Researchers at the Icahn School of Medicine, Mount Sinai have discovered that high levels of a specific protein increase the likelihood of developing severe kidney disease. The study – performed with mice – revealed that certain variations in the gene RTN1 led to the over-expression of RTN1 protein, causing kidney cells to self-destruct.

Chronic Kidney Disease

Healthy kidneys filter blood, produce urine for excretion and filter necessary proteins back to the bloodstream. In chronic kidney disease (CKD) – affecting around 10 percent of Americans adults – these natural processes fail to function, eventually leading to end-stage renal disease, dialysis and kidney transplant.

John Cijiang He, MD, PhD explained that current therapeutic treatments for chronic kidney disease offer only partial protection. Thus, there is an urgent and significant need to identify the major causes and mediators of the disease, so that its progression and can be managed efficiently.

Finding The Link

In pursuit of finding an answer, researchers observed that the over-expression of RTN1 gene produces excessive amounts of RTN1 protein – known as reticulon. The latter alter the shape of the endoplasmic reticulum (part of the protein-building machinery) in kidney cells, signaling them to self-destruct. Prior to this study, RTN1 had never been studied in the context of kidney disease.

Following these findings, the researchers used mice as subjects to study which genes were under or over-expressed in cases of progressive kidney damage. All genes whose expression was associated with intense renal damage were recorded, including RTN1. To ensure that the findings could be applicable to humans, the scientists confirmed that similar genetic discrepancies were also observed during human kidney disease.

Prospects Of The Findings: Protein Increases Risk For Kidney Disease

The results of this study can help scientists comprehend kidney disease better, especially since its causation is generally linked with diabetes, hypertension and cancer.

“These findings will shape upcoming research efforts and hopefully lead to future classes of therapeutics”, stated John Cijiang He, 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. “We believe we have found a target for the development of drugs to prevent chronic kidney disease from becoming severe”. The study was recently published in Nature Communications.