Contrast-induced Acute Kidney Injury Research Articles

Neutrophil gelatinase-associated lipocalin (NGAL) levels for early prediction and ruling out future contrast nephropathy in patients undergoing primary coronary intervention

Abstract Funding Acknowledgements None. Background Neutrophil gelatinase-associated lipocalin (NGAL), is an early marker of acute kidney injury(AKI) . We aimed to investigate the diagnostic utility of sequential NGAL measurements for both prediction and ruling out of contrast induced AKI (CI-AKI) among patients with ST segment elevation (STEMI) undergoing primary coronary intervention (PCI). Methods We included 133 patients with STEMI treated with PCI. Blood samples for plasma NGAL were drawn immediately before PCI (NGAL 0) and 24 hours after PCI (NGAL 24). Optimal threshold for the development of CI-AKI were determined using receiver operating characteristic curves (ROC). Patients were also assessed for the dynamics between NGAL 0 and NGAL 24 levels. Results Mean age was 62 ±13 years and 78% were men, and a total of 20 (15%) developed CI-AKI . Patients with CI-AKI demonstrated higher plasma NGAL 0 levels (164 ± 42 vs. 95 ± 30 ng/mL; p < 0.001) as well as NGAL 24 levels (142 ± 41 vs. 93 ± 36 ng/mL; p < 0.001). There were no significant changes between NGAL 0 & 24 hours within the 2 groups( figure 1). According to the ROC curve analysis (figure 2), the optimal NGAL 0 level for CI-AKI prediction was >125 ng/mL (AUC 0.841, 95% CI 0.801–0.961, p < 0.001), with a sensitivity of and specificity of 70% and 84% respectively, while the negative predictive value of NGAL 0<125 ng/mL was 94%. Conclusions Among STEMI patients, NGAL levels before primary PCI may be utilized both for ruling out and for the prediction of CI-AKI.NGAL 0 vs 24 according to CI-AKINGAL AUC

Layer-by-Layer Assembly of Renal-Targeted Polymeric Nanoparticles for Robust Arginase-2 Knockdown and Contrast-Induced Acute Kidney Injury Prevention.

The mitochondrial enzyme arginase-2 (Arg-2) is implicated in the pathophysiology of contrast-induced acute kidney injury (CI-AKI). Therefore, Arg-2 represents a candid target for CI-AKI prevention. Here, layer-by-layer (LbL) assembled renal-targeting polymeric nanoparticles are developed to efficiently deliver small interfering RNA (siRNA), knockdown Arg-2 expression in renal tubules, and prevention of CI-AKI is evaluated. First, near-infrared dye-loaded poly(lactic-co-glycolic acid) (PLGA) anionic cores are electrostatically coated with cationic chitosan (CS) to facilitate the adsorption and stabilization of Arg-2 siRNA. Next, nanoparticles are coated with anionic hyaluronan (HA) to provide protection against siRNA leakage and shielding against early clearance. Sequential electrostatic layering of CS and HA improves loading capacity of Arg-2 siRNA and yields LbL-assembled nanoparticles. Renal targeting and accumulation is enhanced by modifying the outermost layer of HA with a kidney targeting peptide (HA-KTP). The resultant kidney-targeting and siRNA loaded nanoparticles (PLGA/CS/HA-KTP siRNA) exhibit proprietary accumulation in kidneys and proximal tubular cells at 24 h post-tail vein injection. In iohexol-induced in vitro and in vivo CI-AKI models, PLGA/CS/HA-KTP siRNA delivery alleviates oxidative and nitrification stress, and rescues mitochondrial dysfunction while reducing apoptosis, thereby demonstrating a robust and satisfactory therapeutic effect. Thus, PLGA/CS/HA-KTP siRNA nanoparticles offer a promising candidate therapy to protect against CI-AKI.

Berberine alleviated contrast-induced acute kidney injury by mitophagy-mediated NLRP3 inflammasome inactivation in a mice model

The incidence of contrast-induced acute kidney injury (CI-AKI) has escalated to become the third most prevalent cause of hospital-acquired AKI, with a lack of efficacious interventions. Berberine (BBR) possesses diverse pharmacological effects and exhibits renoprotective properties; however, limited knowledge exists regarding its impact on CI-AKI. Therefore, our study aimed to investigate the protective effects and underlying mechanisms of BBR on CI-AKI in a mice model, focusing on the nucleotide-binding oligomerization domain-like pyrin domain-containing protein 3 (NLRP3) inflammasome and mitophagy. The CI-AKI mice model was established by administering NG-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg), indomethacin (10 mg/kg), and iohexol (11 g/kg) following water deprivation. A pretreatment of 100 mg/kg of BBR was orally administered to the mice for two weeks. Renal injury markers, damage-associated molecular patterns (DAMPs), renal histopathology, mitochondrial morphology, autophagosomes, and potential mechanisms were investigated. BBR effectively reduced levels of renal injury biomarkers such as serum cystatin C, urea nitrogen, and creatinine, downregulated the protein level of kidney injury molecule 1 (KIM1), and mitigated renal histomorphological damage. Moreover, BBR reduced DAMPs, including high mobility group box-1 (HMGB1), heat shock protein 70 (HSP70), and uric acid (UA). It also alleviated oxidative stress and inflammatory factors such as monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β). Furthermore, the activation of NLRP3 inflammasome was attenuated in the BBR pretreatment group, as evidenced by both mRNA and protein levels. Electron microscopy and western blotting examination revealed that BBR mitigated mitochondrial damage and enhanced mitophagy. Additionally, BBR increased the P-AMPK/AMPK ratio. These findings indicated that BBR exerted a protective effect against CI-AKI by suppressing NLRP3 inflammasome activation and modulating mitophagy, providing a potential therapeutic strategy for its prevention.

B-34 | Effects of Artificial Intelligence Clinical Decision Support Tools (Terumo Health Outcomes, ePRISM) on Contrast Induced Acute Kidney Injury (CI-AKI) in Patients Undergoing Percutaneous Coronary Intervention (PCI)

B-34 | Effects of Artificial Intelligence Clinical Decision Support Tools (Terumo Health Outcomes, ePRISM) on Contrast Induced Acute Kidney Injury (CI-AKI) in Patients Undergoing Percutaneous Coronary Intervention (PCI)

NMR-based metabolomic analysis of plasma from elderly patients with CVD before and after using contrast media

Contrast-induced acute kidney injury (CI-AKI) is a growingly common kidney problem caused by medical procedures involving contrast media (CM), especially in older patients with existing health issues. It is crucial to pinpoint potential biomarkers for the early detection of CI-AKI. Previously, we observed that iodixanol affects glucose, choline, and glutathione metabolism in endothelial cells under laboratory conditions. In this study, we used 1H NMR-based metabolomics to examine the metabolic changes in the blood plasma of elderly patients with cardiovascular disease (CVD) before and after receiving iodixanol. We identified altered metabolites in plasma 24 and 48 h after iodixanol injection compared to levels before injection. Notably, metabolites such as glucose, unsaturated fatty acids (UFA), low-density lipoprotein (LDL)/very low-density lipoprotein (VLDL), pyruvate, choline, and glycine showed potential as biomarkers at 24 h post-injection compared to levels before injection. Similarly, glucose, pyruvate, lactate, choline, and glycine in plasma could serve as potential biomarkers at 48 h post-injection. Iodixanol notably affected pathways related to glycolysis, fatty acid breakdown, and amino acid metabolism according to our metabolic pathway analysis. The altered levels of specific metabolites in plasma could be indicative of CM-induced kidney injury. Overall, this research aids in understanding the physiological mechanisms involved and in identifying early biomarkers and prevention strategies for CI-AKI.

Effect of SGLT2 Inhibitors on Post-PCI Outcomes after Acute Myocardial Infarction in Diabetic Patients: A Systematic Review and Meta-Analysis

Background: Acute myocardial infarction (AMI) is related with poor outcomes in patients with diabetes mellitus (DM). Whether diabetic patients with AMI undergoing percutaneous coronary intervention (PCI) benefit from sodium–glucose cotransporter 2 inhibitors (SGLT2i) in terms of cardiovascular mortality, myocardial damage, and left ventricular function is unclear. Methods: Through a comprehensive search in PubMed, EMBASE, and Web of science databases from January 2018 to September 2023, randomized controlled trials were performed to compare SGLT2i with other oral antidiabetic medications in diabetic patients with AMI undergoing PCI. Cardiovascular mortality constituted the primary outcome. Secondary outcomes were high-sensitivity troponin I (hs-TnI) levels, left ventricular ejection fraction (LVEF), and contrast-induced acute kidney injury (CI-AKI). Results: SGLT2i significantly reduced cardiovascular mortality risk versus other antidiabetic agents (hazard ratio (HR): 0.35, 95% confidence interval (CI): 0.21–0.58, p < 0.0001). SGLT2i also lowered hs-TnI levels across all time points (mean difference: –2931 ng/L, p < 0.001). After adjustment for publication bias, this difference was no longer significant. However, peak hs-TnI levels remained significantly lower with SGLT2i (mean difference: –3836 ng/L, p < 0.001). Finally, SGLT2i improved LVEF versus comparators, with a mean difference of –5.00% (95% CI: –6.69 to –3.31, p < 0.001) at hospital discharge. SGLT2i was also associated with 60% lower odds of CI-AKI (odds ratio (OR): 0.40, 95% CI: 0.22–0.75, p = 0.004). Conclusions: Compared with other antidiabetic medications, SGLT2i may lower cardiovascular mortality, infarct size, and prevent left ventricle (LV) systolic dysfunction in diabetic patients with AMI undergoing PCI. The use of SGLT2i in this high-risk group is supported by these findings.

Value of Soluble Urokinase-Type Plasminogen Activator Receptor in Contrast-Induced Acute Kidney Injury in Percutaneous Coronary Intervention Patients

Value of Soluble Urokinase-Type Plasminogen Activator Receptor in Contrast-Induced Acute Kidney Injury in Percutaneous Coronary Intervention Patients

Contrast-Induced Acute Kidney Injury in Patients with Heart Failure on Sodium-Glucose Cotransporter-2 Inhibitors Undergoing Radiocontrast Agent Invasive Procedures: A Propensity-Matched Analysis.

(1) Background: This single-center retrospective study aimed to evaluate whether sodium-glucose cotransporter-2 inhibitors (SGLT2-i) therapy may have a nephroprotective effect to prevent contrast-induced acute kidney injury (CI-AKI) in patients with heart failure (HF) undergoing iodinated contrast medium (ICM) invasive procedures. (2) Methods: The population was stratified into SGLT2-i users and SGLT2-i non-users according to the chronic treatment with gliflozins. The primary endpoint was CI-AKI incidence during hospitalization. Secondary endpoints were all-cause mortality and the need for continuous renal replacement therapy (CRRT). (3) Results: In total, 86 patients on SGLT2-i and 179 patients not on SGLT2-i were enrolled. The incidence of CI-AKI in the gliflozin group was lower than in the non-user group (9.3 vs. 27.3%, p < 0.001), and these results were confirmed after propensity matching analysis. Multivariable logistic regression showed that only SGLT2-i treatment was an independent preventive factor for CI-AKI (OR: 0.41, 95% CI: 0.16-0.90, p = 0.045). The need for CRRT was reported only in five patients in the non-SGLT2-i-user group compared to zero patients in the gliflozin group (p = 0.05). (4) Conclusions: SGLT2-i therapy was associated with a lower risk of CI-AKI in patients with HF undergoing ICM invasive procedures.

Acute Kidney Injury After Percutaneous Coronary Intervention Guided by Intravascular Ultrasound.

Purpose We investigated the impact of intravascular ultrasound guidance on reducing the incidence of contrast-induced acute kidney injury (CI-AKI) in patients undergoing percutaneous coronary intervention (PCI). Methods Ninety-nine patients were enrolled in this prospective cohort who were not randomly assigned to angiography-guided percutaneous coronary intervention or intravascular ultrasound-guided percutaneous coronary intervention. The patients were hospitalized at the Vietnam National Heart Institute - Bach Mai Hospital between 2019 and 2020. Acute kidney injury incidence during hospitalization was the primary endpoint. Results A total of 99 patients were divided into two groups: the intravascular ultrasound-guided group (33 participants) and the angiography-guided group (66 participants). The mean ± SD contrast volume of each group was 95.2 ± 37.1 mL and 133.0 ± 36.0 mL for the ultrasound-guided and angiography-guided groups, with P < 0.0001. Intravascular imaging-guided percutaneous coronary intervention (IVUS-guided PCI) was associated with reduced acute kidney injury incidence during hospitalization: 0.0% vs. 12.12% and P = 0.049. Conclusions Intravascular ultrasound is a safe imaging tool that guides percutaneous coronary intervention and significantly reduces the rate of acute kidney injury compared to angiography alone. Patients who have a high chance of experiencing acute kidney injury benefit from using intravascular ultrasound.

Biomarkers in Contrast-Induced Acute Kidney Injury: Towards A New Perspective.

Contrast-Induced Acute Kidney Injury (CI-AKI) remains a frequent iatrogenic condition since radiological procedures using intra-vascular iodinated contrast media (CM) are being widely administered for diagnostic and therapeutic purposes. Despite the improvement of the medical healthcare system worldwide, CI-AKI is still associated with direct short-term and indirect long-term outcomes including increased morbidity and mortality, especially in patients with underlying pre-existing renal function impairment, cardiovascular disease, or diabetes that could rapidly progress into Chronic Kidney Disease. Although the RIFLE (Risk, Injury, Failure, Loss, End-Stage Kidney Disease), AKIN (Acute Kidney Injury Network), and KDIGO (Kidney Disease Improving Global Outcomes) clinical criteria and recommendation guidelines are based on traditional "gold standard" biomarkers known as serum creatinine, glomerular filtration rate, and urinary output, new reliable serum and urinary biomarkers are still needed for an effective unified diagnostic strategy for AKI. Starting from previous and recent publications on the benefits and limitations of validated biomarkers responding to kidney injury, glomerular filtration, and inflammation among others, this review unravels the role of new emerging biomarkers used alone or in combination as reliable tools for early diagnosis and prognosis of CI-AKI, taking into account patients and procedures-risk factors towards a new clinical perspective.

High-mobility group box 1 and its related receptors: potential therapeutic targets for contrast-induced acute kidney injury.

Percutaneous coronary intervention (PCI) is a crucial diagnostic and therapeutic approach for coronary heart disease. Contrast agents' exposure during PCI is associated with a risk of contrast-induced acute kidney injury (CI-AKI). CI-AKI is characterized by a sudden decline in renal function occurring as a result of exposure to intravascular contrast agents, which is associated with an increased risk of poor prognosis. The pathophysiological mechanisms underlying CI-AKI involve renal medullary hypoxia, direct cytotoxic effects, endoplasmic reticulum stress, inflammation, oxidative stress, and apoptosis. To date, there is no effective therapy for CI-AKI. High-mobility group box 1 (HMGB1), as a damage-associated molecular pattern molecule, is released extracellularly by damaged cells or activated immune cells and binds to related receptors, including toll-like receptors and receptor for advanced glycation end product. In renal injury, HMGB1 is expressed in renal tubular epithelial cells, macrophages, endothelial cells, and glomerular cells, involved in the pathogenesis of various kidney diseases by activating its receptors. Therefore, this review provides a theoretical basis for HMGB1 as a therapeutic intervention target for CI-AKI.

An Investigation of Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention: A Cross-Sectional Study From Pakistan.

Background and objective Contrast-induced acute kidney injury (CIAKI) is a complicationobserved among individuals undergoing primary percutaneous coronary intervention (PCI) and is associated with high morbidity and mortality rates. It is characterized by an elevation in serum creatinine (SCr) levels >0.5 mg/dl or a 50% relative increase in SCrfrom the baseline value following exposure to contrast within a 48- to 72-hour timeframe, in the absence of any alternative causes foracute kidney injury (AKI). This study aimed to assess the incidence of CIAKI in patients following PCI. Methods This prospective study was conducted from July to December 2022, after obtaining ethical approval from the institutional ethics committee (reference no: 147/LRH/MTI). A total of 159 consecutive patients who met the selection criteria were enrolled. A detailed patient and family history was obtained, and a thorough physical examination was conducted. Baseline tests, including SCr, were performed, with SCr repeated 72 hours post-PCI. All investigations were performed in the affiliated hospital's main laboratory and conducted by the same biochemist. Results The study included 159 patients presenting with myocardial infarction, angina pectoris, or ischemic features on EKG, exercise tolerance test (ETT), or echocardiogram and underwent PCI. The patients had a mean age of 51 ± 9 years, baseline SCr of 0.77 ± 0.41 mg/dl, SCr 72 hours post-procedure of 0.83 ± 0.41 mg/dl, and an average contrast volume of 128.6 ± 63 ml; 87 (55%) patients were male, and 72 (45%) were female. CIAKI was observed in 15 (9.4%) patients. Hypertensionand diabetes mellitus were the most prevalent comorbidities. Male gender, diabetes mellitus, and hypertension had a clinically significant association with the development of CIAKI (p<0.05). ST-elevation myocardial infarction (STEMI) was the predominant clinical presentation in 81 (50.9%) cases. Conclusions This study examines the frequency, risk factors, and associations of CIAKI following PCI at a tertiary care hospital in a low-middle-income country. We believe our findings provide future directions for identifying and minimizing the risk of CIAKI in this patient population.

Effect of Curcuminoids on Contrast-Induced Acute Kidney Injury after Elective Coronary Angiography or Intervention: A Pilot Randomized, Double-Blind, Placebo-Controlled Study.

The role of curcuminoids, a striking antioxidant, in prevention of contrast-induced acute kidney injury (CI-AKI) remains unknown. We aimed to evaluate the efficacy and safety of curcuminoids in preventing CI-AKI in patients undergoing elective coronary angiography (CAG) and/or percutaneous coronary intervention (PCI). We randomized 114 patients who were undergoing elective CAG and/or PCI to receive curcuminoids, 4 g/day (1 day before and 1 day after the procedure, n = 56), or placebo (n = 58). Serum creatinine was assessed at baseline, 12, 24, and 48 h after contrast exposure. The primary endpoint was development of CI-AKI defined as serum creatinine increase ≥0.3 mg/dL within 48 h after contrast exposure. The secondary endpoint was the occurrence of kidney injury defined by &gt;30% increase in urine neutrophil gelatinase-associated lipocalin (NGAL). Baseline characteristics were comparable between the two groups. Seven (12.7%) in curcuminoids group and eight (14.0%) in placebo group developed CI-AKI (p = 0.84). The incidence of increased urine NGAL was comparable in the placebo and curcuminoids group (39.6% vs. 50%, respectively; p = 0.34). None in both groups had drug-related adverse events. This is a pilot study to demonstrate the safety and tolerability of curcuminoids in patients undergoing elective CAG and/or PCI. Curcuminoids have no protective effects against kidney injury after elective CAG and/or PCI.

SGLT2 inhibitors and the risk of contrast-induced acute kidney injury: Time for a PCI Trial?

SGLT2 inhibitors and the risk of contrast-induced acute kidney injury: Time for a PCI Trial?

Letter to the editor regarding ‘Correlation between neutrophil-to-lymphocyte ratio and contrast-induced acute kidney injury and the establishment of machine-learning-based predictive models’

Letter to the editor regarding ‘Correlation between neutrophil-to-lymphocyte ratio and contrast-induced acute kidney injury and the establishment of machine-learning-based predictive models’

Contrast-induced acute kidney injury; possible ameliorative effect of sodium-glucose co-transporter 2 inhibitors

Contrast-associated acute renal injury is a common complication that occurs after the administration of contrast media for diagnostic or therapeutic purposes. It is characterized by a sudden decline in kidney function within 48-72 hours after the administration of contrast media. The incidence of contrast-associated acute renal injury varies depending on the patient’s risk factors and the type and amount of contrast media used. Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a group of antidiabetic drugs that inhibit the reabsorption of glucose in the nephrons, running to raise urinary glucose excretion and improve glycemic control. Recent studies have shown that SGLT2 inhibitors may have a protective effect against contrast-associated acute renal injury. Preventive measures for contrast-associated acute renal injury include hydration, minimizing contrast volume and rate of administration, and avoiding contrast in high-risk patients. The administration of SGLT2 inhibitors may also be a useful preventive measure in patients at risk for contrast-associated acute renal injury.

The use of intravascular contrast media in patients with impaired kidney function - joint clinical practice position statement of the Polish Society of Nephrology and the Polish Medical Society of Radiology.

Radiological procedures utilising intravascular contrast media (ICM) are fundamental to modern medicine, enhancing diagnostics and treatment in diverse medical fields. However, the application of ICM has been constrained in patients with compromised kidney function due to perceived nephrotoxic risks, called contrast-induced nephropathy or contrastinduced acute kidney injury. Historical evidence marked ICM as a possible contributor to kidney damage. This led to restrictive guidelines advocating limited ICM use in patients with impaired renal function, preventing crucial radiographic interventions in patients with acute kidney injury (AKI) and chronic kidney disease. Recent advances challenge these traditional views. In particular, no direct causal relationship has been confirmed between contrast admi-nistration and elevated serum creatinine concentrations in humans. Furthermore, contemporary research models and meta-analyses do not associate AKI with contrast usage. This paper, prepared by a cross-disciplinary team of nephrologists and radiologists, presents updated guidelines for ICM application amid renal function impairments, emphasising the reduced nephrotoxic risks currently understood and loosening the previous restrictive approach in patients with renal dysfunction.

Prevention of Contrast-induced Nephropathy in Patients Undergoing Percutaneous Coronary Intervention.

Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury has varying definitions, but in general, increased serum creatinine level by ≥ 0.3 mg/dL (26.5 µmol/L) or 1.5x of baseline value or urine output <0.5 mL/kg/h within 1-7 days after contrast media (CM) administration can be considered as CIN. CIN is one of the most common complications and is associated with increased mortality in patients undergoing percutaneous coronary intervention (PCI). Thus, risk stratification for CIN should be made and preventive strategies should be employed in which the intensity of the approach must be tailored to patient's risk profile. In all patients, adequate hydration is required, nephrotoxic medications should be discontinued, and pre-procedural high-intensity statin is recommended. In patients with an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2, IV hydration should be started 12 hours pre-procedure up until 12-24 hours after the procedure. Remote ischemic preconditioning may be performed pre-procedurally. Radial first approach for vascular access is recommended. During the procedure, low or iso-osmolar CM should be used and its volume should be limited to eGFR x 3.7. In patients at high risk for CIN, additional contrast-sparing strategies may be applied, such as using a contrast reduction system, 5 Fr catheter with no sideholes, CM dilution, limiting test injection, confirming placement using guidewire, use of stent enhancing imaging technology, using metallic/software roadmap to guide PCI, use of IVUS or dextran-based OCT, and coronary aspiration. A more advanced hydration technique based on central venous pressure, left ventricular end-diastolic pressure, or using furosemide-matched hydration, might be considered.

The Effects of Coenzyme Q10 on Contrast-Induced Acute Kidney Injury in Type 2 Diabetes: A Randomized Clinical Trial.

Contrast-induced acute kidney injury (CI-AKI) is a frequent challenge following the injection of contrast media and its subsequent oxidative stress. The aim of the present study was to evaluate the preventive effects of coenzyme Q10 (Q10), as a mitochondrial-targeted antioxidant in CI-AKI in diabetic patients, who account for a large proportion of angiographic cases. A total of 118 diabetic patients were randomly assigned to receive 120 mg of oral coenzyme Q10 (Q10 group) or placebo (Placebo group) for four days, starting 24 hours before contrast media injection. Blood urea nitrogen (BUN), serum and urinary creatinine, estimated glomerular filtration rate (eGFR), urinary malondialdehyde (UMDA), urinary total antioxidant capacity (UTAC), and urinary mitochondrial to nuclearDNA ratios (mtDNA/nDNA ratio) were evaluated before and after the treatment period. Urine sediments were also evaluated to report the urine microscopy score (UMS).The levels of BUN, serum and urine creatinine, and UMS were similar in the Q10 and placebo groups. EGFR was lower in the Q10 group before the treatment (p=0.013) but not after. The urinary mtDNA/nDNA ratio was 3.05±1.68 and 3.69±2.58 in placebo and Q10 groups, but UTAC was found to be lower in Q10 both before (p=0.006) and after the treatment (p<0.001). The incidence of CI-AKI was 14.40% and the mtDNA/nNDA ratio was similar between CI-AKI and non-CI-AKI patients. In conclusion, Q10 treatment shows no favorable effect on prevention of CI-AKI or a urinary mtDNA/nDNA ratio among diabetic patients.

A Systematic Review of Contrast-Induced Acute Kidney Injury

A Systematic Review of Contrast-Induced Acute Kidney Injury