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Contrast‐induced nephropathy (CIN) is a condition that causes kidney damage in patients receiving angiography with iodine‐based contrast agents. This study investigated the potential protective effects of berberine (BBR) against CIN and its underlying mechanisms. The researchers conducted both in vivo and in vitro experiments to explore BBR's renal protective effects. In the in vivo experiments, SD rats were used to create a CIN model, and different groups were established. The results showed that CIN model group exhibited impaired renal function, severe damage to renal tubular cells and increased apoptosis and ferroptosis. However, BBR treatment group demonstrated improved renal function, decreased apoptosis and ferroptosis. Similar results were observed in the in vitro experiments using HK‐2 cells. BBR reduced ioversol‐induced apoptosis and ferroptosis, and exerted its protective effects through Akt/Foxo3a/Nrf2 signalling pathway. BBR administration increased the expression of Foxo3a and Nrf2 while decreasing the levels of p‐Akt and p‐Foxo3a. In conclusion, this study revealed that BBR effectively inhibited ioversol‐induced apoptosis and ferroptosis in vivo and in vitro. The protective effects of BBR were mediated through the modulation of Akt/Foxo3a/Nrf2 signalling pathway, leading to the alleviation of CIN. These findings suggest that BBR may have therapeutic potential for protecting against CIN in patients undergoing angiography with iodine‐based contrast agents.

Background Ultra‐low contrast administration during coronary angiography has been previously shown to be feasible and safe among patients with stable chronic kidney disease. In the present study, we investigate the safety of ultra‐low contrast coronary angiography in patients with pre‐existing acute kidney injury (AKI). Methods The study was a retrospective single‐center evaluation of hospitalized patients who had AKI and required coronary angiography. Ultra‐low contrast use was defined as ≤18 mL of contrast media. Results The cohort consisted of a case series of eight inpatients with AKI who required coronary angiography. The mean age was 57 (±16) years and half were females. All patients had chronic kidney disease with a mean baseline estimated glomerular filtration rate of 34 (±17) mL/min/1.73 m2. The mean creatinine before angiography was 3 (±1) mg/dL and volume of contrast administered was 14 (±4) mL. One patient had a 0.1 mg/dL increase in creatinine during admission, and no patients had further AKI up to 1‐week postprocedure. Conclusions The current data suggest that ultra‐low contrast coronary angiography can be safely performed in patients with pre‐existing AKI The study should be viewed as hypothesis‐generating due to its small sample size. A larger cohort is required to validate the results. Eight patients who had acute kidney injury (AKI) and an indication for coronary angiography were included. After 24 h of stabile serum creatinine, patients underwent ultra‐low contrast angiography. None of the participants had further AKI postprocedure. This hypothesis‐generating small sample study suggests that ultra‐low contrast coronary angiography can be safely performed in patients with pre‐existing AKI.

An increasing number of diagnostic imaging and interventional procedures require the use of radiographic contrast agents which has led to a parallel increase in the incidence of contrast-induced nephropathy (CIN). CIN is a serious clinical problem associated with increased morbidity and mortality, particularly in patients with chronic renal failure (see the Case Report). A key step to minimize CIN is to identify patients at risk of CIN. The aim of the present review was to summarize the knowledge about the risk factors of CIN, including the review of ultimate clinical research and developments.

This study was to investigate the safety of transarterial chemoembolization (TACE) which required injection of contrast medium on renal function in combined hepatocellular carcinoma and chronic kidney disease (CKD) patients. A total of 265 patients admitted for the first session of TACE were included for analysis. CKD was defined as Cockcroft‐Gault glomerular filtration rate (CG‐GFR) < 60 mL/min/1.73 m2. The odds ratio (OR) and 95% confident interval (CI) were calculated to show the influence of factors on renal function. Overall, 24.07% patients with CKD and 31.21% patients without CKD showed exacerbated renal function at discharge. However, 73.15% patients with CKD and 63.69% patients without CKD showed significantly improved renal function (all p = 0.00001). No significant difference in influence of TACE on renal function between patients with and without CKD (p = 0.20509). Factors to exacerbate the serum creatinine level at the third day after TACE included proteinuria ≥1+ (OR 2.2469, 95% CI = 1.1559–4.3675) and glycated hemoglobin ≥7% (OR 2.0796, 95% CI = 1.0497–4.1200). These factors could be obliterated by admission for more than 3 days after TACE. Serum albumin level <3 g/dL at admission was the only factor to exacerbate renal function at discharge (OR 4.4179, 95% CI = 1.3964–13.9776). In conclusion, TACE exerted same influence on renal function between patients with and without CKD. Most patients showed improved renal function at discharge. Low serum albumin level, proteinuria and poor diabetes mellitus control were factors to exacerbate renal function after TACE.

Background Adequate hydration remains the mainstay of contrast‐induced nephropathy prevention, and nitrates could reduce cardiac preload. Hypothesis This study aimed to explore the adequate hydration with nitrates for patients with chronic kidney disease (CKD) and congestive heart failure (CHF) to reduce the risk of contrast‐induced nephropathy (CIN) and at the same time avoid the acute heart failure. Methods Three hundred and ninty‐four consecutive patients with CKD and CHF undergoing coronary procedures were randomized to either adequate hydration with nitrates (n = 196) or to routine hydration (control group; n = 198). The adequate hydration group received continuous intravenous infusion of isosorbide dinitrate combined with intravenous infusion of isotonic saline at a rate of 1.5 mL/kg/h during perioperative period. The definition of CIN was a 25% or 0.5 mg/dL rise in serum creatinine over baseline. This trial is registered with www.clinicaltrials.gov, number NCT02718521. Results Baseline characteristics were well‐matched between the two groups. CIN occurred less frequently in adequate hydration group than the control group (12.8% vs 21.2%; P = 0.018). The incidence of acute heart failure did not differ between the two groups (8 [4.08%] vs 6[3.03%]; P = 0.599). Cumulative major adverse events (death, myocardial infarction, stoke, hospitalization for acute heart failure) during the 90‐day follow‐up were lower in the adequate hydration with nitrates group (P = 0.002). Conclusions Adequate hydration with nitrates can safely and effectively reduce the risk of CIN in patients with CKD and CHF.

Background Numerous trials have investigated the effect of remote ischemic conditioning (RIC) in preventing contrast‐induced nephropathy (CIN) in patients receiving contrast medium (CM). This meta analysis aims to validate the role of RIC in preventing CIN. Methods We searched the PubMed, EMBASE, and Web of Science databases for eligible randomized controlled trials (RCTs) published before April 27, 2019. Two investigators independently extracted basic characteristics from each study. Odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were used to examine the treatment effect. Results A total of 18 studies comprising 2,503 patients were included in our meta‐analysis. Compared with conventional therapy, RIC significantly reduced the risk of CIN (OR = 0.43, 95% CI: 0.33, 0.56, p < .05). Subgroup analyses showed that the protective effect of RIC was stronger in the low‐osmolar contrast media group (OR = 0.32; 95% CI: 0.23, 0.45, p < .05) and the nondiabetic group (OR = 0.39; 95% CI: 0.29, 0.53 p < .05). RIC also significantly reduced major adverse cardiovascular events within the first 6 months (OR = 0.39; p < .05), but the influence was not present after long‐term follow‐up. Conclusions Our meta‐analysis showed that RIC could effectively reduce CIN risk and decrease the short‐term incidence of relevant adverse events. Furthermore, the effects of CIN are more pronounced in nondiabetic patients and with the use of low‐osmolar contrast medium. This meta‐analysis of small trials suggests a possible protective effect of RIC on contrast‐induced nephropathy and favors the performance of a large randomized trial to further investigate this strategy.

Objective: Promising results of CHA2DS2-VASc score have been reported for the prediction of contrast-induced acute kidney injury (CI-AKI) after percutaneous coronary intervention (PCI). However, data of its predictive strength in the context of primary PCI are not available. Therefore, in this study, we have assessed predictive value of CHA2DS2-VASc score for CI-AKI after primary PCI. Methods: This analytical cross-sectional study was conducted between January 2021 and June 2021 at the National Institute of Cardiovascular Diseases (NICVD), Karachi, Pakistan. Inclusion criteria of the study was consecutive adult patients who had undergone primary PCI. Baseline CHA2DS2-VASc score was calculated, and either a 25% or 0.5 mg/dL increase in post-procedure serum creatinine level as compared to baseline level was categorized as CI-AKI. Results: A total of 691 patients were included, of which 82.1% (567) were male. CI-AKI after primary PCI was observed in 63 (9.1%) patients, out of which 66.7% (42) of patients had CHA2DS2-VASc score of ≥ 2. The area under the curve (AUC) for the score was 0.725 [0.662 to 0.788] with a sensitivity and specificity of 66.7% [63.1% to 70.2%] and 66.7% [53.7% to 78.1%], respectively, at a cut-off value of ≥ 2. In multivariable analysis, left ventricular ejection fraction ≤ 30% and CHA2DS2-VASc ≥ 2 were found to be independent predictors with adjusted odds ratios of 2.19 [1.06– 4.5] and 2.13 [1.13– 4.01], respectively. Conclusion: CHA2DS2-VASc score has a good predictive value for the prediction of CI-AKI after primary PCI. Criteria of CHA2DS2-VASc ≥ 2 can be used for the risk stratification of CI-AKI after primary PCI.

Abstract Aims Data regarding contrast-induced nephropathy (CIN) after cardiac resynchronization therapy (CRT) implant are limited. We aimed to investigate the incidence and determinants of CIN and its impact on CRT response and outcomes. Methods and results Patients who underwent CRT implant were retrospectively analysed, and CIN was defined as an increase of serum creatinine ≥0.3 mg/dL or ≥1.5 times the baseline value. Response to CRT was defined as a reduction of left ventricle end-systolic volume (LVESV) of 15% or the increase of five percentage points in ejection fraction (EF) as assessed by echocardiography at 6 months. Follow-up visits were scheduled at 3, 6, and 12 months. Contrast-induced nephropathy occurred in 13/107 patients (12%). Among baseline clinical, echocardiographic, and laboratory characteristics, only a high baseline serum creatinine was associated with the occurrence of CIN. Symptoms, EF, and LVESV at 6 months improved in both CIN and non-CIN patients, and the rate of responders to CRT was similar. Among responders, at 6 months, those with CIN had significantly lower EF (28.5% vs. 35.7% P = 0.003). At a median follow-up of 112 weeks, 43% of patients experienced a clinical event with similar incidence in CIN and non-CIN patients, and likewise survival was similar. Non-responders to CRT had worse survival while among responders those with CIN had worse survival than non-CIN patients (71% vs. 90%, P = 0.0035). Conclusions The incidence of CIN is rather high. Although CIN does not influence response to CRT overall, however among responders impairs the recovery of EF and survival.

It is occasionally observed that patients without contrast-induced nephropathy (CIN) develop kidney injury within 1-6 months after coronary angiography (CAG), termed delayed CIN or delayed kidney injury (DKI) following CAG. The present study aimed to investigate the associated risk factors of delayed CIN and its possible pathogenesis. Subjects with CAG or coronary stenting from January 2008 to December 2009 were studied. A retrospective survey on DKI after CAG was conducted and the risk factors were analyzed. There were 436 cases receiving CAG with complete medical records enrolled in the present cohort, in which the DKI incidence was 7.1% (31/436). Patients with DKI after CAG exhibited lower hemoglobin (121.2±17.3 vs. 133.8±18.6 g/l), estimated glomerular filtration rate (eGFR; 66.4±30.2 vs. 71.9±28.6 ml/min), higher serum creatinine (110.9±43.2 vs. 91.7±37.6 µmol/l), higher rate of heart failure (22.6 vs. 5.4%) and 300 mg aspirin therapy (29 vs. 5.7%) compared with non-DKI patients (all P<0.05). However, no differences were observed in morbidities of diabetes, hypertension, hyperlipidemia and proteinuria, or in the treatments with angiotensin converting enzyme (ACE) inhibitors/angiotensin II receptor-1 blockers (ARBs), diuretics, statins and other anti-platelets between the two groups (P>0.05). Logistic regression revealed that anemia, heart failure and 300 mg aspirin intake were risk factors of DKI (P<0.05), while the contrast level, isotonic contrast, diabetes, ACE inhibitors/ARBs, eGFR and other factors were not associated with DKI (P>0.05). Heart dysfunction and 300 mg aspirin therapy may contribute to DKI after CAG, and iodinated contrast media administration is not a risk factor.

Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury observed after intravascular administration of contrast media for intravascular diagnostic procedures or therapeutic angiographic intervention. High risk patients including those with chronic kidney disease (CKD), diabetes mellitus with impaired renal function, congestive heart failure, intraarterial intervention, higher volume of contrast, volume depletion, old age, multiple myeloma, hypertension, and hyperuricemia had increased prevalence of CIN. Although CIN is reversible by itself, some patients suffer this condition without renal recovery leading to CKD or even end-stage renal disease which required long term renal replacement therapy. In addition, both CIN and CKD have been associated with increasing of mortality. Three pathophysiological mechanisms have been proposed including direct tubular toxicity, intrarenal vasoconstriction, and excessive production of reactive oxygen species (ROS), all of which lead to impaired renal function. Reports from basic and clinical studies showing potential preventive strategies for CIN pathophysiology including low- or iso-osmolar contrast media are summarized and discussed. In addition, reports on pharmacological interventions to reduce ROS and attenuate CIN are summarized, highlighting potential for use in clinical practice. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating CIN.