Hemolysis is associated with acute kidney injury during major aortic surgery

Windsant, Iris C. Vermeulen; Snoeijs, Maarten G.; Hanssen, Sebastiaan J.; Altintas, Sibel; Heijmans, John; Koeppel, Thomas A.; Schurink, Geert Willem H.; Buurman, Wim A.; Jacobs, Michael J.

doi:10.1038/ki.2010.24

Cited by 149 publications

(140 citation statements)

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“…Data have implicated pump-induced hemolysis for mediating AKI with the release of free plasma hemoglobin and iron. 67 Free iron may induce changes in tubular epithelial function, including impaired proliferation and induction of free radical toxicity. Free iron released during CPB can catalyze formation of hydroxyl radicals.…”

Section: Syndromes Of Acute Kidney Injurymentioning

confidence: 99%

Review article: Acute kidney injury in critical illness

Bagshaw

Bellomo

Devarajan

et al. 2010

Can J Anesth/J Can Anesth

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Purpose This review provides a focused and comprehensive update on emerging evidence related to acute kidney injury (AKI).Principal findings Acute kidney injury is a significant clinical problem that increasingly complicates the course of hospitalization and portends worse clinical outcome for sick hospitalized patients. The recent introduction of consensus criteria for the diagnosis of AKI (i.e., RIFLE/AKIN classification) have greatly improved our capacity not only to standardize the diagnosis and classification of severity of AKI, but also to facilitate conducting comparative epidemiologic studies in an effort to better understand the burden of adult and pediatric AKI and its syndromes (i.e., septic, cardio-renal, hepato-renal). The characterization of several novel AKI-specific biomarkers (i.e., neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, and interleukin-18) is extending our understanding of the pathophysiology of AKI. Moreover, these biomarkers appear to have clinical relevance for early detection and they provide prognostic value. These innovations are aiding in the design of epidemiologic surveys and randomized trials of therapeutic interventions. Strategies for prevention Editor's Note: This article is the first of two linked special review articles published in this issue of the Journal. The concept of these articles emerged from the scientific content of the 2010 Acute Kidney Injury (AKI) and Renal Support in Critical Illness Symposium, hosted in Edmonton, Alberta. This review (Part 1) provides a focused and comprehensive update on emerging evidence in the diagnosis and classification of AKI, on specific AKI syndromes, and on the prevention and conservative management of hospitalized patients with AKI. Abstracts presented at this meeting were selected on the basis of peer review by the Scientific Committee and were accepted for presentation at the AKI 2010 Symposium, and appear as Electronic Supplementary Material at

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Section: Syndromes Of Acute Kidney Injurymentioning

confidence: 99%

Review article: Acute kidney injury in critical illness

Bagshaw

Bellomo

Devarajan

et al. 2010

Can J Anesth/J Can Anesth

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“…Possible explanations of how free iron causes AKI in this context include oxidative stress via the HaberWeiss reaction and hemolysis due to pump use causing depletion of nitric oxide (NO). In patients undergoing CPB, there are elevations of markers of systemic inflammation [28][29][30] and significant hemolysis [18,31,32] . Old-stored red blood cell transfusion also potentially contributes free hemoglobin which has been found to scavenge NO [33] .…”

Section: Discussionmentioning

confidence: 99%

Urine Catalytic Iron and Neutrophil Gelatinase Associated Lipocalin as Companion Early Markers of Acute Kidney Injury After Cardiac Surgery: A Prospective Pilot Study

2013

American Journal of Kidney Diseases

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Background: Open heart surgery with cardiopulmonary bypass is recognized as a common cause of acute kidney injury (AKI). The conventional biomarker creatinine is not sensitive enough to detect AKI until a significant decline in renal filtration has occurred. Urine neutrophil gelatinase-associated lipocalin (NGAL), part of an acute response to the release of tissue iron from cells, is an early biomarker and a predictor of AKI in a variety of clinical settings. We sought to evaluate the relationship between urine catalytic iron (unbound iron) and NGAL over the course of AKI due to cardiac surgery. Methods: Fourteen patients who underwent open heart surgery had the following measured: serum creatinine (0, 12, 24, 48 and 72 h postoperatively), urine NGAL and urine catalytic iron (0, 8, 24 and 48 h postoperatively). Urine NGAL and urine catalytic iron were quantified by immunoassay and bleomycin-detectable iron assay, respectively. AKI was defined by the Acute Kidney Injury Network (AKIN) criteria. Results: Urine catalytic iron increased significantly (p < 0.05) within 8 h and peaked at 24 h postoperatively in patients who developed AKI (n = 8, baseline 101.96 ± 177.48, peak 226.35 ± 238.23 nmol/l, p = 0.006), but not in non-AKI patients (n = 6, baseline 131.08 ± 116.21, peak 163.99 ± 109.62 nmol/l, p = 0.380). Urine NGAL levels also peaked at 24 h with significant increase observed only in AKI patients: AKI -baseline 34.88 ± 26.47, peak 65.50 ± 27.03 ng/ml, p = 0.043; non-AKI -baseline 59.33 ± 31.72, peak 71.00 ± 31.76 ng/ml, p = 0.100. The correlation between baseline levels of urine catalytic iron and NGAL and peak levels of urine catalytic iron and NGAL was r = 0.86, p < 0.0001. Conclusion: Urine catalytic iron appears to rise and fall in concert with NGAL in patients undergoing cardiac surgery and may be indicative of early AKI. Future research into the role that catalytic iron plays in acute organ injury syndromes and its potential diagnostic and therapeutic implications is warranted.

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“…[6][7][8] Cardiac surgery results in a postoperative systemic inflammatory response syndrome due to a variety of factors including surgical trauma, exposure of blood to the artificial surface of the bypass circuit, tissue hypoperfusion, hemolysis, hemodilution, blood transfusion, and hypothermia. [9][10][11][12] Inflammation is believed to play a key role in the pathophysiology of AKI after cardiac surgery with CPB. A number of proinflammatory pathways are activated during CPB and can lead to leukocyte extravasation, lipid peroxidation, renal medullary congestion, and tubular cell injury.…”

mentioning

confidence: 99%

“…During CPB, blood is exposed to nonphysiologic surfaces and shear forces, leading to cell lysis and release of free hemoglobin into the circulation. 11,12,20 Free hemoglobin is removed from the circulation through binding to CD163, 21 a scavenger receptor on the cell surface of monocytes and macrophages that is upregulated by glucocorticoids in multiple cell lines. [22][23][24] Hence, enhanced removal of free hemoglobin through upregulated CD163 represents a biologically plausible pathway through which glucocorticoids may decrease the incidence of CPB-associated AKI.…”

mentioning

confidence: 99%

Intraoperative High-Dose Dexamethasone and Severe AKI after Cardiac Surgery

Jacob

Leaf

Dieleman³

et al. 2015

Journal of the American Society of Nephrology

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Administration of prophylactic glucocorticoids has been suggested as a strategy to reduce postoperative AKI and other adverse events after cardiac surgery requiring cardiopulmonary bypass. In this post hoc analysis of a large placebo-controlled randomized trial of dexamethasone in 4465 adult patients undergoing cardiac surgery, we examined severe AKI, defined as use of RRT, as a primary outcome. Secondary outcomes were doubling of serum creatinine level or AKI-RRT, as well as AKI-RRT or in-hospital mortality (RRT/death). The primary outcome occurred in ten patients (0.4%) in the dexamethasone group and in 23 patients (1.0%) in the placebo group (relative risk, 0.44; 95% confidence interval, 0.19 to 0.96). In stratified analyses, the strongest signal for potential benefit of dexamethasone was in patients with an eGFR,15 ml/min per 1.73 m 2 . In conclusion, compared with placebo, intraoperative dexamethasone appeared to reduce the incidence of severe AKI after cardiac surgery in those with advanced CKD. 26: 294726: -295126: , 201526: . doi: 10.1681 Acute kidney injury is one of the most ominous complications after cardiac surgery with cardiopulmonary bypass (CPB). Approximately 1% of patients undergoing cardiac surgery require RRT for severe postoperative AKI, and experience strikingly high in-hospital mortality rates exceeding 40%. 1-3 Less severe AKI is far more common and identifies patients still at increased risk of shortand long-term mortality, prolonged length of hospital stay, and higher hospital costs. 4,5 The pathogenesis of AKI after cardiac surgery is complex and includes patient-related factors such as age and comorbidities (e.g., CKD and diabetes mellitus) as well as surgical factors such as type of procedure and duration of CPB. [6][7][8] Cardiac surgery results in a postoperative systemic inflammatory response syndrome due to a variety of factors including surgical trauma, exposure of blood to the artificial surface of the bypass circuit, tissue hypoperfusion, hemolysis, hemodilution, blood transfusion, and hypothermia. 9-12 Inflammation is believed to play a key role in the pathophysiology of AKI after cardiac surgery with CPB. A number of proinflammatory pathways are activated during CPB and can lead to leukocyte extravasation, lipid peroxidation, renal medullary congestion, and tubular cell injury. 1,9 Multiple strategies have been proposed to attenuate the inflammatory response after cardiac surgery with CPB, including the use of glucocorticoids. To date, the effect of glucocorticoids on AKI after cardiac surgery has been evaluated as a primary outcome in 14 randomized controlled trials, the largest of which included 216 patients. 3 A meta-analysis of these studies (which included a total of 888 patients) concluded that glucocorticoids have no protective effect on AKI after cardiac surgery. 3 However, these studies were underpowered, particularly to detect severe AKI. J Am Soc NephrolWe therefore conducted a post hoc analysis of severe AKI in the Dexamethasone for Cardiac Surgery (DE...

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Hemolysis is associated with acute kidney injury during major aortic surgery

Cited by 149 publications

References 40 publications

Review article: Acute kidney injury in critical illness

Review article: Acute kidney injury in critical illness

Urine Catalytic Iron and Neutrophil Gelatinase Associated Lipocalin as Companion Early Markers of Acute Kidney Injury After Cardiac Surgery: A Prospective Pilot Study

Intraoperative High-Dose Dexamethasone and Severe AKI after Cardiac Surgery

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