morbidity. The optimal intravenous hydration strategy to prevent CI-AKI is not well-established. The primary objective is to determine if a tailored hydration strategy reduces the risk of CI-AKI and of major adverse cardiovascular events (MACE) in patients undergoing coronary angiography compared with a non-tailored hydration strategy., Methods: A study-level meta-analysis of randomized controlled trials comparing tailored versus non-tailored hydration strategies for the prevention of CI-AKI (primary outcome) and of MACE (main secondary outcome) in patients undergoing coronary angiography for any indication was performed. Tailored hydration was defined as the administration of intravenous fluids based on patient-specific parameters other than weight only., Results: A total of 13 studies were included (n = 4,458 participants). The overall risk of bias was moderate. A tailored strategy was associated with a significant reduction in the risk of CI-AKI (RR=0.56, 95% CI, [0.46-0.69], p<0.00001; I 2 =26%), and of MACE (RR=0.57, 95% CI, [0.42-0.78], p=0.0005; I 2 =12%). A tailored hydration strategy was not associated with a significant reduction in the other pre-specified secondary outcomes, except for all-cause mortality (RR=0.57, 95% CI, [0.35, 0.94], p=0.03; I 2 =0%). The impact of a tailored strategy on the primary outcome was consistent in sensitivity analyses., Conclusion: These results suggest that tailored hydration is superior to non-tailored hydration in reducing the risk of CI-AKI and MACE in patients undergoing coronary angiography. Future trials are required to identify the optimal tailored hydration strategy., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025. Published by Elsevier Inc.)

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., (© 2024 International Society for Apheresis and Japanese Society for Apheresis.)

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., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Introduction: Contrast nephropathy (CN) is characterized by oxidative stress, vasoconstriction, tubular toxicity, and hypoxia of the renal medulla. We aimed to test the therapeutic effects of an α7 nicotinic acetylcholine receptor (nAChR) agonist, GTS-21, in an experimental CN model., Methods: Male Sprague-Dawley rats (n = 40) were divided into 4 groups: saline-treated control, GTS-21-treated control, contrast, and GTS-21-treated contrast groups. Starting on the 1st day, GTS-21 (4 mg/kg, intraperitoneally) or saline was administered twice a day for 3 days. CN was induced on the second day by intravenous injection of indomethacin (10 mg/kg), l-NAME (10 mg/kg), and a contrast agent with high osmolarity (6 mL/kg; Urografin 76%). At the 72nd hour, blood and kidney samples were obtained for the determination of biochemical, histological, and gene expression parameters., Results: Compared to those in control rats, the elevated serum BUN level in the contrast group decreased with GTS-21 treatment, while H&E staining and TUNEL assays showed that contrast-induced renal injury was improved by GTS-21. Moreover, GTS-21 treatment in the CN also increased the antioxidant glutathione level. In the contrast group, a significant increase in IL-6 expression and a decrease in TGF-β expression were observed; however, GTS-21 treatment decreased IL-6 expression and increased TGF-β expression., Conclusion: GTS-21 significantly alleviated renal injury parameters through antioxidant, anti-inflammatory, and antiapoptotic mechanisms in the CN model., (© 2024 The Author(s). Published by S. Karger AG, Basel.)

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 β2 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.

Objective: Patients with chronic kidney disease (CKD) who undergo peripheral vascular interventions (PVI) with iodinated contrast are at higher risk of post-contrast acute kidney injury (PC-AKI). Carbon dioxide (CO 2 ) angiography can reduce iodinated contrast volume usage in this patient population, but its impact on PC-AKI has not been studied. We hypothesize that CO 2 angiography is associated with a decrease in PC-AKI in patients with advanced CKD., Methods: The Vascular Quality Initiative PVI dataset from 2010 to 2021 was reviewed. Only patients with advanced CKD (estimated glomular filtration rate <45 ml/min/1.73 m 2 ) treated for peripheral arterial disease were included. Propensity matching and multivariate logistic regression based on demographics, comorbidities, CKD stage, and indications were used to compare the outcomes of patients treated with and without CO 2 ., Results: There were 20,706 PVIs performed in patients with advanced CKD, and only 22% utilized CO 2 angiography. Compared with patients treated without CO 2 , patients who underwent CO 2 angiography were younger and less likely to be women or White, and more likely to have poor renal function, diabetes, cardiac comorbidities, and present with tissue loss. Propensity matching yielded well-matched groups with 4472 patients in each group. The procedural details after matching demonstrated 50% reduction in the volume of contrast used (32±33 vs 65±48 mL; P < .01). PVI with CO 2 angiography was associated with lower rates of PC-AKI (3.9% vs 4.8%; P = .03) and cardiac complications (2.1% vs 2.9%; P = .03) without a significant difference in technical failure or major/minor amputations. Low contrast volumes (≤50 mL for CKD3, ≤20 mL for CKD4, and ≤9 mL for CKD5) are associated with reduced risk of PC-AKI (hazard ratio, 0.59; P < .01)., Conclusions: CO 2 angiography reduces iodinated contrast volume usage during PVI and is associated with decreased cardiac complications and PC-AKI. CO 2 angiography is underutilized and should be considered for patients with advanced CKD who require endovascular therapy., (Copyright © 2023 Society for Vascular Surgery. All rights reserved.)

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., (© 2022 International Society for Apheresis and Japanese Society for Apheresis.)

Background: Rotational atherectomy (RA) is a complex procedure often associated with high contrast load. Known risk scores do not predict contrast-induced acute kidney injury (CI-AKI) before RA. We aim to investigate pre-procedural predictors of CI-AKI after RA, and the role of the target vessel SYNTAX score (tvSS)., Methods: Among 295 patients who underwent RA between 01.2010 and 02.2019 at a single center, 49 developed CI-AKI. Those who were on chronic hemodialysis or with no available 48-h' kidney function tests were excluded. Predictors of CI-AKI were assessed in the whole cohort and those with no basal renal impairment., Results: The rate of CI-AKI was 16.6 %. The tvSS was 18 [14-23] vs. 12 [9-18] in patients with vs. without CI-AKI (p < 0.001). The tvSS cut-off value of 15 provided 75 % sensitivity and 60 % specificity for predicting CI-AKI. Consequently, a tvSS ≥15 emerged as an independent pre-procedural predictor for CI-AKI (adjusted OR: 4.94, 95 % CI: 2.38-10.20, p < 0.001), along with left ventricular ejection fraction (LVEF) ≤35 % (p = 0.016) and glomerular filtration rate (GFR) <45 ml/min (p = 0.004). TvSS was the only independent pre-procedural predictor for CI-AKI in patients with GFR ≥60 ml/min (p < 0.001). The contrast volume/GFR ratio and peri-procedural myocardial infarction (MI) were independent procedural predictors for CI-AKI in the whole cohort and in patients with basal GFR ≥60 ml/min., Conclusion: CI-AKI after RA is frequent. The tvSS is an efficient pre-procedural predictor for CI-AKI after RA, along with LVEF ≤35 % and GFR <45 ml/min. Contrast volume/GFR ratio and peri-procedural MI emerged as procedural predictors for CI-AKI., Competing Interests: Declaration of competing interest Dr. Hemetsberger received a speaker's honoraria from Boston Scientific. Dr. Abdel-Wahab reports that his hospital receives speaker's honoraria and/or consultancy fees on his behalf from Medtronic and Boston Scientific. Dr. Richardt received an institutional research grant from Boston Scientific. Dr. Allali is a proctor for Boston Scientific. The other authors have no conflicts of interest to declare., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Competing Interests: Declaration of competing interest Dr. Finn, Dr. Turco and Dr. Reisman are consultants to RenalPro Medical, Inc. Dr. Chen has no competing interests. CVPath Institute received Grant/Research/Clinical Trial Support from NIH-HL141425, Leducq Foundation Grant, 4C Medical, 4Tech, Abbott Vascular, Ablative Solutions, Absorption Systems, Advanced NanoTherapies, Aerwave Medical, Alivas, Amgen, Asahi Medical, Aurios Medical, Avantec Vascular, BD, Biosensors, Biotronik, Biotyx Medical, Bolt Medical, Boston Scientific, Canon USA,Cardiac Implants, Cardiawave, CardioMech, Cardionomic, Celonova, Cerus EndoVascular, Chansu Vascular Technologies, Childrens National Medical Center, Concept Medical, Cook Medical, Cooper Health, Cormaze Technologies GmbH, CRL/AccelLab, Croivalve, CSI, Dexcom, Edwards Lifesciences, Elucid Bioimaging, eLum Technologies, Emboline, Endotronix, Envision, Filterlex, Imperative Care, Innovalve, Innovative Cardiovascular Solutions, Intact Vascular, Interface Biolgics, Intershunt Technologies, Invatin Technologies, Lahav CRO, Limflow, L&J Biosciences, Lutonix, Lyra Therapeutics, Mayo Clinic, Maywell, MD Start, MedAlliance, Medanex, Medtronic, Mercator, Microport, Microvention, Neovasc, Nephronyx, Nova Vascular, Nyra Medical, Occultech, Olympus, Ohio Health, OrbusNeich, Ossio, Phenox, Pi-Cardia, Polares Medical, Polyvascular, Profusa, ProKidney LLC, Protembis, Pulse Biosciences, Qool Therapeutics, Recombinetics, Recor Medical, Regencor, Renata Medical, Restore Medical, Ripple Therapeutics, Rush University, Sanofi, Shockwave, Sahajanand Medical Technologies, SoundPipe, Spartan Micro, Spectrawave, Surmodics, Terumo Corporation, The Jacobs Institute, Transmural Systems, Transverse Medical, TruLeaf Medical, UCSF, UPMC, Vascudyne, Vesper, Vetex Medical, Whiteswell, WL Gore, Xeltis. Aloke V. Finn received consultant fees/honoraria from Abbott Vascular, Amgen, Biosensors, Boston Scientific, Celonova, Cook Medical, CSI, Lutonix Bard, Sinomed, RenalPro and Terumo Corporation. Drs Turco Chen and Reisman are consults to RenalPro

Background: Acute kidney injury (AKI) after contrast-guided interventions is associated with adverse outcomes, but the role of contrast in the context of renal function is less well described for patients undergoing transcatheter aortic valve replacement (TAVR)., Methods: Patients from the Michigan TAVR registry between January 2016 and December 2019 were included. AKI was defined using Valve Academic Research Consortium 2 definitions. An integer cut point for the ratio of contrast volume (CV) to renal function (estimated glomerular filtration rate [eGFR]) as a predictor of AKI was calculated., Results: Of 7112 cases, AKI occurred in 629 (8.8%) patients. Unadjusted mortality was higher among patients with AKI (32.5% vs 9.0%, P  ​< ​.0001). AKI remained significantly associated with the risk of mortality after multivariable adjustment (hazard ratio = 4.50, P  ​< ​.001). Procedural characteristics associated with AKI included CV/eGFR >2 (adjusted odds ratio [aOR] = 1.36, P = .003, 95% CI = 1.10-1.67), CV/eGFR >3 (aOR = 1.38, P  ​= ​.009, 95% CI = 1.09-1.77), and use of general anesthesia (aOR = 1.67, P  ​< ​.0001, 95% CI = 1.38-2.03)., Conclusions: CV in the context of renal function administrated during TAVR is a robust tool to predict AKI. AKI after TAVR is associated with an increased risk of mortality. Incorporation of thresholds of >2× and > 3× eGFR into procedural planning should be considered as a quality initiative., Competing Interests: S. Gualano, W. Merhi, C. Schwartz, and F. Shannon have no disclosures. S. Chetcuti has been a consultant and proctor for Medtronic, with research support from 10.13039/100004374Medtronic, Gore, 10.13039/100008497Boston Scientific, 10.13039/100006520Edwards Lifesciences, and JenaValve. D. Sukul receives research funding from 10.13039/100001502Blue Cross Blue Shield of Michigan. H. Patel is a consultant for Medtronic and WL Gore. H. Gurm receives research funding from 10.13039/100001502Blue Cross Blue Shield of Michigan and the 10.13039/100000002National Institutes of Health Center for Accelerated Innovation and is a consultant for Osprey Medical. W. O’Neill is a consultant for Abbott, Edwards Lifesciences, Boston Scientific, and Abiomed, with research grant support from Abiomed, 10.13039/100001316Abbott, 10.13039/100006520Edwards Lifesciences, and 10.13039/100004374Medtronic. P. Grossman is a consultant for Medtronic Cardiovascular, has research support from 10.13039/100004374Medtronic Cardiovascular, 10.13039/100006520Edwards Life Sciences, and 10.13039/100016476Cardiovascular Systems Incorporated, has registry support from 10.13039/100001502Blue Cross Blue Shield of Michigan, and has research support from 10.13039/100000002National Institutes of Health. None of the authors have any conflicts directly relevant to this study.

Objective: To perform a detailed analysis of published data regarding intravascular volume expansion to prevent contrast-associated acute kidney injury (CA-AKI) and to determine if an ideal dose of IV fluids can be recommended., Background: Administration of contrast media during invasive angiography is associated with CA-AKI. Intravascular volume expansion is the most effective intervention to prevent CA-AKI, yet evidenced based protocols are lacking., Methods: Literature review and meta-analysis of randomized controlled trials (RCT) of patients receiving IV volume expansion as prophylaxis for CA-AKI was performed. Normal saline, Lactated Ringer's and sodium bicarbonate were included. The primary outcome was incidence of CA-AKI., Results: 37 RCTs studying 12,166 patients were included. Mean age was 67 ± 5 years, 70% of the patients were male. 68% had chronic kidney disease, 41% diabetes, and 30% heart failure. The incidence of CA-AKI was 9.5% (95% CI: 8-12%). IV expansion versus no volume administration was associated with a lower risk of CA-AKI (RR:0.62; 95% CI: 0.49-0.77, p < .001). Intensive IV volume expansion was associated with a reduced risk of CA-AKI(RR: 0.66; 95%CI: 0.52-0.85, p < .01). The intensive IV volume expansion arm received significantly more fluids than the standard protocols: 1,574(1,123 - 1,913) ml versus 849(558-1,067) ml (p = .03) without significant difference in the duration of infusion (median of 12 vs. 17 hr, p = .1) or pulmonary edema (1.7% vs 1.3%, p = .7)., Conclusions: Despite high variability in protocols used, IV volume expansion is effective in preventing CA-AKI. Intensive IVF expansion (median 1.6 L over 17 hr) was associated with decreased risk of CA-AKI., (© 2020 Wiley Periodicals LLC.)

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.

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., Competing Interests: No potential conflict of interest was reported by the authors., (© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group on behalf of Greater Baltimore Medical Center.)

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., (© 2021 The Author(s).)

Background/purpose: Chronic kidney disease (CKD) is a risk factor for contrast associated acute kidney injury (CA-AKI). The risk of renin-angiotensin-aldosterone system inhibitor (RASi) use in patients with CKD before the administration of contrast is not clear., Methods: In this nested case-control study, 8668 patients received contrast computed tomography (CT) from 2013 to 2018 during index administration in a multicenter hospital cohort. The identification of AKI is based on the Kidney Disease: Improving Global Outcomes (KDIGO) serum creatinine criteria within 48 h after contrast medium used., Results: Finally, 986 patients (age, 63.36 ± 12.22; men, 72.92%) with CKD (estimated glomerular filtration rate (eGFR) = 35.0 ± 19.8 mL/min/1.73 m 2 ) were eligible for analysis. After the index date, RASi users (n = 315) were less likely to develop CA-AKI (13.65% vs 30.4%, p < 0.001), and had a lower hospital mortality (8.25% vs 19.23%, p < 0.001) compared with non-users. The pre-contrast use of RASi decrease the risk of AKI (OR, 0.342, p < 0.001) and hospital mortality (OR, 0.602, p = 0.045). Even a few defined daily doses (DDDs) of RASi treatment, more than 0.02 prior to contrast CT could attenuate CA-AKI. The hospital mortality was higher in RASi non-users if their eGFR value was more than 17.9 mL/min/1.73 m 2 ., Conclusion: RASi use in patients with CKD prior to contrast CT has the potential to mitigate the incidence of AKI and hospital mortality. Even a low dose of RASi will noticeably decrease the risk of AKI and will not increase the risk of hyperkalemia., Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest relevant to this article., (Copyright © 2020. Published by Elsevier B.V.)

Contrast media administration has been associated with complications such as nephropathy, cardiovascular morbidity, and neurovascular events, particularly in patients with renal insufficiency. This association has been questioned in recent studies. This review was performed to summarize the most current evidence on contrast induced nephropathy (CIN), contributing factors, and considerations in patients with renal insufficiency. The risk of CIN was over-estimated by the previous studies, due to a lack of control groups or presence of non-randomized control groups, which led to a selection bias. However, the thresholds associated with an increased risk of CIN are controversial and require risk-benefit analysis on an individual basis. Regarding the administration of contrast media (CM) in the emergency setting, the majority of studies suggested that CM exposure does not meaningfully increase the risk of acute kidney injury in critically ill patients (including trauma patients). Several strategies have been suggested to reduce the risk of CIN, including volume expansion to increase renal blood flow, sodium bicarbonate or N-acetylcysteine administration, and use of low-osmolal contrast media in end-stage renal disease., (Copyright © 2020 Elsevier Inc. All rights reserved.)

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., Competing Interests: There are no conflicts of interest., (Copyright: © 2020 Indian Journal of Nephrology.)

Background: Acute kidney injury (AKI) frequently co-prevails with acute coronary syndromes (ACS), which could improve post percutaneous coronary intervention (PCI). We sought to evaluate the impact of PCI on post-procedural renal function in patients with impaired baseline serum creatinine (Cr)., Methods: Retrospective evaluation of 185 patients undergoing PCI with impaired basal serum Cr (≥ 1.5 mg/dl) was done, including 88 (47.5%) patients with recent ACS (≤2 weeks old) in group I and 97 (52.4%) patients in group II (stable angina or ACS >2 weeks old). Patients were classified into worsening or improving renal function based on a corresponding increase or decrease of ≥0.5 mg/dl (ΔCr) in serum Cr 24-48 h post PCI. ΔCr < 0.5 mg/dl was termed as no change., Results: A trend towards improving renal function was seen in the study cohort (mean serum Cr: 2.37 ± 1.25 mg/dl vs 2.28 ± 1.59 mg/dl); (p = 0.09) with decrease in group I from 2.28 ± 1.09 mg/dl to 2.12 ± 1.44 mg/dl (p = 0.03) and in group II from 2.45 ± 1.38 mg/dl to 2.43 ± 1.71 mg/dl (p = 0.81). Post PCI, worsening occurred in 20/185 (10.8%) patients in the total study cohort, 5/88 (5.6%) in group I and 15/97 (15.4%) in group II (p = 0.03). Improvement in serum Cr was seen in 49/185 (26.4%) in the total study cohort, 30/88 (34.1%) in group I and 19/97 (19.6%) patients in group II (p = 0.03)., Conclusion: - Post PCI, only a small proportion of patients with impaired baseline creatinine showed worsening in renal function. Improved renal function was observed in at least one-third of the patients with recent ACS., Competing Interests: Declaration of competing interest None., (Copyright © 2020 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.)

Objective: Postcontrast acute kidney injury (PC-AKI) is a dreaded complication of peripheral vascular interventions (PVIs) that depends on the volume of contrast administered as well as a patient's baseline kidney function. However, there is currently no guidance on the volume of contrast that is considered safe especially for patients with advanced chronic kidney disease (CKD). This study aims to characterize the incidence, risk factors for, and outcomes after PC-AKI and define thresholds of safety for contrast volume., Methods: The Vascular Quality Initiative files for PVI (2010-2018) were reviewed. Patients on dialysis, with renal transplants, or who developed a bleeding complication were excluded. Only records with complete data on baseline creatinine, contrast volume, and PC-AKI (creatinine increase of ≥0.5 mg/dL, or new dialysis requirement) were included. The cumulative incidence of PC-AKI with contrast volume at each stage of CKD was derived. A safe threshold for contrast volume was defined as the volume at which the cumulative incidence of PC-AKI is 0.5% or less. Multivariable logistic regression was used to define risk factors for PC-AKI, and survival analysis was performed using Kaplan-Meier and multivariable Cox proportional hazards regression., Results: A total of 53,780 procedures were included. There were 16,062 patients (29%) with normal kidney function or CKD1, 21,769 (39%) with CKD2, 14,234 (25%) with CKD3, 1471 (3%) with CKD4, and 199 (<1%) with CKD5. The incidence of PC-AKI was 0.9% and increased with each stage of CKD (CKD1, 0.39%; CKD2, 0.45%; CKD3, 1.5%; CKD4, 4.3%; and CKD5, 7.5%). The safe thresholds for contrast volume for advanced CKD were 50, 20, and 9 mL for CKD3, CKD4, and CKD5, respectively. Regression analysis demonstrated that white race (odds ratio [OR], 0.67; 95% confidence interval [CI], 0.54-0.82) and elective surgery (OR, 0.77; 95% CI, 0.62-0.95) were associated with decreased risk of PC-AKI, whereas inpatient status (OR, 14.5; 95% CI, 9.97-21.2), diabetes (OR, 1.27; 95% CI, 1.02-1.58), advanced CKD (CKD3: OR, 3.65; 95% CI, 2.68-4.98; CKD4: OR, 6.98; 95% CI, 4.72-10.3; CKD5: OR, 8.94; 95% CI, 4.53-17.6), critical limb ischemia (OR, 1.51; 95% CI, 1.14-2.00), acute limb ischemia (OR, 2.47; 95% CI, 1.70-3.59), and contrast-to-eGFR ratio (CGR) (2 ≤ CGR < 3: OR, 1.33; 95% CI, 1.02-1.74; 3 ≤ CGR < 4: OR, 1.90; 95% CI, 1.32-2.75; CGR ≥ 4: OR, 1.79; 95% CI, 1.18-2.70) were significantly associated with increased risk for PC-AKI. Patients who developed PC-AKI had worse in-hospital (16.1% vs 0.45%; P < .01) mortality and long-term survival (log-rank P < .01) compared with those without PC-AKI., Conclusions: PVI are associated with low risk of PC-AKI that significantly increases when patients with advanced CKD undergo high acuity cases. Given the strong association with short-term and long-term mortality, risk of PC-AKI should be minimized by using safe thresholds of contrast volume., (Copyright © 2019 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.)

Contrast-induced acute kidney injury (CI-AKI) is a common complication after intravascular injection of iodinated contrast media, and it is associated with a prolonged in-hospital stay and unfavorable outcome. CI-AKI occurs in 5% to 20% among hospitalized patients. Its diagnosis relies on the increase in serum creatinine levels, which is a late biomarker of kidney injury. Novel and early serum and urinary biomarkers have been identified to detect kidney damage before the expected serum creatinine increase., (Copyright © 2020 Elsevier Inc. All rights reserved.)

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.

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., (© 2019 The Author(s) Published by S. Karger AG, Basel.)

Objective: This study aims to investigate the changes in renal function and levels of urinary biomarkers before and after cardiac angiography in children with congenital heart disease (CHD)., Setting: Children with CHD are at a risk for kidney injury during contrast exposure in cardiac angiography., Outcome Measures: We measured urinary protein, albumin, N-acetyl-β-D-glucosaminidase (NAG), β2-microglobulin (BMG), and liver-type fatty acid-binding protein (L-FABP) levels, as well as serum creatinine and cystatin C levels, before and after cardiac angiography in 33 children with CHD., Results: No significant decrease was noted in either the creatinine-based or cystatin C-based estimated glomerular filtration rate at 24 hours after angiography compared with that before angiography. Urinary protein, NAG, BMG, and L-FABP levels were significantly increased at 24 hours after angiography, all of which returned to baseline levels at more than 7 days after angiography. An increase in urinary level of protein, albumin, NAG, or BMG was mostly associated with increased urinary L-FABP level. An increase in both urinary BMG and L-FABP, but not that in urinary L-FABP alone, was associated with increased levels of urinary protein and NAG, as well as the greater dose of contrast media., Conclusions: Transient increases of kidney injury biomarkers following cardiac angiography are not necessarily associated with the impairment of renal function in a short time period; however, the increase in urinary protein, albumin, NAG, or BMG level may indicate greater stresses to the kidneys than the increase in urinary L-FABP alone in children with CHD., (© 2019 Wiley Periodicals, Inc.)

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., (© 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group on behalf of Greater Baltimore Medical Center.)

Background: Although some strategies are used for prophylaxis of contrast induced nephropathy, their efficacy is not fully established. Sarpogrelate can relieve vasospasm and have anti-inflammatory action. This study examined whether sarpogrelate reduces the incidence of contrast induced nephropathy (CIN) or subsequent renal impairment during four weeks after coronary angiography compared with a control group., Methods: Seventy-four participants with chronic renal failure were randomly assigned to the sarpogrelate or control group. Patients assigned to the sarpogrelate group received oral saporogelate from 24 hours before contrast exposure up to one month after contrast exposure. The primary outcome of this study was the incidence of CIN within 48 hours after exposure to the contrast agent., Results: Thirty-one subjects in the control group and 35 subjects in the sarpogrelate group were used for the analysis. Cumulative CIN occurred numerically more at 48 hours in the sarpogrelate group and less at one month without statistical significance (11.4% vs. 6.5% at 48 hours and 11.4% vs. 16.1% at one month, respectively). Baseline renal function was similar in both groups, but the estimated glomerular filtration rate (eGFR) was lower in the sarpogrelate group at 12 and 48 hours compared with the control group (45.6 vs. 54.7 mL/min/1.73m²; P = 0.023 and 39.9 vs. 50.6 mL/min/1.73m²; P = 0.020, respectively). At one month, the eGFR became comparable between the two groups because the eGFR was aggravated in the control group and maintained in the sarpogrelate group., Conclusion: This study failed to demonstrate that sarpogrelate has a renoprotective effect against contrast induced acute kidney injury., Trial Registration: ClinicalTrials.gov Identifier: NCT01165567., Competing Interests: The authors have no potential conflicts of interest to disclose., (© 2019 The Korean Academy of Medical Sciences.)

Purpose: Contrast-induced acute kidney injury (CI-AKI) is a common and potentially serious complication of percutaneous coronary interventions (PCI). In this study, we tested the hypothesis whether serum and urinary hepcidin could represent early biomarkers of CI-AKI in patients with normal serum creatinine undergoing PCI. In addition, we assessed serum and urinary neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, eGFR and serum creatinine in these patients., Methods: Serum and urinary hepcidin and NGAL, serum cystatin C, were evaluated before, and after 2, 4, 8, 24 and 48 h after PCI using commercially available kits. Serum creatinine was assessed before, 24 and 48 h after PCI., Results: We found a significant rise in serum hepcidin as early as after 4 and 8 h when compared to the baseline values. Serum NGAL increased after 2, 4 and 8 h, and in urinary NGAL after 4, 8 and 24 h after PCI. We found a significant fall in urinary hepcidin after 8 and 24 h after PCI. Serum cystatin C increased significantly 8 h after PCI, reaching peak 24 h after PCI and then decreased after 48 h. The prevalence of CI-AKI was 8%. Urine hepcidin was significantly lower 8 and 24 h after PCI in patients with CI-AKI, while serum and urine NGAL were significantly higher in patients with CI-AKI., Conclusions: Our findings suggest that serum hepcidin might be an early predictive biomarker of ruling out CI-AKI after PCI, thereby contributing to early patient risk stratification. However, our data needs to be validated in large cohorts with various stages of CKD., (Copyright © 2018 Medical University of Bialystok. Published by Elsevier B.V. All rights reserved.)

Contrast nephropathy (CN) is acute kidney injury (AKI) that occurs within 24 to 72 hours of iodinated contrast medium (ICM) administration. Mechanisms of CN include hyperviscosity, free radical formation, and renal medullary oxygen supply/demand mismatch. Although risk factors for CN have been identified, it remains uncertain whether ICM causes or is simply associated with AKI. The cornerstones of CN prevention are using low-osmolal ICM, intravenous hydration, and statins, especially in patients with chronic kidney disease. With appropriate CN risk mitigation, coronary angiography and intervention should not be routinely withheld from patients with acute coronary syndromes., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Different methods to prevent contrast-associated acute kidney injury (CA-AKI) have been proposed in recent years. We performed a mixed treatment comparison to evaluate and rank suggested interventions., Methods: A comprehensive Systematic review and a Bayesian network meta-analysis of randomised controlled trials was completed. Results were tabulated and graphically represented using a network diagram; forest plots and league tables were shown to rank treatments by the surface under the cumulative ranking curve (SUCRA). A stacked bar chart rankogram was generated. We performed main analysis with 200 RCTs and three analyses according to contrast media and high or normal baseline renal profile that includes 173, 112 & 60 RCTs respectively., Results: We have included 200 trials with 42,273 patients and 44 interventions. The primary outcome was CI-AKI, defined as ≥25% relative increase or ≥ 0.5 mg/dl increase from baseline creatinine one to 5 days post contrast exposure. The top ranked interventions through different analyses were Allopurinol, Prostaglandin E1 (PGE1) & Oxygen (0.9647, 0.7809 & 0.7527 in the main analysis). Comparatively, reference treatment intravenous hydration was ranked lower but better than Placebo (0.3124 VS 0.2694 in the main analysis)., Conclusion: Multiple CA-AKI preventive interventions have been tested in RCTs. This network evaluates data for all the explored options. The results suggest that some options (particularly allopurinol, PGE1 & Oxygen) deserve further evaluation in a larger well-designed RCTs.

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.

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&#95;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., Systematic Review Registration: PROSPERO CRD42016033178.

Contrast-induced acute kidney injury is a phenomenon that has been extensively studied throughout the years. There is a large volume of literature documenting this risk, and most radiology departments and radiologists use this information when making decisions regarding contrast administration. A review of the current information on the topic of contrast-induced acute kidney injury is necessary to ensure that the risks of intravenous contrast are properly weighed against the benefits of a contrast-enhanced computed tomography scan., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Acute kidney injury causes great morbidity and mortality in both the community and hospital settings. Understanding the etiological factors and the pathophysiological principles resulting in acute kidney injury is essential in prompting appropriate therapies. Recently hyperuricemia has been recognized as a potentially modifiable risk factor for acute kidney injury, including that associated with cardiovascular surgery, radiocontrast administration, rhabdomyolysis, and associated with heat stress. This review discussed the evidence that repeated episodes of acute kidney injury from heat stress and dehydration may also underlie the pathogenesis of the chronic kidney disease epidemic that is occurring in Central America (Mesoamerican nephropathy). Potential mechanisms for how uric acid might contribute to acute kidney injury are also discussed, including systemic effects on renal microvasculature and hemodynamics, and local crystalline and noncrystalline effects on the renal tubules. Pilot clinical trials also show potential benefits of lowering uric acid on acute kidney injury associated with a variety of insults. In summary, there is mounting evidence that hyperuricemia may have a significant role in the development of acute kidney injury. Prospective, placebo controlled, randomized trials are needed to determine the potential benefit of uric acid lowering therapy on kidney and cardio-metabolic diseases.

Background: Contrast-induced nephropathy (CIN) in native kidneys is associated with a significant increase in mortality and morbidity. Data regarding CIN in renal allografts are limited, however. We retrospectively studied CIN in renal allografts at our institution: its incidence, risk factors, and effect on long-term outcomes including allograft loss and death., Methods: One hundred thirty-five renal transplant recipients undergoing 161 contrast-enhanced computed tomography (CT) scans or coronary angiograms (Cath) between years 2000 and 2014 were identified. Contrast agents were iso- or low osmolar. CIN was defined as a rise in serum creatinine (SCr) by >0.3 mg/dl or 25% from baseline within 4 days of contrast exposure. After excluding 85 contrast exposures where patients had no SCr within 4 days of contrast administration, 76 exposures (CT: n  = 45; Cath: n  = 31) in 50 eligible patients were analyzed. Risk factors assessed included demographics, comorbid conditions, type/volume of contrast agent used, IV fluids, N -acetylcysteine administration, and calcineurin inhibitor use. Bivariate and multivariable analyses were used to assess the risk of CIN., Results: Incidence of CIN was 13% following both, CT (6 out of 45) and Cath (4 out of 31). Significant bivariate predictors of CIN were IV fluid administration ( p  = 0.05), lower hemoglobin ( p  = 0.03), and lower albumin ( p  = 0.02). In a multivariable model, CIN was predicted by N -acetylcysteine ( p  = 0.03) and lower hemoglobin ( p  = 0.01). Calcineurin inhibitor use was not associated with CIN. At last follow-up, CIN did not affect allograft or patient survival., Conclusion: CIN is common in kidney transplant recipients, and there is room for quality improvement with regards to careful renal function monitoring post-contrast exposure. In our study, N -acetylcysteine exposure and lower hemoglobin were associated with CIN. Calcineurin inhibitor use was not associated with CIN. Our sample size is small, however, and larger prospective studies of CIN in renal allografts are needed.

Contrast-induced acute kidney injury (CI-AKI) is one of the most common causes of AKI in clinical practice. CI-AKI has been found to be strongly associated with morbidity and mortality of the patients. Furthermore, CI-AKI may not be always reversible and it may be associated with the development of chronic kidney disease. Pathophysiology of CI-AKI is not exactly understood and there is no consensus on the preventive strategies. CI-AKI is an active research area thus clinicians should be updated periodically about this topic. In this review, we aimed to discuss the indications of contrast-enhanced imaging, types of contrast media and their impact on nephrotoxicity, major pathophysiological mechanisms, risk factors and preventive strategies of CI-AKI and alternative non-contrast-enhanced imaging methods., Competing Interests: Conflict-of-interest statement: Authors declare no conflict of interests for this article.

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., (Copyright © 2016 John Wiley & Sons, Ltd.)

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 allopurinol (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 allopurinol in the prevention of contrast nephropathy. However, only allopurinol was superior to placebo. In our study, hyperuricemia and baseline serum creatinine were the only risk factors associated with CIN., Competing Interests: There are no conflicts of interest.

Background: Percutaneous coronary intervention (PCI) use is low in the setting of stable symptomatic angina in individuals with advanced chronic kidney disease (CKD) despite high cardiovascular risk in this population, and PCI is frequently deferred out of concern for precipitating dialysis therapy. Whether this is appropriate is uncertain, and patient-centered data comparing the relative risks and benefits of continued medical therapy versus PCI in patients with advanced CKD and stable angina are scarce., Study Design: Decision analysis., Setting & Population: Hypothetical cohort of individuals with advanced CKD (stages 4-5 with estimated glomerular filtration rates ≤ 20mL/min/1.73m 2 ) and stable angina., Model, Perspective, & Timeline: A Markov model with a Monte Carlo simulation through 12 cycles, that is, 3 years of 3-month intervals, with 10,000 microsimulations predicted mean quality-adjusted life-years., Intervention: PCI first, medical management, or dialysis (hemodialysis [HD]) followed by PCI., Outcomes: Outcomes modeled were progression to HD therapy (for those not assigned to the preemptive HD strategy), catheter infection, and death., Results: Our analysis showed mean quality-adjusted life-years of 1.103 ± 0.69 for PCI first, 1.088±0.70 for medical management, and 0.670±0.58 for HD followed by PCI. Probabilistic sensitivity analysis found PCI as the preferred strategy > 60% of the time., Limitations: Values for probabilities and utilities were estimated and/or derived from multiple sources that were not uniform in their populations in terms of age, comorbid condition burden, and degree of kidney failure, and several simplifying assumptions were made., Conclusions: Our analysis demonstrates that quality-adjusted life expectancy is similar for the PCI first and medical management strategies in patients with advanced CKD with stable angina and that the decision depends on patient preferences other than those incorporated in our model. Both strategies are superior to preemptive dialysis., (Copyright © 2016 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

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, I 2 = 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.

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. Further in vivo and in vitro studies are required.

Introduction: Although contrast induced nephropathy (CIN) is a well-known complication of radiocontrast media administration among patients with underlying renal insufficiency, however the data about CIN among patients with normal renal function are few and it seems that CIN often remained under-diagnosed among these patients., Objectives: The aim of present study was evaluation of CIN in diabetic and nondiabetic patients with normal renal function undergoing coronary angiography., Patients and Methods: This cross-sectional and prospective study has conducted on patients with normal renal function candidate for diagnostic coronary angiography at Imam hospital, Ahvaz, Iran from October 2010 to February 2011. CIN defined as an increase in serum creatinine (sCr) >0.5 mg/dL after two days of contrast administration. A standardized questionnaire was used to collect demographics, clinical and laboratory data., Results: A total of 254 patients (140 males and 114 Females with mean age of 56.6 ± 11.9 years) were included in the study. Of them, 60 patients (23.6%) had congestive heart failure (CHF) and 57 patients (22.4%) had diabetes mellitus (DM). The mean sCr levels before contrast administration in men and women were 1.05 ± 0.22 and 0.93 ± 0.17 mg/dL respectively. In overall CIN occurred in 27 patients (10.6%) with no difference between males and females (P = 0.386) and in patients with or without CHF (P = 0.766). There was a significant association between CIN and DM (P = 0.001) and mean volume of contrast administration (P = 0.001)., Conclusion: Although CIN is a common problem in patients with diabetic nephropathy undergoing coronary angiography, diabetic patients without diabetic nephropathy and also patients without DM who had normal renal function are also at risk of contrast nephropathy.

Transjugular intrahepatic portosystemic shunts (TIPS) have been used for almost 40 years as a safe and effective alternative to surgical shunts, mostly in the setting of portal hypertension. Well described procedural complications include hepatic encephalopathy, hemorrhage, liver infarction and failure. The risk of post procedural acute kidney injury (AKI) associated with intraprocedural intravenous contrast administration has not been evaluated. Using a retrospective chart review of all consecutive patients undergoing a TIPS procedure as part of routine clinical care between 2001 and 2011, we examined whether the volume of administered intravenous contrast was associated with AKI. Of 163 patients who had a TIPS procedure, 16% developed AKI as defined by a 0.3 mg/dl increase in serum creatinine within 48 h of the procedure. In adjusted analysis, a 50 ml increase of intravenous contrast was associated with a 1.27 (95% CI 1.01-1.60), p = 0.04 increased risk of AKI. Baseline serum creatinine was also associated with post procedural AKI; a 0.1 mg/dl increase in creatinine was associated with a 1.17 (1.04-1.31), p = 0.008 risk. In patients with underlying kidney dysfunction, a 50 ml increase of intravenous contrast was associated with a 1.63 (1.20-2.31), p = 0.003 adjusted risk of AKI. In conclusion, intravenous contrast administered during a TIPS procedure is associated with an increased risk of AKI, particularly in patients with impaired renal function at baseline.

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., (© 2015 World Stroke Organization.)

We conducted a pooled analysis of clinical trials comparing intravenous Fenoldopam (FP) with Saline/Placebo/N-acetyl cysteine (NAC) for the prevention of contrast-induced nephropathy (CIN). Five studies were eligible. Quantitative analyses were done with Review Manager (RevMan version 5.2.). A total of 85 out of 353 patients in Fenoldopam group while 73 among 366 in the control group were affected due to CIN. The risk ratio for the development of CIN in the Fenoldopam group was 1.19 compared to the control group. This was not statistically significant. Fenoldopam is no better than Placebo/Saline or NAC in preventing CIN, but more studies are required., (Copyright © 2015 Elsevier Inc. All rights reserved.)