Levels of oxidative stress, mitochondrial respiration and mitochondrial dynamics in CKD patients receiving contrast media during PCI. (A) Cellular oxidative stress levels, (B) Mitochondrial oxidative stress levels, (C) ATP production, (D) Basal respiration, (E) Maximal respiration, (F) Spare respiratory capacity, (G) Mitochondrial fission marker (p‐Drp1ser616/Actin) with immunoblot analysis, (H) Mitochondrial fusion marker (Mfn1/Actin) with immunoblot analysis, (I) Mitochondrial fusion marker (OPA1/Actin) with immunoblot analysis. *p < 0.05 vs. baseline. ATP, adenosine triphosphate; CI‐AKI, contrast‐induced acute kidney injury; CKD, chronic kidney disease; DCF, dichlorofluorescein; Drp1, dynamin related protein 1; Mfn1, mitofusin 1; OCR, oxygen consumption rate; OPA1, optic atrophy protein 1; PCI, percutaneous coronary intervention.

Levels of oxidative stress, mitochondrial respiration and mitochondrial dynamics in CKD patients receiving contrast media during PCI. (A) Cellular oxidative stress levels, (B) Mitochondrial oxidative stress levels, (C) ATP production, (D) Basal respiration, (E) Maximal respiration, (F) Spare respiratory capacity, (G) Mitochondrial fission marker (p‐Drp1ser616/Actin) with immunoblot analysis, (H) Mitochondrial fusion marker (Mfn1/Actin) with immunoblot analysis, (I) Mitochondrial fusion marker (OPA1/Actin) with immunoblot analysis. *p < 0.05 vs. baseline. ATP, adenosine triphosphate; CI‐AKI, contrast‐induced acute kidney injury; CKD, chronic kidney disease; DCF, dichlorofluorescein; Drp1, dynamin related protein 1; Mfn1, mitofusin 1; OCR, oxygen consumption rate; OPA1, optic atrophy protein 1; PCI, percutaneous coronary intervention.

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Contrast-induced acute kidney injury (CI-AKI) is the common hospitalized acute kidney injury (AKI). However, the diagnosis by serum creatinine might not be early enough. Currently, the roles of circulating mitochondria in CI-AKI are still unclear. Since early detection is crucial for treatment, the association between circulating mitochondrial func...

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... Previous studies have revealed that iohexol induced changes in over 30 metabolites (including pyruvate, choline, glycine, etc.) in the kidneys, plasma, and urine of CI-AKI rats, closely associated with disrupted energy and amino acid metabolism [20]. In CKD patients undergoing PCI, contrast media significantly induced mitochondrial dysfunction and oxidative stress in peripheral blood mononuclear cells (PBMCs) post-exposure, leading to decreased ATP levels and disturbed energy metabolism [32]. Our findings indicated a significant disturbance in the energy-related metabolic pathway following iodixanol injection, including glycine, serine, and threonine metabolism. ...
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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.
... Thus, although CM decreases GFR almost immediately, is not until 24-48 h later that this is reflected in a Scr increase, making it not an effective biomarker [28]. For all these reasons, SCr becomes a retrospective, late, insensitive, and misleading measure of kidney damage [28,30,32]. ...
... Moreover, its elevation could persist markedly for up to 5 days if the initial injury is severe. For this reason, among all new biomarkers, NGAL is one of the most widely investigated, also in the setting of CI-AKI [32]. ...
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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.
... The objective was to uncover connections between these factors and the occurrence of CIAKI. This study reported that the mitochondrial dysfunction in PBMCs occurs before the rise in SCr, indicating its potential utility as an early biomarker for CIAKI [19]. A study by Qiu et al. found high-sensitivity C-reactive protein (hs-CRP) to be an independent risk factor for CIAKI. ...
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Background and objective Contrast-induced acute kidney injury (CIAKI) is a complication observed 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 SCr from the baseline value following exposure to contrast within a 48- to 72-hour timeframe, in the absence of any alternative causes for acute 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. Hypertension and 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.