Cardiac Surgery-Associated Acute Kidney Injury

Abstract

Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common and serious postoperative complication of cardiac surgery requiring cardiopulmonary bypass (CPB), and it is the second most common cause of AKI in the intensive care unit. Although the complication has been associated with the use of CPB, the etiology is likely multifactorial and related to intraoperative and early postoperative management including pharmacologic therapy. To date, very little evidence from randomized trials supporting specific interventions to protect from or prevent AKI in broad cardiac surgery populations has been found. The definition of AKI employed by investigators influences not only the incidence of CSA-AKI, but also the identification of risk variables. The advent of novel biomarkers of kidney injury has the potential to facilitate the subclinical diagnosis of CSA-AKI, the assessment of its severity and prognosis, and the early institution of interventions to prevent or reduce kidney damage. Further studies are needed to determine how to optimize cardiac surgical procedures, CPB parameters, and intraoperative and early postoperative blood pressure and renal blood flow to reduce the risk of CSA-AKI. No pharmacologic strategy has demonstrated clear efficacy in the prevention of CSA-AKI; however, some agents, such as the natriuretic peptide nesiritide and the dopamine agonist fenoldopam, have shown promising results in renoprotection. It remains unclear whether CSA-AKI patients can benefit from the early institution of such pharmacologic agents or the early initiation of renal replacement therapy.

Minor Postoperative Increases of Creatinine Are Associated With Higher Mortality and Longer Hospital Length of Stay in Surgical Patients

“…3,4 Similarly, the much higher AKI incidence (35%) in cardiac surgery patients corresponds with previous studies. 8 Moreover, our findings indicate that the manifestation of more severe forms of AKI occurs less frequently in surgical patients. However, the risk of death gradually increased dependent on the severity of AKI.…”

“…This epidemiology in surgical patients is consistent with previous studies in other cohorts of hospitalized patients. [7][8][9]18,20,22,32 In contrast, the association of minor creatinine increases not fulfilling AKI criteria with adverse outcome has not been shown in noncardiac surgical patients before. Some studies have linked minor creatinine increases to higher mortality in small subsets of cardiac surgery patients.…”

“…17,42,43 The duration of intraoperative CPB has thus been linked to the incidence and severity of postcardiac surgery AKI. 8,15,[44][45][46][47] However, the fact that AKI in noncardiac surgery patients has a more profound impact on mortality and HLOS suggests that "low-grade AKI" caused by CPB is likely an event that the kidneys can recover from in most instances, whereas "low-grade AKI" without the use of CPB indicates a more severe form of intrinsic injury to the kidneys. Indeed, these findings alert to the fact that clinicians should take subclinical increases of creatinine levels in general surgery patients very seriously.…”

Lipids, blood pressure and kidney update 2014

“…In a large study including 820 patients receiving elective cardiac surgery, there were no favorable effects of statin administration on AKI incidence. Following cardiac surgery and cardiopulmonary bypass renal ischemia-reperfusion injury, impaired vasodilatation, neurohormonal activation, oxidative stress, inflammation, and atheroembolism may promote AKI [139]. Statins administration might reduce oxidative stress, improve endothelial function and decrease inflammation [140,141].…”

Sodium bicarbonate infusion for prevention of acute kidney injury: No evidence for superior benefit, but risk for harm?

“…Hemolysis and release of free hemoglobin during CPB is a well-recognized nephrotoxic mechanism. Increased levels of free red blood cell constituents together with exhaustion of their scavengers result in a variety of serious sequelae such as increased vascular resistance, altered coagulation activity, platelet dysfunction and renal tubular damage [35].…”