According to research published in the journal Nature Communications, patients with higher levels of a certain protein are at greater risk of developing severe kidney disease.
Four per cent of adults in England have the condition, and the NHS believes another million people could be living with it undiagnosed.
The study, led by researchers from the Icahn School of Medicine at Mount Sinai, claims that variations in the gene RTN1 cause a greater production of a protein called reticulon, which causes kidney cells to self-destruct.
To establish this the research team looked at which genes were expressed more as kidney damage grew more severe. They found that high levels of reticulon corresponded with intense renal damage.
The research was carried out in mice, but to ensure the results are relevant to humans, the researchers confirmed that similar genetic differences are seen in human kidney disease.
John Cijiang He, chief of nephrology in the school’s department of medicine, hopes the research will have practical benefits:
‘We are excited because these findings will shape our upcoming research efforts and hopefully lead to future classes of therapeutics. We believe we have found a target for the development of drugs to prevent chronic kidney disease from becoming severe.’
Early diagnosis is crucial because chronic kidney disease greatly increases the risk of other vascular events, such as stroke and heart failure. This risk can be reduced if chronic kidney disease is identified and managed at an early stage.
‘Right now, therapeutic options for chronic kidney disease are limited, and only offer partial protection against disease protection. Therefore, there is an urgent need to identify key causes and mediators of chronic kidney disease progression so that we can find the best way to fight it.’