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Acute kidney injury in critically ill patients with COVID-19.
Intensive Care Med. 2020 Jul; 46(7):1339-1348.IC

Abstract

Acute kidney injury (AKI) has been reported in up to 25% of critically-ill patients with SARS-CoV-2 infection, especially in those with underlying comorbidities. AKI is associated with high mortality rates in this setting, especially when renal replacement therapy is required. Several studies have highlighted changes in urinary sediment, including proteinuria and hematuria, and evidence of urinary SARS-CoV-2 excretion, suggesting the presence of a renal reservoir for the virus. The pathophysiology of COVID-19 associated AKI could be related to unspecific mechanisms but also to COVID-specific mechanisms such as direct cellular injury resulting from viral entry through the receptor (ACE2) which is highly expressed in the kidney, an imbalanced renin-angotensin-aldosteron system, pro-inflammatory cytokines elicited by the viral infection and thrombotic events. Non-specific mechanisms include haemodynamic alterations, right heart failure, high levels of PEEP in patients requiring mechanical ventilation, hypovolemia, administration of nephrotoxic drugs and nosocomial sepsis. To date, there is no specific treatment for COVID-19 induced AKI. A number of investigational agents are being explored for antiviral/immunomodulatory treatment of COVID-19 and their impact on AKI is still unknown. Indications, timing and modalities of renal replacement therapy currently rely on non-specific data focusing on patients with sepsis. Further studies focusing on AKI in COVID-19 patients are urgently warranted in order to predict the risk of AKI, to identify the exact mechanisms of renal injury and to suggest targeted interventions.

Authors+Show Affiliations

Medical Intensive Care Unit, Hopital Saint-Louis, Assistance Publique des Hôpitaux de Paris, University of Paris, Paris, France.Medical Intensive Care Unit, Hopital Saint-Louis, Assistance Publique des Hôpitaux de Paris, University of Paris, Paris, France.Medical Intensive Care Unit, Hopital Saint-Louis, Assistance Publique des Hôpitaux de Paris, University of Paris, Paris, France.Medical Intensive Care Unit, Hopital Saint-Louis, Assistance Publique des Hôpitaux de Paris, University of Paris, Paris, France.Medical Intensive Care Unit, Hopital Saint-Louis, Assistance Publique des Hôpitaux de Paris, University of Paris, Paris, France.Medical Intensive Care Unit, Hopital Saint-Louis, Assistance Publique des Hôpitaux de Paris, University of Paris, Paris, France. lara.zafrani@aphp.fr. UMR 976, INSERM, Paris, France. lara.zafrani@aphp.fr.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

32533197

Citation

Gabarre, Paul, et al. "Acute Kidney Injury in Critically Ill Patients With COVID-19." Intensive Care Medicine, vol. 46, no. 7, 2020, pp. 1339-1348.
Gabarre P, Dumas G, Dupont T, et al. Acute kidney injury in critically ill patients with COVID-19. Intensive Care Med. 2020;46(7):1339-1348.
Gabarre, P., Dumas, G., Dupont, T., Darmon, M., Azoulay, E., & Zafrani, L. (2020). Acute kidney injury in critically ill patients with COVID-19. Intensive Care Medicine, 46(7), 1339-1348. https://doi.org/10.1007/s00134-020-06153-9
Gabarre P, et al. Acute Kidney Injury in Critically Ill Patients With COVID-19. Intensive Care Med. 2020;46(7):1339-1348. PubMed PMID: 32533197.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acute kidney injury in critically ill patients with COVID-19. AU - Gabarre,Paul, AU - Dumas,Guillaume, AU - Dupont,Thibault, AU - Darmon,Michael, AU - Azoulay,Elie, AU - Zafrani,Lara, Y1 - 2020/06/12/ PY - 2020/04/30/received PY - 2020/06/03/accepted PY - 2020/6/14/pubmed PY - 2020/7/16/medline PY - 2020/6/14/entrez KW - Acute kidney injury KW - COVID-19 KW - Intensive care unit KW - Renin–angiotensin–aldosterone system SP - 1339 EP - 1348 JF - Intensive care medicine JO - Intensive Care Med VL - 46 IS - 7 N2 - Acute kidney injury (AKI) has been reported in up to 25% of critically-ill patients with SARS-CoV-2 infection, especially in those with underlying comorbidities. AKI is associated with high mortality rates in this setting, especially when renal replacement therapy is required. Several studies have highlighted changes in urinary sediment, including proteinuria and hematuria, and evidence of urinary SARS-CoV-2 excretion, suggesting the presence of a renal reservoir for the virus. The pathophysiology of COVID-19 associated AKI could be related to unspecific mechanisms but also to COVID-specific mechanisms such as direct cellular injury resulting from viral entry through the receptor (ACE2) which is highly expressed in the kidney, an imbalanced renin-angotensin-aldosteron system, pro-inflammatory cytokines elicited by the viral infection and thrombotic events. Non-specific mechanisms include haemodynamic alterations, right heart failure, high levels of PEEP in patients requiring mechanical ventilation, hypovolemia, administration of nephrotoxic drugs and nosocomial sepsis. To date, there is no specific treatment for COVID-19 induced AKI. A number of investigational agents are being explored for antiviral/immunomodulatory treatment of COVID-19 and their impact on AKI is still unknown. Indications, timing and modalities of renal replacement therapy currently rely on non-specific data focusing on patients with sepsis. Further studies focusing on AKI in COVID-19 patients are urgently warranted in order to predict the risk of AKI, to identify the exact mechanisms of renal injury and to suggest targeted interventions. SN - 1432-1238 UR - https://www.unboundmedicine.com/medline/citation/32533197/Acute_kidney_injury_in_critically_ill_patients_with_COVID_19_ L2 - https://dx.doi.org/10.1007/s00134-020-06153-9 DB - PRIME DP - Unbound Medicine ER -