COVID-19 directly affects the kidneys, too

SARS-CoV-2 can directly infect the kidneys, leading to tubular pathogenesis and acute kidney injury (AKI), a recent study has found.

Researchers conducted a retrospective analysis of 85 patients with laboratory-confirmed novel coronavirus disease (COVID-19). Post-mortem kidney histopathology was also performed in six additional COVID-19 autopsies; in all cases, acute respiratory distress syndrome was the cause of death.

Of the patients, 23 had AKI while the remaining 62 did not, yielding a prevalence rate of 27 percent. AKI was diagnosed based on estimated glomerular filtration rate (eGFR). Severe disease and mortality both overlapped with AKI, though statistical significance was not achieved. Patients who were older or had comorbidities were much more likely to develop AKI.

Dividing the patients into three severity groups (mild/moderate, severe, and critical) showed that eGFR was significantly lowered among critically ill patients, while serum urea and creatinine concentrations were dramatically raised, suggesting that in these patients, AKI was relatively common.

Post-mortem histopathological studies showed varying degrees of tubular necrosis, luminal brush border sloughing, vacuole degeneration, and leukocyte infiltration. Four of the autopsy samples showed signs of benign hypertensive glomerulosclerosis, though none had severe glomerular injury.

“[P]atients infected by SARS-CoV-2 presented kidney defects that appear different from nephritis and nephrotic syndrome, in which the pathological signs are mainly shown in the glomerulus, rarely accompanied by tubular injury,” the researchers said.

“[W]e have demonstrated that the SARS-CoV-2 virus can directly infect human renal tubules and consequently lead to renal tubular injury and AKI, suggesting that the risk of AKI in COVID-19 patients should be kept in mind and alleviation of renal injury would benefit COVID-19 patients,” they added.