News release

From: Federation University Australia

A new study led by Federation University researchers has identified a specific biological signature within the human kidney that could hold the key to predicting and managing age-related organ failure.

The research shows that the shortening of telomeres within kidney cells, coupled with specific chemical changes to DNA, may contribute to the development of nephrosclerosis – the hardening and scarring of kidneys often associated with ageing and a major contributor to chronic kidney disease (CKD).

Telomeres are the protective caps at the ends of chromosomes and while it has long been known that these shorten with age, the study provides evidence that telomere shortening within kidney tissue may provide a clearer picture of kidney health than measurements taken from  blood cells.

CKD is often called a silent killer because it is largely irreversible and asymptomatic until it reaches an advanced stage. Many patients only discover the damage when they are already facing dialysis or a transplant.

By identifying specific markers of ‘biological ageing’ within the kidney, the researchers were able to distinguish between people whose organs were ageing at a normal rate and ‘fast agers’ who are at high risk for organ failure, potentially identifying individuals at increased risk long before symptoms appear.

The research team analysed tissue from 200 participants through the Human Kidney Tissue Resource, the world’s largest resource of the organ. The collaboration included researchers from the University of Manchester and the team analysed healthy tissue samples from patients undergoing surgery.

They discovered that the way a kidney ages is unique and does not always match the ageing process seen in blood or skin cells.

Federation University researcher Dr Arinola Akinnibosun, who led the study, said while chronological age is a known factor in kidney disease, the research shows that a person’s birth year doesn't always tell the full story.

She said some younger individuals possess kidneys that are biologically ‘older’ than their years, leaving them more vulnerable to early-onset disease.

“By looking at telomeres within kidney cells, we wanted to see if they could signal these changes early – before they progress to chronic disease.

“We also monitored epigenetic markers. By measuring these changes at a genetic level, we can identify ‘fast kidney agers,’ or those whose kidneys are ageing more rapidly than expected.”

By identifying the specific genes and patterns linked to kidney damage, the findings could eventually allow doctors to identify high-risk patients decades before they ever need dialysis or a transplant.

Dr Akinnibosun said lifestyle changes are known to be effective in delaying kidney disease, but many people assume that they don’t have to worry about the illness until they are in their 60s or 70s.

“We're trying to get to a place where we can be a bit more personalised in the way that we deal with individuals and where we can assess people’s risk to know if they are fast agers or slow agers,” she said.

“For those who are fast agers, they can start implementing lifestyle changes early. If the treatment can be more personalised to them, they will have a much higher chance of avoiding serious health problems later.”

Dr Arinola Akinnibosun said the study, published in the journal Cardiovascular Research, would allow other researchers to begin building on their work. She said there were also implications for clinical practice.

"If you know early that your kidneys are ageing faster than expected, you can take steps to delay your risk,” Dr Akinnibosun said.

“Ultimately, lifestyle plays a key role and it starts early on. We know we can't change every factor, but when we have a clearer picture of how different organs in the body are ageing, we can better understand what steps may help protect them.”