Kidney involvement and anemia in COVID-19 infection.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is responsible for coronavirus disease 2019 (COVID-19), has infected > 700 million people and led to > 7 million deaths worldwide. Although COVID-19 primarily affects the lungs, it can also affect the kidneys through various pathways. SARS-CoV-2 affects the kidney via several common mechanisms, such as dysregulation of angiotensin-converting enzyme 2, transmembrane serine protease 2 and tissue proteinase L expression in kidney tissue. People with chronic kidney disease (CKD) and COVID-19 have an increased risk of mortality and hospitalization in the intensive care unit. Anemia, a common consequence of CKD, is also associated with worsening outcomes in COVID-19 patients. In these patients with multiple comorbidities, there is a sharp increase in D-dimers, inflammatory parameters, creatinine and blood urea nitrogen. COVID-19 patients also present with resistance to erythropoietin (EPO)-stimulating agents, which necessitates elevated dosages even several months post-infection. In CKD, anemia is exacerbated by decreased EPO production, red blood cell (RBC) fragmentation due to impairment of the renovascular endothelium in situations such as glomerulopathy and malignant hypertension. Other factors include iron and/or folic acid deficiency, bleeding due to platelet dysfunction, inflammation, reduced RBC lifespan, poor iron utilization, uremia, and atypical blood loss after dialysis. Excessive hepcidin synthesis impairs the absorption of dietary iron and the mobilization of iron from endogenous reserves, thus contributing significantly to anemia and poor iron regulation in CKD. These findings suggest that CKD may contribute to the occurrence of anemia in COVID-19 patients, especially in older people with comorbidities. Our review aims to explore the complex relationship between CKD, COVID-19 and anemia to improve our understanding of the underlying mechanisms of the disease and the potential cofactors that worsen outcomes in these patients.