Acute kidney injury after cardiac surgery: a preventable event?
Acute kidney injury after cardiac surgery: a preventable event?
Kenta Kubota
Moritoki Egi
Satoshi Mizobuchi
Cardiovascular surgery (CVS) is one of the major causes of acute kidney injury (AKI). A recently published singlecenter retrospective study conducted in 767 adult critically ill patients, mainly cardiac and postoperative patients, showed that the incidence of AKI was high in this cohort (51.9%) and that the mortality rate increased with progression of the AKI stage [1]. A similar high incidence of AKI and its association with poor outcomes have also been reported in post-CVS patients in several studies [2-5]. In the past decade, many studies have been carried out with the aim to identify a sensitive biomarker for the early diagnosis of AKI in patients who had undergone CVS. To date, several useful biomarkers have been reported, including urine neutrophil gelatinase-associated lipocalin (NGAL), kidney injury marker 1, N-acetyl-βd -glucosaminidase (NAG), cystatin C, liver-type fatty acid-binding protein (L-FABP) and interleukin-18 [6, 7]. Among these biomarkers, NGAL, NAG, cystatin C and L-FABP are covered by Japan's National Heath Insurance system. Early identification of AKI using such biomarkers may improve the outcome by widening the therapeutic time window in post-CVS patients. Thus, it is time to ask whether the development of AKI in patients who have undergone CVS is a preventable event or not. Multiple pathophysiologies are considered to be involved in the development of AKI in patients post-CVS. Numerous risk factors have been reported, including advanced age, anemia, diabetes, chronic lung disease, chronic heart failure, chronic renal dysfunction, administration Vol.:(011233456789)
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of nephrotoxic agents, hypoperfusion, embolization and
increased aortic clamp time [
8
]. Some of the risk factors
can be treated or avoided. For example, it may be crucial
to avoid ischemic damage during renal hypoperfusion due
to perioperative low cardiac output syndrome and
cardiogenic shock [
8, 9
]. A systematic review by Brienza et al.
showed that postoperative AKI was significantly reduced
using perioperative hemodynamic optimization [10].
However, it is not easy to achieve perioperative hemodynamic
optimization in CVS patients, especially in those with low
output syndrome. In this context, recent studies have
provided useful information for determining the optimal
inotrope in CVS patients [
11–13
]. Levosimendan is a calcium
sensitizer that binds to troponin-C, thereby sensitizing the
myocardial filaments to calcium. Although several
metaanalyses of small trials have suggested that levosimendan
improves the survival rates among patients undergoing
cardiac surgery [
11, 13, 14
], a recently published randomized
controlled trial has shown that levosimendan does not
reduce the incidence of AKI and other clinical outcomes,
including 30-day mortality and duration of mechanical
ventilation and hospital stay, respectively [
15
]. In this regard,
the optimal inotrope to improve outcomes, including the
prevention of AKI, remains unidentified.
Pharmacologic renal protection is another important
issue in patients undergoing CVS. Various agents,
including dopamine, fenoldopam, statins, sodium bicarbonate,
mannitol, N-acetylcysteine, atrial natriuretic peptide and
free hemoglobin scavengers, have been proposed as agents
providing pharmacologic renal protection [
16–19
].
However, the results of studies in which the impact of such
pharmacologic renal protection was assessed have not been
consistent.
Studies have been carried out recently to assess the risks
and benefits of various interventions to prevent AKI in
patients who have undergone CVS [
16–19
], but as yet no
definitive strategy to prevent AKI has been identified.
Considering the multiple pathophysiologies of AKI post-CVS,
it is possible that the prevention of AKI in this context can
not be achieved through a single intervention [20]. It may
therefore be better to consider combination interventions in
future trials.
J Anesth
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