Association of Serum Calcium-Phosphorus Product with Blood Pressure and Renal Parameters in Early Chronic Kidney Disease

Background & Objectives: Chronic kidney disease (CKD) is a progressive condition associated with dysregulation of mineral metabolism, including alterations in serum calcium and phosphorus. The calcium-phosphorus (Ca×P) product is a clinically significant marker reflecting the risk of vascular calcification and cardiovascular morbidity. This study aimed to evaluate the association of serum Ca×P product with systolic/diastolic blood pressure and renal biochemical parameters in patients with early-stage CKD (stages 1–3).

Methods: A hospital-based cross-sectional observational study was conducted at MGM Medical College & LSK Hospital, Kishanganj, Bihar, involving 100 diagnosed CKD patients (stages 1–3 by KDIGO criteria) and 50 age- and sex-matched healthy controls. Serum calcium, phosphorus, creatinine, urea, uric acid, eGFR (CKD-EPI equation), 24-hour urine protein, and blood pressure were measured. The Ca×P product was calculated and correlated with clinical and biochemical variables using Pearson’s correlation and multivariate linear regression.

Results: The mean Ca×P product in CKD patients was significantly elevated compared to controls (42.6 ± 8.4 vs 28.3 ± 5.1 mg²/dL²; p < 0.001). A strong positive correlation was found between Ca×P product and systolic blood pressure (r = 0.621, p < 0.001) and diastolic blood pressure (r = 0.574, p < 0.001). Ca×P product correlated significantly with serum creatinine (r = 0.683), serum urea (r = 0.659), uric acid (r = 0.541), and 24-hour urinary protein (r = 0.612) (all p < 0.001). An inverse correlation was noted with eGFR (r = −0.712, p < 0.001). On multivariate analysis, Ca×P product emerged as an independent predictor of both elevated blood pressure (β = 0.48, p < 0.001) and reduced eGFR (β = −0.52, p < 0.001).

Conclusion: The serum Ca×P product is significantly elevated even in early CKD and shows robust associations with blood pressure elevation and deterioration of renal function. Monitoring Ca×P product in early CKD may facilitate timely intervention to reduce cardiovascular and renal progression.