SARS-CoV-2 Infection and the Kidneys: An Evolving Picture

Abstract

Since December 2019, a novel coronavirus known as Severe Acute Respiratory Virus 2 (SARS-CoV-2) has caused an outbreak of a respiratory illness worldwide. Even though SARS-CoV-2 primarily affects the respiratory system, other organs such as the heart and kidneys are implicated. The pathophysiology of Acute Kidney Injury (AKI) in coronavirus 2019 (COVID-19) patients is not clearly defined. Direct kidney injury results from virus entry through angiotensin-converting enzyme-2 (ACE2) receptors which are highly expressed by the podocytes and proximal convoluted tubules, as suggested by “viral-like” particles on electron microscopy. However, the link between the presence of viral particles in kidney tissue and kidney injury has not been fully explained. Furthermore, it is also hypothesized that collapsing focal segmental glomerulosclerosis (FSGS), myoglobin toxicity, sepsis-linked, and glomeruli fibrin thrombi is part of the mechanism for AKI. Reported cases link FSGS and high-risk apolipoprotein 1 (APOL1) alleles in patients of African ancestry. Typically, these patients present with AKI and nephrotic-range proteinuria. The rate of AKI in hospitalized patients is high and associated with a higher mortality rate in older patients with comorbidities. Even higher mortality is now being reported in patients with chronic kidney disease and kidney transplant recipients due to immune system dysfunction. Herein, we review the current literature on kidney disease and pathogenesis in COVID-19 patients.