Effect on BP and Renal Outcomes with Cilnidipine-based therapy in Hypertensive CKD Patients with or without T2DM: A Two-Year Real-World Analysis

Hypertension and chronic kidney disease (CKD) form a bidirectional clinical challenge, each accelerating the progression of the other, contributing to high cardiovascular risk. The coexistence of diabetes further amplifies this risk, making effective blood pressure (BP) control and organ-protection a cornerstone of management. In India, where hypertension frequently presents early and diabetic kidney disease is highly prevalent, selection of the right antihypertensive therapy is crucial. Amongst CCBs, Cilnidipine, a 4th generation L/N-type CCB, has exhibited sympatholytic and reno-protective actions in documented studies. This study aimed to assess the long-term effects of cilnidipine-based therapy on BP and urinary albumin excretion (UAE) in Indian hypertensive-CKD patients, with or without type 2 diabetes mellitus (T2DM), under real-world clinical conditions.

Data from 200 adult hypertensive-CKD patients, with or without T2DM, who initiated cilnidipine (10–20 mg once daily) were analysed. All patients had been on stable background antihypertensive therapy prior to cilnidipine initiation, and no additional antihypertensive agents were introduced during follow-up. Baseline assessments corresponded to the time of cilnidipine initiation, and follow-up data was recorded at 24 months. The effect on BP and UAE, upon initiation of cilnidipine-based therapy, in hypertensive diabetic or non-diabetic patients was analysed. Within-group comparisons were performed using paired t-tests, and between-group comparisons (diabetic vs. non-diabetic) used independent t-tests.

Of 200 included patients, 60 (30%) were diabetic and 140 (70%) were non-diabetic. Both diabetic and non-diabetic groups showed significant reductions in systolic BP [SBP], diastolic BP [DBP], and UAE after 24 months of treatment. The mean baseline SBP and DBP were 156 ± 11 mmHg and 86 ± 7 mmHg, respectively. After 24 months of cilnidipine therapy, mean SBP decreased to 137 ± 9 mmHg and DBP to 79 ± 6 mmHg (p < 0.001 for both). Among diabetics, the mean SBP reduction was −14.2 mmHg and DBP reduction was −8.1 mmHg, while in non-diabetics the respective reductions were −12.6 mmHg and −5.1 mmHg; both groups demonstrated statistically significant within-group improvements, with no significant difference between them (p > 0.05).

Mean UAE decreased from 84.2 ± 30 mg/dL at baseline to 33 ± 18 mg/dL at 24 months (p < 0.001 within groups). The mean reduction in UAE was −61.6 mg/dL in diabetics and −47 mg/dL in non-diabetics; reflecting a substantial fall of nearly 50–65% from baseline in both subgroups. While the between-group difference was not statistically significant (p = 0.10), the reduction was clinically significant, indicating meaningful improvement in UAE over the two-year period. No major adverse events or need for treatment modification were reported.

Cilnidipine-based antihypertensive therapy achieved sustained and statistically significant reductions in both SBP and DBP and UAE in hypertensive CKD patients, irrespective of diabetic status. Although the decline in urinary albumin excretion did not reach statistical significance between groups, the magnitude of reduction was clinically meaningful, reflecting cilnidipine’s potential reno-protective action. These findings reinforce the benefits of cilnidipine-based therapy for hypertension management in CKD, offering sustained BP control with proteinuria reduction, particularly also valuable in those with concomitant diabetes.