Open AccessThe etiology and pathophysiology of COVID-19 associated acute kidney injury
Author(s) -
Andrei Niculae,
Mirela Țigliș,
Tiberiu Paul Neagu,
Ana-Maria Nechita,
Ileana Peride,
Ionel-Alexandru Checherita
Publication year - 2021
Publication title -
romanian medical journal
Language(s) - English
Resource type - Journals
eISSN - 2069-606X
pISSN - 1220-5478
DOI - 10.37897/rmj.2021.4.13
Subject(s) - acute kidney injury , pathophysiology , medicine , etiology , acute tubular necrosis , azotemia , kidney , pathology , renal function
Hospitalized COVID-19 patients often develop acute kidney injury (AKI), leading to increased mortality. In order to improve patients’ survival rate, it is important to understand the pathophysiology mechanism of AKI. In this brief review, we highlight the most important elements of the etiology and pathophysiology of COVID-19 associated AKI. Acute tubular injury seems to be more frequent than prerenal azotemia in COVID-19 patients and collapsing glomerulopathy is the most encountered form of glomerular disease. Another important role in acute kidney injury seems to play immune cell infiltration, inflammation, endothelial injury and microvascular thrombi. Renin-angiotensin-aldosterone system is also important in the pathophysiology of COVID-19 associated AKI.