Abstract
Background. The new coronavirus SARS-CoV-2, responsible for the Covid-19 pandemic, uses the angiotensin converting enzyme type 2 (ACE2), a physiological inhibitor of the renin angiotensin aldosterone system (RAAS), as a cellular receptor to infect cells. Since the RAAS can induce and modulate pro-inflammatory responses, it could play a key role in the pathophysiology of Covid-19. Thus, we aimed to determine the levels of plasma renin and aldosterone as indicators of RAAS activation in a series of consecutively admitted patients for Covid-19 in our clinic. Methods. Plasma renin and aldosterone levels were measured, among the miscellaneous investigations needed for Covid-19 management, early after admission in our clinic. Disease severity was assessed using a seven-category ordinal scale. Primary outcome of interest was the severity of patients’ clinical courses. Results. Forty-four patients were included. At inclusion, 12 patients had mild clinical status, 25 moderate clinical status and 7 severe clinical status. In univariate analyses, aldosterone and C-reactive protein (CRP) levels at inclusion were significantly higher in patients with severe clinical course as compared to those with mild or moderate course (p < 0.01 and p = 0.03, respectively). In multivariate analyses, only aldosterone and CRP levels remained positively associated with severity. We also observed a positive significant correlation between aldosterone and CRP levels among patients with an aldosterone level greater than 102.5 pmol/L. Conclusions. Both plasmatic aldosterone and CRP levels at inclusion are associated with the clinical course of Covid-19. Our findings may open new perspectives in the understanding of the possible role of RAAS for Covid-19 outcome.
Highlights
A new coronavirus called SARS-CoV-2 is responsible for the pandemic of Covid-19, which has led to tens of thousands of deaths around the world so far [1]
As compared to patients withInmcluilsdiono:rDmayo0derate cliDnaiyca2l status, CRPOSleMveaxls were significantly higherr=in0.6p1atients with ordinal scale (OS) ≥ 5 o50n0 Day 2 or at OS max (p = 0.01 and p = 0.02, respectively) 1(F50i0gure 3A).pC= o0.n00s6idering the hypothe4s0i0s that aldosterone may be i*nvolved in inflam*matory damages of Covid-19, we searched for a relationship between the aldosterone and C-reactive protein (CRP) levels
In the present study based upon data collected in the real-life settings of the brutal SARS-CoV-2 outbreak, we report an association between the plasma levels of aldosterone close to admission and the severity of Covid-19 course, as defined by the ordinal scale grade
Summary
A new coronavirus called SARS-CoV-2 is responsible for the pandemic of Covid-19, which has led to tens of thousands of deaths around the world so far [1]. The disease develops in two phases: the first one is linked to the viral invasion, and the second one consists of a severe acute inflammatory immune response, including a “cytokine storm”, which results in severe morbidity and mortality, mainly related to lung injury [2] In this context, the intensity of the inflammatory process contributes to the disease severity and the plasmatic level of C-reactive protein (CRP) (a biomarker of systemic inflammation) could represent a marker of poor outcomes in Covid-19 patients [3,4,5,6]. The new coronavirus SARS-CoV-2, responsible for the Covid-19 pandemic, uses the angiotensin converting enzyme type 2 (ACE2), a physiological inhibitor of the renin angiotensin aldosterone system (RAAS), as a cellular receptor to infect cells. Our findings may open new perspectives in the understanding of the possible role of RAAS for Covid-19 outcome
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