1\. Research background 1. Research hypothesis The development of acute kidney injury (AKI) can be predicted using urine mitochondrial deoxyribonucleic acid (UmtDNA), serum and urine beta-2 microglobulin (β2-MG) in critically ill surgical patients 2. Basis of research hypothesis i. Correlation between mitochondria and renal function (Results of previous studies) * Mitochondria are involved in development and recovery of diabetic nephropathy. * UmtDNA can be used as early marker to detect the development of AKI ※ Mitochondria * As an organelle located within the cell, it is an organ that produces energy through adenosine triphosphate (ATP) through cellular oxidative phosphorylation. * The kidney has the second most mitochondria after the heart. II. Correlation between elevation of β2-MG and renal function * Circulating β2-MG infiltrates the glomerulus and is reabsorbed and metabolized in the proximal tubule of the kidney. Therefore, it increases in the blood due to a decrease in metabolism when renal function is abnormal. ※ Beta 2-microglobulin * As the light chain of the class I major histocompatibility antigen, it is a protein distributed in nucleated cells (especially lymphocytes and monocytes) in the body. III. Mechanism of acute kidney injury in critically ill surgical patients * Blood flow to the kidneys is reduced due to decreased cardiac output, vasoconstriction due to systemic inflammatory response, hemodynamic changes, and decreased body fluid. This leads to renal tubular injury along with ischemic reperfusion injury. * Renal tubular injury increases the permeability of the transition pore that connects the outer and inner mitochondrial membranes, resulting in mitochondrial structural damage and oxidative injury. It causes a decrease of ATP in kidney cells and induces apoptosis of kidney cells. * Urine mtDNA, a product of this kidney injury, could be used as a biomarker to predict impairment of renal function in critically ill surgical patients. * Serum β2-MG maybe increase due to a decrease of metabolism of β2-MG in AKI.
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Acute kidney injury (dichotomous)
Timeframe: Within 30 days after ICU admission
Acute kidney injury recovery (dichotomous)
Timeframe: Within 30 days after ICU admission