CovidFranceV1, Main, Exploration, bibRecord, 001761

Acute kidney injury in critically ill patients with COVID-19.

Identifieur interne : 001761 ( Main/Exploration ); précédent : 001760; suivant : 001762

Acute kidney injury in critically ill patients with COVID-19.

Auteurs : Paul Gabarre [France] ; Guillaume Dumas [France] ; Thibault Dupont [France] ; Michael Darmon [France] ; Elie Azoulay [France] ; Lara Zafrani [France]

Source :

Intensive care medicine [ 1432-1238 ] ; 2020.

RBID : pubmed:32533197

Descripteurs français

KwdFr :
- Atteinte rénale aigüe (physiopathologie), Atteinte rénale aigüe (thérapie), Atteinte rénale aigüe (traitement médicamenteux), Atteinte rénale aigüe (virologie), Betacoronavirus (isolement et purification), Betacoronavirus (physiologie), Créatinine (sang), Examen des urines (MeSH), Humains (MeSH), Hématurie (étiologie), Infections à coronavirus (complications), Infections à coronavirus (métabolisme), Infections à coronavirus (urine), Maladie grave (MeSH), Pandémies (MeSH), Pneumopathie virale (complications), Pneumopathie virale (métabolisme), Pneumopathie virale (urine), Protéinurie (étiologie), Rein (physiopathologie), Rein (virologie), Système rénine-angiotensine (physiologie), Troubles de l'hémostase et de la coagulation (virologie), Urine (composition chimique), Urine (virologie).
MESH :
- composition chimique : Infections à coronavirus, Pneumopathie virale, Urine.
- isolement et purification : Betacoronavirus.
- métabolisme : Infections à coronavirus, Pneumopathie virale.
- physiologie : Betacoronavirus, Système rénine-angiotensine.
- physiopathologie : Atteinte rénale aigüe, Rein.
- sang : Créatinine.
- thérapie : Atteinte rénale aigüe.
- traitement médicamenteux : Atteinte rénale aigüe.
- virologie : Atteinte rénale aigüe, Rein, Troubles de l'hémostase et de la coagulation, Urine.
- étiologie : Hématurie, Infections à coronavirus, Pneumopathie virale, Protéinurie.
- Examen des urines, Humains, Maladie grave, Pandémies.

English descriptors

KwdEn :
- Acute Kidney Injury (drug therapy), Acute Kidney Injury (physiopathology), Acute Kidney Injury (therapy), Acute Kidney Injury (virology), Betacoronavirus (isolation & purification), Betacoronavirus (physiology), Blood Coagulation Disorders (virology), Coronavirus Infections (complications), Coronavirus Infections (metabolism), Coronavirus Infections (urine), Creatinine (blood), Critical Illness (MeSH), Hematuria (etiology), Humans (MeSH), Kidney (physiopathology), Kidney (virology), Pandemics (MeSH), Pneumonia, Viral (complications), Pneumonia, Viral (metabolism), Pneumonia, Viral (urine), Proteinuria (etiology), Renin-Angiotensin System (physiology), Urinalysis (MeSH), Urine (chemistry), Urine (virology).
MESH :
- chemical , blood : Creatinine.
- chemistry : Urine.
- complications : Coronavirus Infections, Pneumonia, Viral.
- drug therapy : Acute Kidney Injury.
- etiology : Hematuria, Proteinuria.
- isolation & purification : Betacoronavirus.
- metabolism : Coronavirus Infections, Pneumonia, Viral.
- physiology : Betacoronavirus, Renin-Angiotensin System.
- physiopathology : Acute Kidney Injury, Kidney.
- therapy : Acute Kidney Injury.
- urine : Coronavirus Infections, Pneumonia, Viral.
- virology : Acute Kidney Injury, Blood Coagulation Disorders, Kidney, Urine.
- Critical Illness, Humans, Pandemics, Urinalysis.

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.

DOI: 10.1007/s00134-020-06153-9
PubMed: 32533197
PubMed Central: PMC7290076

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000E13
to stream Main, to step Curation: 000E13

Le document en format XML

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<term>Acute Kidney Injury (therapy)</term>
<term>Acute Kidney Injury (virology)</term>
<term>Betacoronavirus (isolation & purification)</term>
<term>Betacoronavirus (physiology)</term>
<term>Blood Coagulation Disorders (virology)</term>
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<term>Coronavirus Infections (urine)</term>
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<term>Kidney (physiopathology)</term>
<term>Kidney (virology)</term>
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<term>Pneumonia, Viral (metabolism)</term>
<term>Pneumonia, Viral (urine)</term>
<term>Proteinuria (etiology)</term>
<term>Renin-Angiotensin System (physiology)</term>
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<term>Atteinte rénale aigüe (traitement médicamenteux)</term>
<term>Atteinte rénale aigüe (virologie)</term>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
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<Title>Intensive care medicine</Title>
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<ArticleTitle>Acute kidney injury in critically ill patients with COVID-19.</ArticleTitle>
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<Abstract><AbstractText>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.</AbstractText>
</Abstract>
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<Initials>P</Initials>
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Acute kidney injury in critically ill patients with COVID-19.

Acute kidney injury in critically ill patients with COVID-19.

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