Pathomorphology of Kidney Damage in Covid-19: Possible Etiological Factors

The study aim was to study the histological picture of damaged kidneys in patients who died from COVID-19, as well as to attempt to find the objective causes of renal pathology at COVID-19.

Kidney damage in this disease is still considered mainly secondary and associated with multiple organ failure, hypoxia, ischemia, disseminated intravascular coagulation (DIC) at severe and extremely severe disease.

At the same time, it was found that the initial clinical and laboratory signs of renal pathology (in the form of an increase in the level of creatinine and urea in the blood, the presence of proteinuria, cylindruria in the form of granular cylinders, and then oliguria) coincide with time (by 5-7 - 10-12 days of the disease) and are in a parallel progress with lung damage or coronavirus "pneumonia", which, both pathogenetically and clinically, is initially interstitial, and then alveolar hemorrhagic pulmonary edema (as in influenza lung disease). A characteristic feature of this "pneumonia" (pulmonary edema) and kidney damage is their "deferred" and gradual, rather slow, but steady development.

Based on the study of macro- and microscopic preparations of damaged kidneys, the conclusion is that with COVID-19 this lesion with an outcome of acute total nephronecrosis is a consequence of a direct combined viral-drug cytotoxic effect on the renal epithelium, which manifests itself pathomorphologically as total nephronecrosis, and clinically, as a form of acute renal failure, usually with a lethal outcome.