2.5 COVID-19 infection and kidney infarction

An increased risk of the formation of blood clot has previously been noted with SARS and MERS, and this is one proposed cause of pre-renal injury in COVID-9 patients (Bandyopadhyay et al., 2020; Dobesh and Trujillo, 2020). The lodging of thrombi in the renal vessels and kidneys increases the likelihood of kidney damage and possibly kidney death due to kidney infarction. This finding supports the observation where platelet-rich fibrin microthrombi scattered in peritubular capillaries and tubules in kidneys of deceased COVID-19 patients (Rapkiewicz et al., 2020). In some COVID-19-positive patients, changes in blood coagulation parameters have been observed (Iba et al., 2020; Post et al., 2020). Disseminated intravascular coagulopathy (DIC; a condition of overactive clotting factors) is observed in COVID-19 patients, particularly in the critically ill patients. DIC arises from cytokine storm syndrome-induced hemophagocytosis and acute consumptive coagulopathy, which leads to enhanced platelet activation, fibrin and thrombus formation (Ortega-Paz et al., 2021). A cross-sectional study from April 13-24 in 2020 revealed elevation of markers of endothelial cells and platelet activation such as von Willebrand factor antigen, coagulation factors and fibrinolytic enzymes (Goshua et al., 2020). These coagulation anomalies were reported in a 71-year-old COVID-19-positive patient, who exhibited thromboembolic events such as ascending aortic thrombosis, renal infarction and a corresponding hypercoagulable state (Mukherjee et al., 2020). However, this may seem a little presumptuous given that the coagulation anomalies were reported in only one patient and over a short period (10 days). In a nutshell, COVID-19 infection increases the likelihood of formation of blood clots in the renal vessels and kidney, which may lead to kidney infarction and possibly death of the patient.