Evaluation of Calcium–Phosphate–Parathyroid Hormone Axis in Secondary Hyperparathyroidism Among Renal Failure Patients

Abstract

Background: Chronic kidney disease (CKD) leads to profound disturbances in mineral metabolism, culminating in secondary hyperparathyroidism (SHPT), a central component of CKD–mineral and bone disorder (CKD-MBD). Objective: To evaluate the biochemical interplay between calcium, phosphate, and parathyroid hormone (PTH) in renal failure patients and assess the severity of SHPT. Methods: A cross-sectional analytical study was conducted on 80 patients with advanced renal failure. Biochemical parameters including calcium, phosphate, PTH, vitamin D, and renal function markers were analyzed. Statistical comparisons were made against healthy reference midpoints using one-sample t-tests. Correlation and regression analyses were performed to assess interrelationships. Results: Mean PTH levels were markedly elevated (789.26 pg/mL, p<0.001), with concomitant hyperphosphatemia (6.49 mg/dL) and vitamin D deficiency (20.53 ng/mL). Despite near-normal mean calcium (9.50 mg/dL), significant endocrine dysregulation was evident. Strong associations were observed between renal dysfunction and metabolic derangements. Conclusion: Severe disruption of the calcium–phosphate–PTH axis is evident in renal failure patients, characterized by vitamin D deficiency, phosphate retention, and compensatory PTH elevation. Early intervention targeting mineral metabolism is critical to reduce morbidity associated with CKD-MBD.