Acute kidney injury after coronary artery bypass grafting: Does rhabdomyolysis play a role?

Benedetto, Umberto; Angeloni, Emiliano; Luciani, Remo; Refice, Simone; Stefanelli, Manuel; Comito, Cosimo; Roscitano, Antonino; Sinatra, Riccardo

doi:10.1016/j.jtcvs.2010.03.028

Cited by 35 publications

(34 citation statements)

References 17 publications

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“…It has been found to independently predict postoperative AKI after coronary artery bypass grafting after adjustment for confounding factors (21). These findings are supported by serum myoglobin being strongly associated with AKI after thoraco-abdominal and thoracic aortic repair (22).…”

Section: Discussionmentioning

confidence: 92%

Urinary Hepcidin-25 and Risk of Acute Kidney Injury Following Cardiopulmonary Bypass

Reslerova²,

Gali³

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Acute kidney injury (AKI) complicating cardiopulmonary bypass (CPB) results in increased morbidity and mortality. Urinary hepcidin-25 has been shown to be elevated in patients who do not develop AKI after CPB using semiquantitative mass spectrometry (SELDI TOF-MS). The goals of this study were to quantitatively validate these findings with ELISA and evaluate the diagnostic performance of hepcidin-25 for AKI.Design, setting, participants, & measurements A nested, case-control analysis of urinary hepcidin-25 in AKI (n ϭ 22) and non-AKI (n ϭ 22) patients was conducted to validate the SELDI TOF-MS data at the following times: preoperatively; the start of CPB; 1 hour on CPB; on arrival to the intensive care unit; and postoperative days (POD) 1 and 3 to 5. The diagnostic performance of hepcidin-25 was then evaluated in the entire prospective observational cohort (n ϭ 338) at POD 1. AKI was defined as Cr Ͼ50% from baseline, within 72 hours postoperatively.Results Urinary hepcidin-25/Cr ratio was significantly elevated in all patients at POD 1 compared with baseline (P Ͻ 0.0005) and was also significantly elevated in non-AKI versus AKI patients at POD 1 (P Ͻ 0.0005). Increased log 10 hepcidin-25/Cr ratio was strongly associated with avoidance of AKI on univariate analysis. On multivariate analysis, the log 10 hepcidin-25/Cr ratio (P Ͻ 0.0001) was associated with avoidance of AKI with an area under the curve of 0.80, sensitivity 0.68, specificity 0.68, and negative predictive value 0.96. ConclusionsElevated urinary hepcidin-25 on POD 1 is a strong predictor of avoidance of AKI beyond postoperative day 1.

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Section: Discussionmentioning

confidence: 92%

Urinary Hepcidin-25 and Risk of Acute Kidney Injury Following Cardiopulmonary Bypass

Reslerova²,

Gali³

et al. 2011

Clinical Journal of the American Society of Nephrology

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“…As skeletal muscle injury occurs during CPB surgery, 21 and release of myoglobin into the circulation could be a source of plasma catalytic iron, we investigated the correlation between serum creatinine phosphokinase (CPK) values (as a surrogate for myoglobinemia) 22 and plasma catalytic iron levels. We found a significant correlation between plasma catalytic iron levels at the end of CPB and serum CPK levels obtained immediately postoperatively ( r s = 0.28, P <0.001).…”

Section: Resultsmentioning

confidence: 99%

“…However, potential mechanisms by which cardiac surgery may induce elevation of plasma catalytic iron include: exposure of RBCs to nonphysiological surfaces resulting in hemolysis; 17 shear stress generated by pumps and suction systems; mechanical fragmentation of RBCs induced by valvular prostheses; skeletal muscle injury during CPB, 21 resulting in the release of iron-rich myoglobin into the circulation; pRBC transfusions; 20 and ischemia/reperfusion injury to the kidneys and other organs. Our findings of a positive correlation between both CPB duration and number of pRBC transfusions with postoperative catalytic iron levels suggest that the rise is at least partially iatrogenic and hence potentially modifiable.…”

Section: Discussionmentioning

confidence: 99%

Increased plasma catalytic iron in patients may mediate acute kidney injury and death following cardiac surgery

Leaf

Rajapurkar

Lele

et al. 2015

Kidney International

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Catalytic iron, the chemical form of iron capable of participating in redox cycling, is a key mediator of acute kidney injury (AKI) in multiple animal models, but its role in human AKI has not been studied. Here we tested in a prospective cohort of 250 patients undergoing cardiac surgery whether plasma catalytic iron levels are elevated and associated with the composite outcome of AKI requiring renal replacement therapy or in-hospital mortality. Plasma catalytic iron, free hemoglobin, and other iron parameters were measured preoperatively, at the end of cardiopulmonary bypass, and on postoperative days 1 and 3. Plasma catalytic iron levels, but not other iron parameters, rose significantly at the end of cardiopulmonary bypass and were directly associated with bypass time and number of packed red blood cell transfusions. In multivariate analyses adjusting for age and preoperative eGFR, patients in the highest compared with the lowest quartile of catalytic iron on postoperative day 1 had a 6.71 greater odds of experiencing the primary outcome, and also had greater odds of AKI, hospital mortality, and postoperative myocardial injury. Thus, our data are consistent with and expand on findings from animal models demonstrating a pathologic role of catalytic iron in mediating adverse postoperative outcomes. Interventions aimed at reducing plasma catalytic iron levels as a strategy for preventing AKI in humans are warranted.

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“…The release of both hemoglobin and myoglobin during CPB surgery has been associated with AKI in prior studies [3,24]. However, the dominant hemeprotein released during CPB surgery is hemoglobin [3].…”

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 and Acute Kidney Injury following Cardiac Surgery

Billings

Byrne

et al. 2014

Cardiorenal Med

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Background: Intraoperative hemolysis and inflammation are associated with acute kidney injury (AKI) following cardiac surgery. Plasma-free hemoglobin induces heme oxygenase-1 (HO-1) expression. HO-1 degrades heme but increases in experimental models of AKI. This study tested the hypothesis that plasma HO-1 concentrations are associated with intraoperative hemolysis and are increased in patients that develop AKI following cardiac surgery. Methods: We measured plasma HO-1, free hemoglobin, and inflammatory markers in 74 patients undergoing cardiopulmonary bypass (CPB). AKI was defined as anincrease in serum creatinine concentration of 50% or 0.3 mg/dl within 72 h of surgery. Results: Twenty-eight percent of patients developed AKI. HO-1 concentrations increased from 4.2 ± 0.2 ng/ml at baseline to 6.6 ± 0.5 ng/ml on postoperative day (POD) 1 (p < 0.001). POD1 HO-1 concentrations were 3.1 ng/ml higher (95% CI 1.1-5.1) in AKI patients, as was the change in HO-1 from baseline to POD1 (4.4 ± 1.3 ng/ml in AKI patients vs. 1.5 ± 0.3 ng/ml in no-AKI patients, p = 0.006). HO-1 concentrations remained elevated in AKI patients even after controlling for AKI risk factors and preoperative drug therapy. Peak-free hemoglobin concentrations correlated with peak HO-1 concentrations on POD1 in patients that developed AKI (p = 0.02). Duration of CPB and post-CPB IL-6 and IL-10 concentrations were also associated with increased HO-1 on POD1. Conclusion: Plasma HO-1 is increased in patients that develop AKI, and CPB duration, hemolysis, and inflammation are associated with increased HO-1 concentrations following cardiac surgery. Strategies that alter hemolysis and HO-1 expression during cardiac surgery may affect risk for AKI.

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Acute kidney injury after coronary artery bypass grafting: Does rhabdomyolysis play a role?

Cited by 35 publications

References 17 publications

Urinary Hepcidin-25 and Risk of Acute Kidney Injury Following Cardiopulmonary Bypass

Urinary Hepcidin-25 and Risk of Acute Kidney Injury Following Cardiopulmonary Bypass

Increased plasma catalytic iron in patients may mediate acute kidney injury and death following cardiac surgery

Heme Oxygenase-1 and Acute Kidney Injury following Cardiac Surgery

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