Evaluation of the Predictive Effect of Inflammatory Markers in MI Patients

Overview

Acute myocardial infarction (AMI), triggered by myocardial ischemia and reperfusion injury, is a disease with high morbidity and mortality, and there is a tendency for its incidence to increase at younger ages. One of the most worrisome complications of primary percutaneous surgery is contrast-induced nephropathy, which is associated with increased mortality and morbidity in myocardial infarction after coronary interventions. In many studies, inflammatory markers, which are thought to give an idea about the development of contrast-related nephropathy, have been examined. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of cytoprotective protein expression driven by antioxidant response agents (AREs) and plays a decisive role in the regulation of oxidative defense and redox homeostasis in cells. There are studies showing the role of Nrf2 in the pathogenesis of kidney damage in some studies. Studies on the effect of Nrf2 level on contrast media nephropathy in patients with contrast media nephropathy (CIN) are limited in the literature. This study also aimed to form a basis for the literature, which is a small number of studies, in later studies.

Acute myocardial infarction (AMI), triggered by myocardial ischemia and reperfusion injury, is a disease with high morbidity and mortality, and there is a tendency for its incidence to increase at younger ages. One of the most worrisome complications of primary percutaneous surgery is contrast-induced nephropathy and acute renal failure, which is associated with increased mortality and morbidity in myocardial infarction after coronary interventions. In many studies, markers that are thought to give an idea about the development of contrast-associated nephropathy have been examined. Acute renal failure (ARF) refers to a sudden decrease in glomerular tissue. Glomerular filtration rate (GFR) causes creatinine accumulation in the body and decreased urine output for various reasons, causing serious complications. Apart from dysfunction during the acute phase, there is a significant risk for permanent tissue damage. Therefore, kidney function cannot be restored, leading to the development of chronic renal failure (CKD), a sustained decrease in GFR, and increased long-term mortality. Incomplete recovery can also lead to the onset or further deterioration of chronic renal failure. Clinically, apart from hemodialysis treatment, few effective methods can treat the formation and development of ARF. Therefore, there is still an urgent need for new targets or better treatment options to prevent ARF and promote adaptive repair after ARF occurs. To date, the molecular mechanism of ARF is unclear, but there is increasing evidence that ARF is directly related to oxidative stress. In some studies, there are studies showing the role of Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) in the pathogenesis of kidney damage. There is an increase in mortality and morbidity rates due to nephrotoxicity after percutaneous intervention after MI. Studies showing that Nrf2 level may have a protective effect in contrast media nephropathy in patients with contrast media nephropathy (CIN) are limited in the literature. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of cytoprotective protein expression driven by antioxidant response agents (AREs) and plays a decisive role in the regulation of oxidative defense and redox homeostasis in cells. Although there are studies examining the epidemiological, demographic and clinical characteristics of patients in our country, studies on the importance of inflammatory parameters and the mortality and morbidity of Nrf2 levels are not available in our country. This study aimed to form the basis of the literature, which is a small number of studies, in later studies.