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.