Blood Pressure Drug Class Linked to Worse Kidney Outcomes in Diabetic Patients, Studies Show
New research presented at the ERA Congress found DCCB blood pressure medications were associated with a 33% increased risk of major adverse kidney events in Type 2 diabetes patients also receiving RAS and SGLT2 inhibitors. A separate study revealed that diabetic nephropathy patients exhibit the most severe biochemical disturbances, including markedly elevated glycemic indices and significantly impaired renal function compared to other groups.
Commonly prescribed blood pressure medications known as dihydropyridine calcium-channel blockers (DCCBs) may be associated with significantly worse kidney outcomes in people with Type 2 diabetes (T2D) and diabetic kidney disease (DKD), according to new research presented at the 63rd European Renal Association (ERA) Congress in Glasgow, Scotland.
Researchers analysed data from 31,031 adults with T2D treated between 2016 and 2021. All participants were receiving both renin-angiotensin system (RAS) inhibitors and sodium-glucose cotransporter-2 (SGLT2) inhibitors — therapies that have transformed outcomes by slowing kidney disease progression and reducing the risk of kidney failure. Of these, 12,172 patients were also prescribed DCCBs, while 18,859 received alternative blood pressure therapies. Participants were followed for a median of approximately 3.5 years.
After adjusting for baseline demographic and clinical differences, DCCB use was associated with a 33% increased risk of major adverse kidney events compared with other antihypertensive treatments. The composite outcome included a decline of at least 40% in estimated glomerular filtration rate (eGFR) or progression to end-stage kidney disease requiring dialysis or kidney transplantation. The researchers proposed that the observed association may stem from the drugs' effects on kidney haemodynamics — by preferentially dilating blood vessels entering the kidney's filtering units, DCCBs may increase pressure within these structures, potentially contributing to ongoing damage despite concurrent kidney-protective therapies.
The investigators emphasised that the study was observational and cannot establish causality, but the results warrant further investigation. Prospective studies and randomised controlled trials will be needed to determine whether alternative blood pressure treatment strategies could offer greater kidney protection for patients with DKD.
Separate research has shed further light on the biochemical disruptions associated with diabetic kidney disease. A prospective case-control study of 200 participants divided into four groups — diabetic nephropathy (DNp), diabetes control (DC), nephropathy control (NC), and healthy controls — found that the DNp group exhibited the most severe biochemical disturbances. Patients with DNp showed augmented fasting glucose (178.75 ± 61 mg/dL), glycated hemoglobin (8.13 ± 1.7%), creatinine (5.67 ± 1.8 mg/dL), and blood urea nitrogen (72.02 ± 22.8 mg/dL), indicating poor glycemic control and impaired kidney function.
The study also revealed distinct patterns across groups: the DC group demonstrated prominent dyslipidemia with the highest lipid levels, including elevated triglycerides (230.67 ± 59 mg/dL), low-density lipoprotein (107.41 ± 16 mg/dL), and cholesterol (169 ± 19 mg/dL). Meanwhile, the NC group showed the highest inflammatory markers, with lactate dehydrogenase levels of 1,216.43 ± 634 U/L. Inflammatory marker C-reactive protein was elevated in both the DNp and NC groups. The researchers concluded that DNp patients presented the most severe glycemic and renal impairment, while the diabetes control group exhibited the most pronounced dyslipidemia.