New research indicates dihydropyridine calcium-channel blockers may be associated with poorer kidney outcomes in people with type 2 diabetes. The findings were presented on June 4, 2026, at the 63rd European Renal Association Congress.
The study analyzed medical data from 31,031 adults with type 2 diabetes, collected between 2016 and 2021. All participants involved in the study were receiving both renin-angiotensin system inhibitors and sodium-glucose cotransporter-2 inhibitors, which constitute standard medical care for most patients with diabetic kidney disease.
Among the participants, 12,172 individuals, representing 39.2 percent of the cohort, were taking these medications. The remaining 18,859 individuals, or 60 percent of the cohort, were receiving other antihypertensive treatments. Patients were followed for a median period of approximately 3.5 years.
After adjusting for baseline clinical and demographic characteristics, the use of the medications correlated with a 33 percent higher risk of a major adverse kidney event. Major adverse kidney events were defined as a decline of 40 percent or more in the estimated glomerular filtration rate or progression to end-stage kidney disease requiring dialysis or transplantation. The calculated risk ratio was 1.33, with a 95 percent confidence interval ranging from 1.03 to 1.73.
This class of blood pressure medications relax blood vessels and are frequently prescribed as second-line therapies for patients with diabetic kidney disease. Diabetic kidney disease develops when persistently high blood sugar damages small blood vessels in the kidneys.
Dr. Timna Agur, the study's lead author, said, "Dihydropyridine calcium-channel blockers are widely used as second-line blood pressure treatments in patients with diabetic kidney disease. Our findings raise important questions about whether these medications are always the best option for patients already receiving modern kidney-protective therapies."
Researchers hypothesize that the medications may preferentially relax blood vessels carrying blood into the kidneys' filtering units without relaxing the vessels carrying blood out. This vascular mechanism could increase pressure within the filtering structures and contribute to kidney damage, researchers suggest. Agur said, "We initially thought the kidney-protective effects of sodium-glucose cotransporter-2 inhibitors might counterbalance the potential harms associated with dihydropyridine calcium-channel blockers. However, the increased risk of kidney disease progression appeared to persist even in this group."
The researchers stated that the study was observational in nature and cannot establish direct causation.
No independent assessment was available for this report.