Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new pathogen that was responsible for the global pandemic that started in Wuhan, China in 2019. It causes COVID-19, manifesting as viral pneumonia with concomitant acute respiratory failure and, in certain cases, multiorgan failure and death. Kidney involvement is common and can be aetiologically heterogeneous. Acute kidney injury is mostly caused indirectly, especially in the context of systemic inflammation, hypoxaemia, hypotension, shock, and increased oxidative stress. Complement activation, tubulointerstitial damage, and endothelial dysfunction with resultant thromboses are also important factors in kidney injury. Histologically, SARS-CoV-2 was found to induce predominant tubulointerstitial changes and in some cases, glomerular changes. In a certain subgroup of patients with the APOL1 high-risk allele variant, a collapsing glomerulopathy, similar to HIV-associated nephropathy, was found. This entity was later named COVID-19-associated nephropathy. In this article, the authors present the pathophysiology behind SARS-CoV-2-related kidney involvement and the development of COVID-19-associated nephropathy.
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