Abstract:
Introduction. Coronavirus disease 2019 (COVID-19) is a pandemic infection caused by the novel severe
acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Although the respiratory system is the major
target, multiple organs, including the kidneys, can be affected. Kidney involvement is frequent, with clinical
presentation ranging from abnormal proteinuria at hospital admission to progressive acute kidney injury
(AKI). AKI is one of the most important complications in critically ill patients with COVID-19. The
estimated incidence of acute kidney injury in patients with COVID-19 varies from 0.5% up to 45%
depending on the severity of the disease. Mortality among hospitalised patients with acute kidney injury
associated-COVID-19 is significantly higher than for those without kidney involvement.
Aim of study. Acute kidney injury is considered a marker of disease severity and negative prognostic factor
for survival. In this context, we explored the potential pathways and pathophysiology of COVID-19
associated with AKI.
Methods and materials. The articles published during the years 2020-2022, were selected, using PubMed
and Google Scholar database according to keywords: ,,COVID-19", „SARS-CoV-2”, „Acute kidney
injury”, „Pathophysiology”. 308 publications were found. Research includes data from 28 publications,
analysed according to selection criteria.
Results. The etiology of renal impairment in patients with COVID-19 is multifactorial. Various
mechanisms have been proposed for kidney injury in SARS-CoV-2 infection, both COVID-19-specific
mechanisms, including direct invasion of the renal parenchyma with SARS-CoV-2 virus, the new
coronavirus can exert direct cytopathic effects on kidney tissue and also non-specific mechanisms, such as:
hemodynamic instability (hypovolemia or fluid overload), local and systemic immune and inflammatory
responses, with macrophage activation and release of circulating proinflammatory cytokines (cytokine
storm), hypoxia, sepsis, rhabdomyolysis, release of tissue factors and activation of coagulation pathways
with the formation of microthrombi and alteration of the microcirculation. Other potential mechanisms are
altered Renin-Angiotensin-Aldosterone regulation, organ interactions between lung, heart, and kidney and
also therapeutic consequences (use of antibiotics and antiviral drugs with nephrotoxic potential, invasive
mechanical ventilation). The most common histopathological findings are: acute tubular injury, thrombotic
microangiopathy, endothelial injury and collapsing glomerulopathy.
Conclusion. This review highlights the importance of understanding the potential mechanisms of renal
involvement in SARS-CoV-2 infection, for the early detection of renal injury and the avoidance of factors
that contribute to progression of kidney injury, including adequate hemodynamic support and avoidance of
nephrotoxic drugs, which will improve vital prognosis of COVID-19.
