Latent Acute Kidney Injury in COVID-19

Abstract

Since the outbreak of COVID-19, a bidirectional interaction between kidney disease and the progression of COVID-19 has been demonstrated. Kidney disease is an independent risk factor for mortality in patients with COVID-19, as well as severe acute respiratory syndrome coronavirus infection 2 (SARS-CoV-2), leading to the development of acute kidney injury (AKI) and chronic kidney disease (CKD) in patients with COVID-19. However, detection of kidney damage in patients with COVID-19 may only occur at a late stage based on current clinical blood and urine tests. Some studies point to the development of a subclinical acute kidney injury syndrome (subAKI) with COVID-19. This syndrome is characterized by significant interstitial tubular damage without altering the estimated glomerular filtration rate. Despite the complexity of the mechanism(s) underlying the development of subAKI, changes in the mechanism of protein endocytosis in proximal tubular epithelial cells have been proposed. This article focuses on data regarding subAKP and COVID-19, as well as the role of PTEC and the mechanism of endocytosis of their proteins in its pathogenesis.