Chronic kidney disease (CKD) generally progresses to end-stage renal disease that requires dialysis or a kidney transplant. Higher levels of a key protein that causes kidney cells to self-destruct may put patients at greater risk of contracting severe kidney disease, revealed a new study.
Corresponding author John Cijiang He, professor at the Icahn School of Medicine at Mount Sinai in the US, said, "We believe we have found a target for the development of drugs to prevent chronic kidney disease from becoming severe. Right now, therapeutic options for chronic kidney disease are limited, and only offer partial protection against disease protection."
For the study, the research team 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 the cells to self-destruct. The researchers 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 severity of renal damage were catalogued, including RTN1. To ensure that the results of the study were relevant to human kidney disease, researchers then confirmed that similar genetic differences are seen in human kidney disease. Earlier, RTN1 had never been examined in the context of kidney disease.
The findings appeared in Nature Communications.