Acute kidney injury associated with COVID-19-Cumulative evidence and rationale supporting against direct kidney injury (infection).

ABSTRACT

Acute kidney injury (AKI) is a common complication, affecting up to 37% of hospitalized patients with SARS-CoV-2 infection and is proportional to its severity and portends poor prognosis. Diverse mechanisms have been proposed and studies reported conflicting results. Moreover, renal tropism of SARS-CoV-2 does not equate to its renal pathogenicity. For a virus to be pathogenic, in addition to its affinity (tropism) for specific tissue(s), host cells must allow viral entry, and discuss the important role played by transmembrane protease, serine 2 (TMPRSS2) and coexpression of both ACE2 and TMPRSS2 in the same cells is important to cause damage. Lack of coexpression of ACE2 and TMPRSS2 in the same cells of the kidneys is the limiting factor of SARS-CoV-2 direct effects in the kidney. We present the rationale and cumulative evidence supporting that AKI is secondary to hemodynamic and immunologic effects of SARS-CoV-2 infection than the direct injury or infection.