Hospitalized patients with COVID-19 are at risk for severe kidney damage, a new study has found. Photo by EPA-EFE/Enric Fontcuberta
Sept. 22 (UPI) -- COVID-19 causes acute kidney injury that can lead to death in some people infected with the virus, a study published Tuesday by the Clinical Journal of the American Society of Nephrology found.
In an analysis of nearly 1,400 patients with the new coronavirus in Wuhan, where the pandemic began, 7% of those who required hospital care developed acute kidney injury, the data showed.
Of those who experienced this complication, 72% died of COVID-19, the researchers said. Among those without kidney damage, 10% died from the virus.
"Prior to this study, there was limited information concerning ... [acute kidney injury] in patients with COVID-19," study co-author Gang Xu, a researcher at Tongji hospital in Wuhan, said in a statement.
"Our results indicate that acute kidney injury is strongly associated with mortality, and that careful monitoring of acute kidney injury is necessary early in the course of infection," Xu said.
Tongji hospital was assigned responsibility for treating severe COVID-19 cases by the local government, researchers said.
Their study evaluated 1,392 patients treated at the hospital. Those with acute kidney injury were five times as likely to die from COVID-19 while in the hospital compared to those without the complication, the data showed.
Factors associated with a higher risk of acute kidney disease included severe COVID-19 disease and high blood creatinine levels -- an indicator of kidney dysfunction -- as well as low blood levels of certain immune cells and high blood levels of a protein fragment indicative of elevated blood clot formation and breakdown.
In a separate study, researchers at Boston University, studying human stem cell-derived lung cells called type 2 pneumocytes that were infected with COVID-19, found the virus also initially suppresses the lung cells' ability to call in the help of the immune system to fight off the disease.
Instead, the virus activates an inflammatory pathway called NFkB, which brings immune cells into lung tissue laden with infected and already dead and dying cells, "driv[ing] up levels of inflammation in the lungs," the researchers said in an article published Monday by the journal Cell Stem Cell.
"Our data confirms that [COVID-19] blocks cells from activating one of the antiviral branches of the immune system early on after infection has set in," Dr. Darrell Kotton, director of the Center for Regenerative Medicine at Boston University, said in a statement.
"The signal the cells would typically send out, a tiny protein called interferon that they exude under threat of disease, are instead delayed for several days, giving [the virus] plenty of time to spread and kill cells, triggering a buildup of dead cell debris and other inflammation," Kotton said.