Determinants of calcium channel blocker-induced gingival hyperplasia among patients undergoing peritoneal dialysis.

OBJECTIVE

This study aimed to assess the prevalence of calcium channel blocker (CCB)–induced gingival hyperplasia (GH) and to identify associated risk factors among patients undergoing peritoneal dialysis (PD).

METHODS

A retrospective analysis was performed on 303 patients receiving CCB therapy while undergoing PD at the General Hospital of Ningxia Medical University. Based on clinical assessment, patients were categorized into a GH group (n = 48) and a non-GH group (n = 255). Demographic characteristics and inflammatory biomarkers were compared between groups. Independent factors associated with GH were evaluated using logistic regression analysis.

RESULTS

Patients with GH were younger and had longer durations of PD and shorter CCB exposure compared to those without GH (all p < 0.05). No significant differences were observed between groups with respect to CCB class or dosage, dialysis dose, volume load, ultrafiltration volume, or residual urine volume (p > 0.05). Compared with the non-GH group, patients with GH showed lower reticulocyte counts and higher levels of alkaline phosphatase, uric acid, and prealbumin (all p < 0.05). Serum calcium, phosphorus, parathyroid hormone, urea, creatinine, C-reactive protein, β₂-microglobulin, albumin, and potassium levels did not differ significantly between groups (p > 0.05). Circulating concentrations of interleukin-6 and transforming growth factor–β1 were also comparable (p > 0.05). Multivariable logistic regression identified shorter duration of PD [odds ratio (OR) = 0.703, 95% confidence interval (CI): 0.581–0.851, p < 0.001] and shorter duration of CCB exposure [OR = 0.959, 95% CI: 0.931–0.988, p = 0.006] as protective factors against the development of CCB-induced GH.

CONCLUSION

Shorter duration of both PD and CCB exposure were associated with lower odds of gingival hyperplasia. These findings underscore the need for careful clinical surveillance in patients receiving long-term CCB therapy during PD.