tetano
Editor, Senior Moderator
Cytokine
. 2022 Jul 25;157:155974.
doi: 10.1016/j.cyto.2022.155974. Online ahead of print.
Acute kidney injury associated to COVID-19 leads to a strong unbalance of circulant immune mediators
Thalia Medeiros[SUP] 1 [/SUP], Gabriel Macedo Costa Guimarães[SUP] 2 [/SUP], Fabiana Rabe Carvalho[SUP] 2 [/SUP], Lilian Santos Alves[SUP] 2 [/SUP], Renan Faustino[SUP] 2 [/SUP], Ana Carolina Campi-Azevedo[SUP] 3 [/SUP], Vanessa Peruhype-Magalhães[SUP] 3 [/SUP], Andréa Teixeira-Carvalho[SUP] 3 [/SUP], Matheus de Souza Gomes[SUP] 4 [/SUP], Laurence Rodrigues do Amaral[SUP] 4 [/SUP], Olindo Assis Martins-Filho[SUP] 3 [/SUP], Jocemir Ronaldo Lugon[SUP] 5 [/SUP], Jorge Reis Almeida[SUP] 5 [/SUP], Andrea Alice Silva[SUP] 6 [/SUP]
Affiliations
Abstract
Background: Severe cases of coronavirus disease 2019 (COVID-19) have increased risk for acute kidney injury (AKI). The exacerbation of the immune response seems to contribute to AKI development, but the immunopathological process is not completely understood.
Objectives: To analyze levels of circulant immune mediators in COVID-19 patients evolving with or without AKI. We have also investigated possible associations of these mediators with viral load and clinical outcomes.
Methods: This is a longitudinal study performed with hospitalized patients with moderate to severe COVID-19. Serum levels of 27 immune mediators were measured by a multiplex immunoassay. Data were analyzed at two timepoints during the follow-up: within the first 13 days of the disease onset (early sample) and from the 14th day to death or hospital discharge (follow-up sample).
Results: We studied 82 COVID-19 patients (59.5 ± 17.5 years, 54.9% male). Of these, 34 (41.5%) developed AKI. These patients presented higher SARS-CoV-2 viral load (P = 0.03), higher frequency of diabetes (P = 0.01) and death (P = 0.0004). Overall, AKI patients presented significantly higher and sustained levels (P < 0.05) of CCL-2, CCL-3, CCL-4, CXCL-8, CXCL-10, IFN-γ, IL-2, IL-6, TNF-α, IL-1Ra, IL-10 and VEGF. Importantly, higher levels of CCL-2, CXCL-10, IL-2, TNF-α, IL-10, FGFb, and VEGF were observed in AKI patients independently of death. ROC curves demonstrated that early alterations in CCL-2, CXCL-8, CXCL-10, IFN-γ, IL-6, IL-1Ra and IL-10 show a good predictive value regarding AKI development. Lastly, immune mediators were significantly associated with each other and with SARS-CoV-2 viral load in AKI patients.
Conclusions: COVID-19 associated AKI is accompanied by substantial alterations in circulant levels of immune mediators, which could significantly contribute to the establishment of kidney injury.
Keywords: Acute kidney injury; COVID-19; Cytokines; Immune mediators.
. 2022 Jul 25;157:155974.
doi: 10.1016/j.cyto.2022.155974. Online ahead of print.
Acute kidney injury associated to COVID-19 leads to a strong unbalance of circulant immune mediators
Thalia Medeiros[SUP] 1 [/SUP], Gabriel Macedo Costa Guimarães[SUP] 2 [/SUP], Fabiana Rabe Carvalho[SUP] 2 [/SUP], Lilian Santos Alves[SUP] 2 [/SUP], Renan Faustino[SUP] 2 [/SUP], Ana Carolina Campi-Azevedo[SUP] 3 [/SUP], Vanessa Peruhype-Magalhães[SUP] 3 [/SUP], Andréa Teixeira-Carvalho[SUP] 3 [/SUP], Matheus de Souza Gomes[SUP] 4 [/SUP], Laurence Rodrigues do Amaral[SUP] 4 [/SUP], Olindo Assis Martins-Filho[SUP] 3 [/SUP], Jocemir Ronaldo Lugon[SUP] 5 [/SUP], Jorge Reis Almeida[SUP] 5 [/SUP], Andrea Alice Silva[SUP] 6 [/SUP]
Affiliations
- PMID: 35907365
- DOI: 10.1016/j.cyto.2022.155974
Abstract
Background: Severe cases of coronavirus disease 2019 (COVID-19) have increased risk for acute kidney injury (AKI). The exacerbation of the immune response seems to contribute to AKI development, but the immunopathological process is not completely understood.
Objectives: To analyze levels of circulant immune mediators in COVID-19 patients evolving with or without AKI. We have also investigated possible associations of these mediators with viral load and clinical outcomes.
Methods: This is a longitudinal study performed with hospitalized patients with moderate to severe COVID-19. Serum levels of 27 immune mediators were measured by a multiplex immunoassay. Data were analyzed at two timepoints during the follow-up: within the first 13 days of the disease onset (early sample) and from the 14th day to death or hospital discharge (follow-up sample).
Results: We studied 82 COVID-19 patients (59.5 ± 17.5 years, 54.9% male). Of these, 34 (41.5%) developed AKI. These patients presented higher SARS-CoV-2 viral load (P = 0.03), higher frequency of diabetes (P = 0.01) and death (P = 0.0004). Overall, AKI patients presented significantly higher and sustained levels (P < 0.05) of CCL-2, CCL-3, CCL-4, CXCL-8, CXCL-10, IFN-γ, IL-2, IL-6, TNF-α, IL-1Ra, IL-10 and VEGF. Importantly, higher levels of CCL-2, CXCL-10, IL-2, TNF-α, IL-10, FGFb, and VEGF were observed in AKI patients independently of death. ROC curves demonstrated that early alterations in CCL-2, CXCL-8, CXCL-10, IFN-γ, IL-6, IL-1Ra and IL-10 show a good predictive value regarding AKI development. Lastly, immune mediators were significantly associated with each other and with SARS-CoV-2 viral load in AKI patients.
Conclusions: COVID-19 associated AKI is accompanied by substantial alterations in circulant levels of immune mediators, which could significantly contribute to the establishment of kidney injury.
Keywords: Acute kidney injury; COVID-19; Cytokines; Immune mediators.