NT-proBNP levels in the identification and classification of pulmonary transfusion reactions.
Journal
Transfusion
ISSN: 1537-2995
Titre abrégé: Transfusion
Pays: United States
ID NLM: 0417360
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
14
06
2020
revised:
29
07
2020
accepted:
07
08
2020
pubmed:
10
9
2020
medline:
29
6
2021
entrez:
9
9
2020
Statut:
ppublish
Résumé
Consensus definitions for transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (TACO) have recently been revised; however, pulmonary transfusion reactions remain difficult to diagnose. We hypothesized that N-terminal pro-brain natriuretic peptide (NT-proBNP) levels could have utility in the identification and classification of pulmonary transfusion reactions. We performed a secondary analysis of a case-control study of pulmonary transfusion reactions at four academic hospitals. We evaluated clinical data and measured NT-proBNP levels prior to and following transfusion in patients with TACO (n = 160), transfused acute respiratory distress syndrome (ARDS) [n = 51], TRALI [n = 12], TACO/TRALI [n = 7], and controls [n = 335]. We used Wilcoxon Rank-Sum tests to compare NT-proBNP levels, and classification and regression tree (CART) algorithms to produce a ranking of covariates in order of relative importance for differentiating TACO from transfused controls. Pre-transfusion NT-proBNP levels were elevated in cases of transfused ARDS and TACO (both P < .001) but not TRALI (P = .31) or TACO/TRALI (P = .23) compared to transfused controls. Pre-transfusion NT-proBNP levels were higher in cases of transfused ARDS or TRALI with a diagnosis of sepsis compared to those without (P < .05 for both). CART analyses resulted in similar differentiation of patients with TACO from transfused controls for models utilizing either NT-proBNP levels (AUC 0.83) or echocardiogram results (AUC 0.80). NT-proBNP levels may have utility in the classification of pulmonary transfusion reactions. Prospective studies are needed to test the predictive utility of pre-transfusion NT-proBNP in conjunction with other clinical factors in identifying patients at risk of pulmonary transfusion reactions.
Sections du résumé
BACKGROUND
Consensus definitions for transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (TACO) have recently been revised; however, pulmonary transfusion reactions remain difficult to diagnose. We hypothesized that N-terminal pro-brain natriuretic peptide (NT-proBNP) levels could have utility in the identification and classification of pulmonary transfusion reactions.
STUDY DESIGN AND METHODS
We performed a secondary analysis of a case-control study of pulmonary transfusion reactions at four academic hospitals. We evaluated clinical data and measured NT-proBNP levels prior to and following transfusion in patients with TACO (n = 160), transfused acute respiratory distress syndrome (ARDS) [n = 51], TRALI [n = 12], TACO/TRALI [n = 7], and controls [n = 335]. We used Wilcoxon Rank-Sum tests to compare NT-proBNP levels, and classification and regression tree (CART) algorithms to produce a ranking of covariates in order of relative importance for differentiating TACO from transfused controls.
RESULTS
Pre-transfusion NT-proBNP levels were elevated in cases of transfused ARDS and TACO (both P < .001) but not TRALI (P = .31) or TACO/TRALI (P = .23) compared to transfused controls. Pre-transfusion NT-proBNP levels were higher in cases of transfused ARDS or TRALI with a diagnosis of sepsis compared to those without (P < .05 for both). CART analyses resulted in similar differentiation of patients with TACO from transfused controls for models utilizing either NT-proBNP levels (AUC 0.83) or echocardiogram results (AUC 0.80).
CONCLUSIONS
NT-proBNP levels may have utility in the classification of pulmonary transfusion reactions. Prospective studies are needed to test the predictive utility of pre-transfusion NT-proBNP in conjunction with other clinical factors in identifying patients at risk of pulmonary transfusion reactions.
Substances chimiques
Peptide Fragments
0
pro-brain natriuretic peptide (1-76)
0
Natriuretic Peptide, Brain
114471-18-0
Types de publication
Clinical Trial
Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
2548-2556Subventions
Organisme : NHLBI NIH HHS
ID : L30 HL129355
Pays : United States
Organisme : The authors were supported by research contracts from the National Heart, Lung, and Blood Institute (NHLBI Contracts HHSN2682011000002I, HHSN2682011000003I, HHSN2682011000004I, HHSN2682011000005I, and HHSN268201100006I for the Recipient Epidemiology and Donor Evaluation Study-III
Organisme : The authors were supported by research contracts from the National Heart, Lung, and Blood Institute (NHLBI Contracts HHSN2682011000002I, HHSN2682011000003I, HHSN2682011000004I, HHSN2682011000005I, and HHSN268201100006I for the Recipient Epidemiology and Donor Evaluation Study-III.
Informations de copyright
© 2020 AABB.
Références
Fatalities Reported to FDA Following Blood Collection and Transfusion 2018. https://www.fda.gov/media/136907/download. .
Roubinian N. TACO and TRALI: Biology, risk factors, and prevention strategies. Hematology Am Soc Hematol Educ Program. 2018;2018(1):585-594.
Vlaar APJ, Toy P, Fung M, et al. A consensus redefinition of transfusion-related acute lung injury. Transfusion. 2019;59(7):2465-2476.
Wiersum-Osselton JC, Whitaker B, Grey S, et al. Revised international surveillance case definition of transfusion-associated circulatory overload: a classification agreement validation study. Lancet Haematol. 2019;6(7):e350-e358.
Looney MR, Roubinian N, Gajic O, et al. Prospective study on the clinical course and outcomes in transfusion-related acute lung injury. Crit Care Med. 2014;42(7):1676-1687.
Vlaar AP, Binnekade JM, Prins D, et al. Risk factors and outcome of transfusion-related acute lung injury in the critically ill: a nested case-control study. Crit Care Med. 2010;38(3):771-778.
Gajic O, Rana R, Winters JL, et al. Transfusion-related acute lung injury in the critically ill: prospective nested case-control study. Am J Respir Crit Care Med. 2007;176(9):886-891.
Roubinian NH, Looney MR, Kor DJ, et al. Cytokines and clinical predictors in distinguishing pulmonary transfusion reactions. Transfusion. 2015;55(8):1838-1846.
Klanderman RB, Bosboom JJ, Migdady Y, et al. Transfusion-associated circulatory overload-a systematic review of diagnostic biomarkers. Transfusion. 2019;59(2):795-805.
Tobian AA, Sokoll LJ, Tisch DJ, Ness PM, Shan H. N-terminal pro-brain natriuretic peptide is a useful diagnostic marker for transfusion-associated circulatory overload. Transfusion. 2008;48(6):1143-1150.
Zhou L, Giacherio D, Cooling L, Davenport RD. Use of B-natriuretic peptide as a diagnostic marker in the differential diagnosis of transfusion-associated circulatory overload. Transfusion. 2005;45(7):1056-1063.
Li G, Daniels CE, Kojicic M, et al. The accuracy of natriuretic peptides (brain natriuretic peptide and N-terminal pro-brain natriuretic) in the differentiation between transfusion-related acute lung injury and transfusion-related circulatory overload in the critically ill. Transfusion. 2009;49(1):13-20.
Roubinian NH, Looney MR, Keating S, et al. Differentiating pulmonary transfusion reactions using recipient and transfusion factors. Transfusion. 2017;57(7):1684-1690.
Callum JL, Cohen R, Cressman AM, et al. Cardiac stress biomarkers after red blood cell transfusion in patients at risk for transfusion-associated circulatory overload: a prospective observational study. Transfusion. 2018;58(9):2139-2148.
Roubinian NH, Hendrickson JE, Triulzi DJ, et al. Contemporary risk factors and outcomes of transfusion-associated circulatory overload. Crit Care Med. 2018;46(4):577-585.
Toy P, Popovsky MA, Abraham E, et al. Transfusion-related acute lung injury: definition and review. Crit Care Med. 2005;33(4):721-726.
Kleinman S, Caulfield T, Chan P, et al. Toward an understanding of transfusion-related acute lung injury: statement of a consensus panel. Transfusion. 2004;44(12):1774-1789.
Toy P, Bacchetti P, Grimes B, et al. Recipient clinical risk factors predominate in possible transfusion-related acute lung injury. Transfusion. 2015;55(5):947-952.
Andrzejewski C Jr, Popovsky MA, Stec TC, et al. Hemotherapy bedside biovigilance involving vital sign values and characteristics of patients with suspected transfusion reactions associated with fluid challenges: can some cases of transfusion-associated circulatory overload have proinflammatory aspects? Transfusion. 2012;52(11):2310-2320.
Looney MR, Gropper MA, Matthay MA. Transfusion-related acute lung injury: a review. Chest. 2004;126(1):249-258.
Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1334-1349.
Semple JW, McVey MJ, Kim M, Rebetz J, Kuebler WM, Kapur R. Targeting transfusion-related acute lung injury: the journey from basic science to novel therapies. Crit Care Med. 2018;46(5):e452-e458.
Eder AF, Dy BA, Perez JM, Rambaud M, Benjamin RJ. The residual risk of transfusion-related acute lung injury at the American Red Cross (2008-2011): limitations of a predominantly male-donor plasma mitigation strategy. Transfusion. 2013;53(7):1442-1449.
Andreu G, Boudjedir K, Muller JY, et al. Analysis of transfusion-related acute lung injury and possible transfusion-related acute lung injury reported to the French hemovigilance network from 2007 to 2013. Transfus Med Rev. 2018;32(1):16-27.
Roubinian NH, Triulzi DJ. Transfusion-associated circulatory overload and transfusion-related acute lung injury: etiology and prevention. Hematol Oncol Clin North Am. 2019;33(5):767-779.
Clifford L, Jia Q, Subramanian A, Yadav H, Schroeder DR, Kor DJ. Risk factors and clinical outcomes associated with perioperative transfusion-associated circulatory overload. Anesthesiology. 2017;126(3):409-418.
Clifford L, Jia Q, Yadav H, et al. Characterizing the epidemiology of perioperative transfusion-associated circulatory overload. Anesthesiology. 2015;122(1):21-28.
Pendergrast J, Armali C, Cserti-Gazdewich C, et al. Can furosemide prevent transfusion-associated circulatory overload? Results of a pilot, double-blind, randomized controlled trial. Transfusion. 2019;59(6):1997-2006.
Hendrickson JE, Roubinian NH, Chowdhury D, et al. Incidence of transfusion reactions: a multicenter study utilizing systematic active surveillance and expert adjudication. Transfusion. 2016;56(10):2587-2596.
Mafirakureva N, Khoza S, Mvere DA, Chitiyo ME, Postma MJ, Van Hulst M. Incidence and pattern of 12 years of reported transfusion adverse events in Zimbabwe: a retrospective analysis. Blood Transfus. 2014;12(3):362-367.
Waiswa MK, Moses A, Seremba E, Ddungu H, Hume HA. Acute transfusion reactions at a national referral hospital in Uganda: a prospective study. Transfusion. 2014;54(11):2804-2810.
Vickery S, Price CP, John RI, et al. B-type natriuretic peptide (BNP) and amino-terminal proBNP in patients with CKD: relationship to renal function and left ventricular hypertrophy. Am J Kidney Dis. 2005;46(4):610-620.
Das SR, Drazner MH, Dries DL, et al. Impact of body mass and body composition on circulating levels of natriuretic peptides: results from the Dallas heart study. Circulation. 2005;112(14):2163-2168.
Clerico A, Franzini M, Masotti S, Prontera C, Passino C. State of the art of immunoassay methods for B-type natriuretic peptides: an update. Crit Rev Clin Lab Sci. 2015;52(2):56-69.