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Acute kidney injury 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 co-expression of both ACE2 and TMPRSS2 in the same cells is important to cause damage. Lack of co-expression 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 acute kidney injury is secondary to hemodynamic and immunologic effects of SARS-CoV-2 infection than the direct injury or infection.
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Acute Kidney Injury associated with COVID-19 - Cumulative Evidence and Rationale supporting Against Direct Kidney Injury (Infection).
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