Coronavirus disease 2019: acute Fanconi syndrome precedes acute kidney injury

Kormann, Raphaël; Jacquot, Audrey; Alla, Asma; Corbel, Alice; Koszutski, Matthieu; Voirin, Paul; Parrilla, Matthieu Garcia; Bévilacqua, S.; Schvoerer, Évelyne; Guéant, Jean‐Louis; Namour, Farès; Lévy, Bruno; Frimat, Luc; Oussalah, Abderrahim

doi:10.1093/ckj/sfaa109

Cited by 49 publications

(76 citation statements)

References 27 publications

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“…One of the hypotheses for the occurrence of acute renal damage is the inadequacy of the inflammatory response linked to the cytokine storm observed in severe forms of COVID-19 and their effect on hypoperfusion of renal tubules [30] . A recent study reported that patients with severe COVID-19 have a high risk of developing Fanconi syndrome, leading to potentially life-threatening plasma disturbances [31] . SARS-CoV-2 infects the cells through its binding to the membrane-bound form of receptor-angiotensin converting enzyme II (ACE2) and subsequent internalization of the complex by the host cell [ 1 , [32] , [33] , [34] ].…”

Section: Discussionmentioning

confidence: 99%

The spectrum of biochemical alterations associated with organ dysfunction and inflammatory status and their association with disease outcomes in severe COVID-19: A longitudinal cohort and time-series design study

Oussalah¹,

Gleye²,

Urmes³

et al. 2020

EClinicalMedicine

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Background: In patients with severe COVID-19, no data are available on the longitudinal evolution of biochemical abnormalities and their ability to predict disease outcomes. Methods: Using a retrospective, longitudinal cohort study design on consecutive patients with severe COVID-19, we used an extensive biochemical dataset of serial data and time-series design to estimate the occurrence of organ dysfunction and the severity of the inflammatory reaction and their association with acute respiratory failure (ARF) and death. Findings: On the 162 studied patients, 1151 biochemical explorations were carried out for up to 59 biochemical markers, totaling 15,260 biochemical values. The spectrum of biochemical abnormalities and their kinetics were consistent with a multi-organ involvement, including lung, kidney, heart, liver, muscle, and pancreas, along with a severe inflammatory syndrome. The proportion of patients who developed an acute kidney injury (AKI) stage 3, increased significantly during follow-up (0¢9%, day 0; 21¢4%, day 14; P<0¢001). On the 20 more representative biochemical markers (>250 iterations), only CRP >90 mg/L (odds ratio [OR] 6¢87, 95% CI, 2¢36À20¢01) and urea nitrogen >0¢36 g/L (OR 3¢91, 95% CI, 1¢15À13¢29) were independently associated with the risk of ARF. Urea nitrogen >0¢42 g/L was the only marker associated with the risk of COVID-19 related death. Interpretation: Our results point out the lack of the association between the inflammatory markers and the risk of death but rather highlight a significant association between renal dysfunction and the risk of COVID-19 related acute respiratory failure and death.

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Section: Discussionmentioning

confidence: 99%

The spectrum of biochemical alterations associated with organ dysfunction and inflammatory status and their association with disease outcomes in severe COVID-19: A longitudinal cohort and time-series design study

Oussalah¹,

Gleye²,

Urmes³

et al. 2020

EClinicalMedicine

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“…Our study highlighted the possible association between ACE-I or ARB use and a significant increase in both ARDS and AKI. The induction of ACE2 expression by RAS blockade might affect the binding of SARS-CoV-2 to kidney tissues, deteriorating renal function, considering that ACE2 is abundantly expressed in the proximal tubules of the kidney and type II alveolar epithelium of lung 34,35 . Little is known about the dose effect of RAS blockade in COVID-19.…”

Section: Discussionmentioning

confidence: 99%

Adverse impact of renin–angiotensin system blockade on the clinical course in hospitalized patients with severe COVID-19: a retrospective cohort study

Lim

Cho

Jeon

et al. 2020

Sci Rep

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The association between angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II receptor blocker (ARB) and the risk of mortality in hospitalized patients with severe coronavirus disease 2019 (COVID-19) was investigated. This retrospective cohort study was performed in all hospitalized patients with COVID-19 in tertiary hospitals in Daegu, Korea. Patients were classified based on whether they received ACE-I or ARB before COVID-19 diagnosis. The analysis of the primary outcome, in-hospital mortality, was performed using the Cox proportional hazards regression model. Of 130 patients with COVID-19, 30 (23.1%) who received ACE-I or ARB exhibited an increased risk of in-hospital mortality (adjusted hazard ratio, 2.20; 95% confidence interval [CI], 1.10–4.38; P = 0.025). ACE-I or ARB was also associated with severe complications, such as acute respiratory distress syndrome (ARDS) (adjusted odds ratio [aOR], 2.58; 95% CI, 1.02–6.51; P = 0.045) and acute kidney injury (AKI) (aOR, 3.06; 95% CI, 1.15–8.15; P = 0.026). Among the patients with ACE-I or ARB therapy, 8 patients (26.7%) used high equivalent doses of ACE-I or ARB and they had higher in-hospital mortality and an increased risk of ARDS and AKI (all, P < 0.05). ACE-I or ARB therapy in patients with severe COVID-19 was associated with the occurrence of severe complications and increased in-hospital mortality. The potentially harmful effect of ACE-I or ARB therapy may be higher in patients who received high doses.

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“…It can be shed into the blood and tubular urine by ADAMS17 (ADAM metallopeptidase domain 17)—a disintegrin and metalloproteinase. 78 – 80 The levels of circulating ACE2, however, can increase moderately in several pathologies, including diabetes mellitus and cardiovascular disease. 25 Full-length ACE2 is widely expressed in the cell membrane of several organs, including kidneys, testicles, and the gastrointestinal tract.…”

Section: Binding Of Sars-cov-2 To Ace2 Receptors and Internalizationmentioning

confidence: 99%

Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor

2020

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Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) originated from Wuhan, China in December 2019, and rapidly spread to other areas worldwide. Since then, COVID-19 has reached pandemic proportions with more than 570,000 deaths globally by mid-July 2020. The magnitude of the outbreak and the potentially severe clinical course of COVID-19 has led to a burst of scientific research on this novel coronavirus and its host receptor, angiotensin converting enzyme-2 (ACE2). ACE2 is a homolog of the angiotensin-I converting enzyme (ACE) that acts on several substrates in the renin-angiotensin system. With unprecedented speed, scientific research has solved the structure of SARS-CoV-2 and imaged its binding with the ACE2 receptor. In SARS-CoV-2 infection, the viral spike (S) protein receptor binding domain (RBD) binds to ACE2 to enter the host cell. ACE2 expression in the lungs is relatively low, but it is present in type II pneumocytes, a cell type also endowed with transmembrane protease serine 2 (TMPRSS2). This protease is critical for priming the SARS-CoV-2 S protein to complex with ACE2 and enter the cells. Herein, we review the current understanding of the interaction of SARS-CoV-2 with ACE2 as it has rapidly unfolded over the last months. While it should not be assumed that we have a complete picture of SARS-CoV-2's mechanism of infection and its interaction with ACE2 much has been learned with clear therapeutic implications. Potential therapies aimed at intercepting SARS-CoV-2 from reaching the full-length membrane-bound ACE2 receptor using soluble ACE2 protein and other potential approaches are briefly discussed as well.

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Coronavirus disease 2019: acute Fanconi syndrome precedes acute kidney injury

Cited by 49 publications

References 27 publications

The spectrum of biochemical alterations associated with organ dysfunction and inflammatory status and their association with disease outcomes in severe COVID-19: A longitudinal cohort and time-series design study

The spectrum of biochemical alterations associated with organ dysfunction and inflammatory status and their association with disease outcomes in severe COVID-19: A longitudinal cohort and time-series design study

Adverse impact of renin–angiotensin system blockade on the clinical course in hospitalized patients with severe COVID-19: a retrospective cohort study

Interaction of SARS-CoV-2 and Other Coronavirus With ACE (Angiotensin-Converting Enzyme)-2 as Their Main Receptor

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