Acute Kidney Injury after Cardiac Surgery: Risk Factors and Novel Biomarkers

Abstract

Acute kidney injury (AKI) is a common and severe complication after cardiac surgery. Currently, a series of novel biomarkers have favored the assessment of AKI after cardiac surgery in addition to the conventional indicators. The biomartkers, such as urinary liver fatty acid binding protein (L-FABP), urinary neutrophil gelatinase-associated lipocalin (NGAL), serum L-FABP, heart-type FABP, kidney injury molecule 1 (KIM-1), and interleukin-18 were found to be significantly higher in patients who developed AKI after cardiac surgery than those who did not. Apart from urinary interleukin-18, the novel biomarkers have been recognized as reliable indicators for predicting the diagnosis, adverse outcome, and even mortality of AKI after cardiac surgery. The timing of the renal replacement therapy is a significant predictor relating to patients’ prognoses. In patients with AKI after cardiac surgery, renal replacement therapy should be performed as early as possible in order to achieve promising outcomes. In children, AKI after cardiac surgery can be managed with peritoneal dialysis. AKI after cardiac surgery has received extensive attention as it may increase early mortality and impact long-term survival of patients as well. The purpose of this article was to analyze the changes of the pertinent biomarkers, to explore the related risk factors leading to the occurrence of AKI after cardiac surgery, and to provide a basis for the clinical prevention and reduction of AKI.

Correlation Between Vasoactive-Inotropic Score and Postoperative Acute Kidney Injury after Cardiovascular Surgery

“…Acute kidney injury (AKI) is a common and serious complication in patients undergoing both cardiac surgery and vascular surgery, occurring in 20% to 70% of cases, depending on the type of surgery and the definition of AKI used [Nadim 2018]. Cardiac and vascular surgery-associated AKI (CVS-AKI) is associated with poor outcomes, including a prolonged hospital stay, an increased duration of mechanical ventilation, and high mortality [Yuan 2019]. It significantly increases mortality and morbidity, and to decrease these adverse events, many studies have focused on identifying preventative strategies as well as risk scores or biomarkers for AKI after cardiac and vascular surgery.…”

Renal Implications Following Cardiac Surgery: A Comprehensive Review

“…6 A figure adapted from Yuan et al has been included in this review to further understand the mechanism of acute kidney injury (Figure 1). 10 The highly regulated renal perfusion system consists of a shunt that helps maintain electrolyte and water concentration gradients in the renal medulla for tubule and collecting system reabsorption but renders the renal medulla and corticomedullary junction hypoxic relative other tissues. This may act as a protective mechanism for oxidative injury but increases susceptibility to ischemia.…”

“…Renal oxygenation may also be impaired due to sympathetic nervous system activation, the endogenous release of circulating catecholamines, and the induction of the renin-angiotensin-aldosterone cascade. 10 Intraoperatively, many factors may alter renal perfusion, such as the vasodilatory effects of anaesthesia, the usage of diuretics, and blood loss which overall accentuates the effect of hypoperfusion on the kidneys. Following a prolonged period of ischaemia, restoration of blood flow may also cause reperfusion injury in which renal tissues are further damaged due to the induction of oxidative stress.…”

“…Although the mechanism behind the inflammation is not completely understood, it may be caused due to a combination of factors including contact activation from the exposure of blood to the CBP circuit, ischemia-reperfusion injury, and oxidative damage. 10 Furthermore, the usage of cardiopulmonary bypass (CPB) itself may evoke renal damage due to the trigger of systemic inflammatory response syndrome (SIRS), the consequences of changes in blood flow and renal vasomotor tone as well as the formation of microemboli. SIRS during CPB is elicited by the contact of blood with the foreign material of the bypass circuit and prompts widespread inflammation and renal damage.…”

“…Haemolysis induced by CPB also worsens SIRS and induces the generation of microemboli, which directly destruct capillaries in the kidneys. 10 Additionally, both hemoglobinemia and myoglobinemia are independent predictors of postoperative AKI. Billings et al, in their study, demonstrated that postoperative AKI is associated with both enhanced intraoperative hemeprotein release and enhanced lipid peroxidation.…”