A type of protein found in urine could help provide a clearer picture of how people with type 2 diabetes and kidney disease respond to finerenone, according to new research.
The study found that treatment with finerenone was associated with reductions in non-albumin proteinuria (NAP), particularly among people with higher levels of proteinuria before starting treatment.
The researchers say the findings suggest NAP could potentially provide a useful additional marker for monitoring treatment response in diabetic kidney disease (DKD).
Looking beyond albuminuria
Diabetic kidney disease is a common complication of diabetes and can lead to a progressive decline in kidney function.
Albuminuria – an increased amount of the protein albumin in the urine – is widely used to assess kidney damage and monitor the progression of DKD.
However, not everyone with DKD follows the same pattern. Some people experience declining kidney function without a corresponding increase in albuminuria, highlighting the need for additional ways to assess kidney health.
Researchers in South Korea therefore investigated non-albumin proteinuria, which includes proteins associated with damage to the kidney tubules.
They wanted to determine whether levels changed following treatment with finerenone and whether NAP could potentially be used as a marker of treatment response.
What did the study find?
The researchers analysed data from 477 adults with Type 2 diabetes who had been treated with finerenone, a non-steroidal mineralocorticoid receptor antagonist used to lower the risk of kidney failure, heart attacks, and death from heart disease in people with chronic kidney disease linked to the disease.
After six months of treatment, albuminuria had fallen by 30.3%, while non-albumin proteinuria had fallen by 17.5%. However, the reduction in NAP differed depending on how much protein participants had in their urine before starting treatment.
Among people with higher baseline proteinuria, NAP fell by 18.8%. In those with lower baseline proteinuria, researchers recorded a 1.3% change, which was not statistically significant.
Changes in NAP were also associated with changes in another urinary marker called N-acetyl-β-D-glucosaminidase (NAG), which is used as a marker of injury to the kidney tubules.
Together, the results raise the possibility that monitoring non-albumin proteins could provide information about kidney changes that are not captured by albuminuria alone.
Could it lead to more personalised treatment?
Finerenone is already used to reduce the risk of kidney and cardiovascular complications in certain people with chronic kidney disease associated with type 2 diabetes.
The researchers suggest that measuring NAP alongside albuminuria could potentially help identify different patterns of kidney disease and provide additional information about how someone is responding to treatment.
Importantly, however, the findings do not yet show that NAP should be routinely used to guide treatment decisions.
The research was a retrospective observational study conducted at a single hospital. This means it can show an association between finerenone treatment and changes in NAP, but cannot establish that the medication directly caused those changes.
The researchers said prospective studies involving multiple centres are now needed to determine whether NAP can reliably predict treatment response and, importantly, whether changes in NAP correspond with better long-term kidney outcomes.
The findings nevertheless suggest that looking beyond albumin alone could offer another way to understand the varied effects of diabetic kidney disease and, in the future, potentially support a more personalised approach to its management.
Reference
Choi M S et al. Non-albumin proteinuria as a candidate biomarker of treatment response to finerenone in diabetic kidney disease: a real-world cohort study. Front. Endocrinol. 2026. 17:1918192.
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