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Use of tocilizumab in kidney transplant recipients with COVID‐19
Author(s) -
PérezSáez María J.,
Blasco Miquel,
RedondoPachón Dolores,
VenturaAguiar Pedro,
BadaBosch Teresa,
PérezFlores Isabel,
Melilli Edoardo,
SánchezCámara Luis A.,
LópezOliva María O.,
Canal Cristina,
Shabaka Amir,
GarraMoncau Núria,
MartínMoreno Paloma L.,
López Verónica,
HernándezGallego Román,
Siverio Orlando,
Galeano Cristina,
EspíReig Jordi,
Cabezas Carlos J.,
Rodrigo María T.,
LlinàsMallol Laura,
FernándezReyes María J.,
CruzadoVega Leónidas,
PérezTamajón Lourdes,
SantanaEstupiñán Raquel,
RuizFuentes María C,
Tabernero Guadalupe,
Zárraga Sofía,
Ruiz Juan C,
GutiérrezDalmau Alex,
Mazuecos Auxiliadora,
SánchezÁlvarez Emilio,
Crespo Marta,
Pascual Julio
Publication year - 2020
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/ajt.16192
Subject(s) - tocilizumab , medicine , cytokine release syndrome , cytokine storm , hazard ratio , gastroenterology , population , confidence interval , immunology , covid-19 , disease , infectious disease (medical specialty) , environmental health
Acute respiratory distress syndrome associated with coronavirus infection is related to a cytokine storm with large interleukin‐6 (IL‐6) release. The IL‐6‐receptor blocker tocilizumab may control the aberrant host immune response in patients with coronavirus disease 2019 (COVID‐19) . In this pandemic, kidney transplant (KT) recipients are a high‐risk population for severe infection and showed poor outcomes. We present a multicenter cohort study of 80 KT patients with severe COVID‐19 treated with tocilizumab during hospital admission. High mortality rate was identified (32.5%), related with older age (hazard ratio [HR] 3.12 for those older than 60 years, P  = .039). IL‐6 and other inflammatory markers, including lactic acid dehydrogenase, ferritin, and D‐dimer increased early after tocilizumab administration and their values were higher in nonsurvivors. Instead, C‐reactive protein (CRP) levels decreased after tocilizumab, and this decrease positively correlated with survival (mean 12.3 mg/L in survivors vs. 33 mg/L in nonsurvivors). Each mg/L of CRP soon after tocilizumab increased the risk of death by 1% (HR 1.01 [confidence interval 1.004‐1.024], P  = .003). Although patients who died presented with worse respiratory situation at admission, this was not significantly different at tocilizumab administration and did not have an impact on outcome in the multivariate analysis. Tocilizumab may be effective in controlling cytokine storm in COVID‐19 but randomized trials are needed.

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