Epigenetic Age Acceleration Tracks Kidney Disease Progression in Type 1 Diabetes

The work is an observational study in people. It cannot show that faster biological ageing causes kidney damage. Researchers analysed two groups of people with type 1 diabetes: 464 in the UK and Republic of Ireland cohort and 795 in the Finnish Diabetic Nephropathy (FinnDiane) cohort. In each, some had diabetic kidney disease (the cases) and some did not (the controls).

The study used epigenetic clocks. These are tools that read chemical marks on DNA, called methylation, to estimate how old the body is biologically rather than by the calendar. The team generated 10 different clocks. They also compared telomere length measured in the lab with telomere length predicted from methylation. Telomeres are the protective caps on the ends of chromosomes.

Two measures stood out. A higher PhenoAge score and a shorter methylationpredicted telomere length were both linked to greater odds of diabetic kidney disease. These results were adjusted for age, white blood cell proportions and sex. For the principal-component version of PhenoAge, the odds ratio was 1.4 (95% confidence interval 1.2–1.8) in the UK and Ireland group and 1.8 (1.5–2.1) in the Finnish group. For predicted telomere length, the odds ratios were 0.6 (0.5–0.8) and 0.7 (0.6–0.8). Values below 1 mean that longer telomeres went with lower odds.

The authors also reported a male-specific link between kidney disease and DunedinPACE, a clock that estimates the pace of ageing. The odds ratio was 1.3 (1.0– 1.7) in the UK and Ireland group and 1.5 (1.3–1.8) in the Finnish group.

The researchers then looked at change over time. In one analysis, 52 people had methylation measured twice, a median of 7.5 years apart. Progression from normal albumin levels in the urine to severely increased levels, a sign of worsening kidney damage, was associated with increased epigenetic age acceleration.

A second analysis followed 384 people who already had kidney disease for a median of 7.7 years, using Cox regression to look at who progressed to end-stage kidney disease. Chronological age, epigenetic age and age acceleration were all significant predictors. For PhenoAge acceleration, the hazard ratio was 1.07 per year (1.03–1.11; P = 0.0011). The C-index was 0.67. That statistic runs from 0.5, no better than chance, to 1.0, perfect. So the signal is real but modest on its own.

The authors conclude that these epigenetic markers show accelerated biological ageing linked to diabetic kidney disease and to progression to end-stage kidney disease. They say the results support developing epigenetic biomarkers to predict onset and progression. That is a goal, not a current test.

This study differs from the paper's October 18 report on longer sleep and kidney disease risk in type 2 diabetes. That story concerned a behavioural signal in a different type of diabetes. This one concerns a molecular signal in type 1. Both are observational and point to possible early warning signs.

What to watch next

Studies that test whether epigenetic age measures can flag kidney risk earlier or more accurately than the tests already in use, and whether the findings hold in more varied groups of people.

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