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Renal tubular injury during cardiopulmonary bypass as assessed by urinary release of N-acetyl-ss-D-glucosaminidase

Artikel i vetenskaplig tidskrift
Författare Lukas Lannemyr
E. Lundin
Björn Reinsfelt
Gudrun Bragadottir
Bengt Redfors
Jonatan Oras
Sven-Erik Ricksten
Publicerad i Acta Anaesthesiologica Scandinavica
Volym 61
Nummer/häfte 9
Sidor 1075-1083
ISSN 0001-5172
Publiceringsår 2017
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för anestesiologi och intensivvård
Sidor 1075-1083
Språk en
Länkar doi.org/10.1111/aas.12946
Ämnesord acute kidney injury, cardiac-surgery, inflammatory response, creatinine, values, minimal changes, failure, association, disease, plasma, risk
Ämneskategorier Klinisk medicin

Sammanfattning

BackgroundAcute kidney injury (AKI) is a common complication with a major impact on morbidity and mortality after cardiac surgery with cardiopulmonary bypass (CPB). The aim of the present study was to perform a detailed analysis on the release of the tubular injury biomarker N-acetyl-b-D-glucosaminidase (NAG) during and early after CPB and to describe independent predictors of maximal tubular injury. We hypothesized that renal tubular injury occurs early after the onset of CPB. MethodsIn this prospective observational study, we included 61 patients undergoing open cardiac surgery with an expected CPB duration exceeding 60min. The urinary NAG levels were measured at 30min intervals during CPB, as well as early (30min) after CPB and post-operatively. Independent predictors of tubular injury were identified using an Interquantile multivariate regression model. ResultsAlready 30min after the onset of CPB, NAG excretion was significantly increased (P<0.001), followed by a sixfold peak increase after discontinuation of CPB (P<0.001). In the multivariable regression model, CPB duration (P<0.05) and the degree of rewarming during CPB (P<0.05), were independent predictors of peak NAG excretion. ConclusionIn cardiac surgery, a renal tubular cell injury is seen early after onset of CPB with a peak biomarker increase early after end of CPB. The magnitude of this tubular injury is independently related to CPB duration and the degree of rewarming. Efforts made to decrease the CPB duration and to avoid hypothermia and the need for rewarming may decrease the risk for tubular injury.

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