COVID-19 drives a more severe form of acute kidney injury, Yale study finds

Illustration, kidney being attacked by virus.
(© stock.adobe.com)

Patients who develop acute kidney injury (AKI) while being treated for COVID-19 have significantly worse kidney function in the months after their hospital discharge than non-COVID patients with AKI, new Yale research finds.

In a study of patients who experienced AKI at five hospitals, researchers found that individuals who were also diagnosed with COVID-19 had a 12-fold greater loss of kidney function six months after hospitalization than those who did not have COVID. The findings were published in JAMA Network Open.

COVID-AKI looks like a different form of AKI in terms of long-term effects,” said lead author Dr. F. Perry Wilson, associate professor of medicine and director of Yale’s Clinical and Translational Research Accelerator.

Acute kidney injury is an abrupt decline in the kidney’s filtration function that is typically found in 15% of hospitalized patients and increases a patient’s likelihood of death ten-fold.

For reasons that are still not clear, the condition is more common in patients with COVID-19. Earlier research has shown that 24% to 57% of patients hospitalized with COVID-19 developed AKI. In fact, this latest research suggests that the disease may cause a more serious form of AKI to develop.

To measure kidney function, researchers looked at the estimated glomerular filtration rate (eGFR), which measures how much blood passes through the glomeruli, small filters in the kidney, each minute. Specifically, they look at how much creatinine — a chemical waste produced by the muscles — is in the blood. A healthy person has an eGFR of 90 or more milliliters per minute. A person with AKI will see a decline of 1 to 2 milliliters per minute, representing a mild loss of kidney function. But in the COVID-AKI patients, Perry said, the decline is about 12 milliliters per minute.

The observed drop in eGFR among patients with COVID-AKI was independent of patient demographics, comorbidities, or the severity of the AKI, suggesting it was the result of the hyperinflammatory state associated with COVID-19 or the residual effects of the virus, researchers said. These patients continued to have faster decline in eGFR after discharge, increasing the likelihood of long-term kidney disease, dialysis, and death.

The study involved 182 patients with COVID-19-associated AKI and 1,430 patients who had AKI but not COVID-19 at five hospitals in Connecticut and Rhode Island.

While researchers do not know what is driving this more aggressive form of AKI in COVID patients, they speculate in the study that COVID-AKI may induce tubulointerstitial fibrosis, or scarring driven by inflammation within the kidney.

It may be possible, in part, to mitigate this progression by optimizing blood pressure control and making sure any diabetes is well controlled, Wilson said. His team will continue to follow these COVID-AKI patients to further understand the long-term effects of the condition, he said.

Share this with Facebook Share this with Twitter Share this with LinkedIn Share this with Email Print this

Media Contact

Fred Mamoun: fred.mamoun@yale.edu, 203-436-2643