The researchers found that excess of this protein causes kidney cells to self-destruct.
"We believe we have found a target for the development of drugs to prevent chronic kidney disease from becoming severe," said corresponding author John Cijiang He, professor at the Icahn School of Medicine at Mount Sinai in the US.
Chronic kidney disease generally progresses to end-stage renal disease that requires dialysis or a kidney transplant.
"Right now, therapeutic options for chronic kidney disease are limited, and only offer partial protection against disease protection," he added.
In the study, the researchers found that when the gene RTN1 is over-expressed, or activated more than normal, it causes an excess of a protein called reticulon to be built.
This in turn changes the protein-building machinery in kidney cells, that signals cells to self-destruct.
The research team examined which genes were expressed more and less in study mice as kidney damage grew more severe.
Genes whose level of expression correlated with the intensity of renal damage were catalogued, including RTN1.
To ensure that the results were relevant to human kidney disease, researchers then confirmed that similar genetic differences are seen in human kidney disease.
Before this study, RTN1 had never been examined in the context of kidney disease, the study said.
The findings appeared in the journal Nature Communications.