Abstract
COVID-19 is mainly considered a respiratory illness, but since SARS-CoV-2 uses the angiotensin converting enzyme 2 receptor (ACE2) to enter human cells, the kidney is also a target of the viral infection. Acute kidney injury (AKI) is the most alarming condition in COVID-19 patients. Recent studies have confirmed the direct entry of SARS-CoV-2 into the renal cells, namely podocytes and proximal tubular cells, but this is not the only pathomechanism of kidney damage. Hypovolemia, cytokine storm and collapsing glomerulopathy also play an important role. An increasing number of papers suggest a strong association between AKI development and higher mortality in COVID-19 patients, hence our interest in the matter. Although knowledge about the role of kidneys in SARS-CoV-2 infection is changing dynamically and is yet to be fully investigated, we present an insight into the possible pathomechanisms of AKI in COVID-19, its clinical features, risk factors, impact on hospitalization and possible ways for its management via renal replacement therapy.
Highlights
COVID-19 is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and it originated in Wuhan, China, in December 2019
There are few possible reasons for acute renal failure, such as inflammatory damage caused by cytokine storm, Acute kidney injury (AKI) related to acute respiratory distress syndrome (ARDS), kidney–lung crosstalk theory, hypovolemia and collapsing glomerulopathy [24,25,26]
Acute kidney injury is common amongst patients with SARS-CoV-2 infection, especially critically ill ones, and is without a doubt associated with higher mortality
Summary
COVID-19 is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and it originated in Wuhan, China, in December 2019. COVID-19 disease mainly affects the respiratory system, which in more severe cases is manifested by pneumonia, hypoxemia and acute respiratory distress syndrome. Acute kidney injury (AKI) is the most common kidney manifestation among patients hospitalized with. According to KDIGO, AKI is defined as any of the following: (1) an increase in serum creatinine (SCr) by ≥0.3 mg/dL (≥26.5 μmol/L) within 48 h; or (2) an increase in SCr ≥ 1.5 times of baseline within the prior 7 days; or (3) urine volume < 0.5 mL/kg/hour for 6 h. AKI can be staged for severity according to KDIGO: stage (1) increase in SCr to 1.5–1.9 times baseline or by ≥0.3 mg/dL; stage (2) increase SCr to 2.0–2.9 times baseline; stage (3) increase SCr to 3.0 times baseline or increase in serum creatinine to.
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