In a new study, researchers found that COVID-19 virus associated acute kidney injury is not uncommon.
Many hospitalized COVID-19 patients—as many as 80% of critically ill COVID-19 patients, according to a current study—develop acute kidney injury, but without requiring dialysis in most cases.
Examinations of renal tissue from deceased patients show injury to the renal corpuscles or filter membrane, and to the renal tubules.
Given that SARS-CoV-2 uses the ACE2 receptor to infect cells, and that tubular cells and podocytes express ACE2, it is clear that the kidney can be a specific tissue targeted by the virus.
The research was conducted by a team at Universitaire Ambroise Paré and elsewhere.
The current study reported two COVID-19 patients with injury to both these renal structures.
Both patients were over 50 years of age and were known to have high blood pressure; one had cardiac insufficiency, the other hepatitis B.
Both had been complaining of coughing for four days; one of them also had a fever. On admission, they had pulmonary CT findings typical of COVID-19 and differently elevated creatinine levels indicating reduced renal function (acute kidney injury).
Within a few days, one patient required ventilation, whereas the other only needed oxygen; dialysis was not required in either case.
Both recovered their pulmonary function within one to two weeks (extubation on day 14). Kidney function also improved, but they both had persistent, high proteinuria (increased levels of protein in the urine).
The team also found tubule injury as well as inflammatory cells.
Although both patients had positive virus detection from the throat swab, SARS-CoV-2 was not detected in blood, urine, or in kidney tissue, despite highly sensitive RT-PCR testing.
Further analysis showed variants in the APOL1 gene, which are known to be linked to a high risk for kidney disease.
The team says the kidney damage was not caused directly by the viral infection, but rather by a SARS-CoV-2-induced inflammatory reaction, particularly in the context of genetic APOL1 risk variants.
The lead author of the study is Professor Ziad Massy.
The study is published in Clinical Kidney Journal.
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