Kidney Disease: Key Gene RTN1 Protein Linked To Health Issue

New findings published in the journal Nature Communications reveal that patients with higher levels of a key protein may be at an increased risk for severe kidney disease.

Researchers at the Icahn School of Medicine at Mount Sinai conducted a study on mice, with findings suggesting that variations in the gene RTN1 led to greater production of the related RTN1 protein that causes kidney cells to self-destruct.

"We are excited because these findings will shape our upcoming research efforts and hopefully lead to future classes of therapeutics," said John Cijiang He, MD, PhD, the Irene and Dr. Arthur M. Fishberg Professor of Medicine and Chief of the Division of Nephrology in the Department of Medicine at the Icahn School of Medicine at Mount Sinai, in a news release. "We believe we have found a target for the development of drugs to prevent chronic kidney disease from becoming severe."

Researchers note how the study results contribute to a better understanding of kidney disease, which is commonly caused by high blood pressure, diabetes and cancer. Chronic kidney disease affects about 10 percent of American adults and can eventually progress to end-stage renal disease, requiring dialysis or a kidney transplant.

During the study, researchers discovered that when the RTN1 gene is overexposed, it results in an excess of a protein known as reticulum to be built, which changes the shape of the endoplasmic reticulum--part of the protein-building machinery in kidney cells that signal cells to sell-destruct as part of the disease. Through the mice used in the study, researchers were able to determine which genes were expressed more and less, resulting in more severe kidney damage.

Genes whose level of expression correlated with the intensity of renal damage were catalogued, including RTN1, according to researchers.

The study authors are hopeful that this and future studies will help bring about more options for chronic kidney disease. As of now, there is an urgent need to identity key causes and mediators of chronic kidney disease progression so as to determine the best way to fight it.

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