According to a recent study led by researchers in the Perelman School of Medicine, metabolic changes related to a coenzyme might serve as the basis for a future treatment for kidney disease.
Penn scientists mapped metabolite changes in healthy and diseased mice and human kidneys. This allowed them to identify differences between the healthy and diseased kidneys and recognize a significant decrease in nicotinamide adenine dinucleotide, a "helper molecule," in the diseased kidneys.
The study was conducted by co-lead investigators Katalin Susztak, professor of nephrology and co-chair of the Kidney Innovation Center at Penn Medicine, and Joseph Baur, professor of physiology at Penn. The first author was Tomohito Doke, a postdoctoral fellow in Susztak’s lab.
“We hope that this research can lead to improved care in the future. So when patients have metabolite changes, they can receive treatment before kidney disorders arise,” Susztak said to Penn Medicine News.
Prior to their study, samples from human patients had not been used in metabolomic studies to study the effects of kidney disease. Throughout the study, the team identified changes in NAD metabolism in mice and human kidneys.
Mice were given an over-the-counter supplement that effectively reversed NAD loss. This provided evidence that NAD could play a significant role in protecting from kidney dysfunction.
They further showed in the mice studies that using supplements such as nicotinamide riboside or nicotinamide mononucleotide to boost NAD protected mice from kidney dysfunction by protecting the kidney tubule mitochondria cells.
Kidney tubule cells return crucial filtered nutrients to the body’s bloodstream. The researchers found that when the mitochondria in those cells are damaged, a pathway that causes inflammation and kidney disease development is activated.
The team hopes that their research will lead to further studies into the significance of metabolite changes in kidney dysfunction and the development of new treatments to prevent and cure kidney disease.
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