Impact of Iso-Osmolar Versus Low-Osmolar Contrast Agents on Contrast-Induced Nephropathy and Tissue Reperfusion in Unselected Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention (From the Contrast Media and Nephrotoxicity Following Primary Angioplasty for Acute Myocardial Infarction [CONTRAST-AMI] Trial)

Association of monocyte to HDL cholesterol level with contrast induced nephropathy in STEMI patients treated with primary PCI

“…In addition, the comorbid conditions of the patients may not be adequately evaluated due the emergency of the situation. Thus, the incidence of CIN is higher after primary PCI compared to elective CAGs and other imaging modalities and is associated with an increased risk of morbidity and mortality [9,30,32,33]. Our findings confirm the clinical use of the Mehran score, AGEF score and CV/eGFR ratio in patients treated with primary PCI.…”

“…In ROC curve analysis, these risk scores and MHR had significant discriminative power for the prediction of CIN. Effectiveness of several preventive strategies for CIN have been reported including preprocedural intravenous volume expansion with isotonic saline or sodium bicarbonate, antioxidant therapy with N-acetylcysteine, theophylline or ascorbic acid and use of low-or iso-osmolality CM [32,[34][35][36]. In addition, high-dose statin treatment may decrease the risk of renal failure and CIN in patients with CAD [10][11][12].…”

Selective Inhibition of the Reverse Mode of Na⁺/Ca²⁺ Exchanger Attenuates Contrast-Induced Cell Injury

“…The demonstration that contrast media with osmolalities of 450-600 mosm (low-osmolar CM) are associated with lower rates of acute kidney injury than earlier contrast media with osmolalities around 1,200 mosm (high-osmolar CM) [16] and that contrast media which are iso-osmolar with osmolalities of 300 mosm may be less nephrotoxic than low-osmolar CM [17] suggested that osmolality per se may play an important pathogenetic role in contrast nephrotoxicity. However, observations which demonstrate no differences in nephrotoxicity between low and iso-osmolar CM [18] and that contrast nephrotoxicity still exists with iso-osmolar contrast agents [18] suggest that contrast nephrotoxicity is not fully explained by hyperosmolality alone. In vitro studies also showed that the direct cytotoxic effects of the contrast molecule contribute to their nephrotoxicities besides hyperosmolality [19].…”

Sodium Bicarbonate Therapy for the Prevention of Contrast-Induced Acute Kidney Injury

“…However, more recent studies have failed to show any statistical difference in the incidence of CI-AKI after the administration of iodixanol or lowosmolar contrast media to high-risk patients. 56- 58 Reed et al conducted a meta-analysis of RCTs of 16 trials including 2,763 patients and found no significant differences in the incidence of CI-AKI, rates of postprocedural dialysis or death. 59 The mechanism responsible for the more pronounced effect of sodium bicarbonate in patients receiving low-osmolar contrast media in our meta-analysis is difficult to elucidate because of the small number of included studies and no adjusted comparison of variable clinical conditions.…”