Endocrine Abstracts

JOINT1929

Background: Aldosterone excess has been implicated in the regulation of bone metabolism, with different studies indicating reduced bone mass in patients with primary hyperaldosteronism (PA) compared to those with essential hypertension (EH). Some authors suggest that these alterations may be linked to aldosterone-induced parathyroid hormone (PTH) release. Additionally, increased levels of 24-hour urinary calcium have been proposed as a mechanism contributing to bone loss. However, it remains unclear whether this 24-hour urinary calcium is a direct effect of aldosterone or a compensatory response to elevated PTH levels. Existing data on bone turnover in PA patients are limited and often conflicting. This study aimed to investigate calcium–phosphorus metabolism and bone turnover markers in PA patients compared to a cohort of EH controls.

Methods: We conducted a retrospective, multi-center study involving 37 patients with PA and 46 EH controls. PTH, 24-hour urinary calcium, alkaline phosphatase (ALP), C-terminal telopeptide (CTX), calcium, phosphate, 25-OH vitamin D, plasma aldosterone concentration, plasma renin activity, and the aldosterone-to-renin ratio were measured in all participants. Bone turnover has been evaluated in the absence of interfering anti-hypertensive medications in both PA and EAH patients.

Results: The two study groups were comparable in terms of age, gender, and BMI. Serum ALP levels were similar between the groups (73 U/L [62–91] in PA vs. 70 U/L [55–73] in EH, P=0.26), as were 25-OH vitamin D levels (27.6 ng/ml [15–34] in PA vs. 19.9 ng/ml [16–28.5] in EH, P=0.33) and PTH levels (52 pg/ml [41–61] in PA vs. 59 pg/ml [44–71] in EH, P=0.25). As expected, 24-hour urinary calcium was significantly higher in PA patients (201 mg/kg/day [149–299]) compared to those with EH (165 mg/kg/day [107–230]). Notably, the PA group exhibited significantly elevated CTX levels compared to EH controls (617 ng/ml [447–779] vs. 410 ng/ml [280–560], P<0.005). Additionally, calcium levels were higher (9.3 mg/dl [8.9–9.6] vs. 9.1 mg/dl [8.8–9.3], P=0.03), while phosphorus levels were lower in PA patients (3.0 mg/dl [2.6–3.5] vs. 3.5 mg/dl [3.2–3.7], P<0.001).

Conclusion: Patients with PA demonstrate increased skeletal turnover compared to EH controls, which does not appear to be linked to elevated PTH levels. These findings suggest that alterations in bone metabolism among PA patients may be partially PTH-independent and potentially driven by other factors, such as changes in phosphorus metabolism induced by aldosterone, as indicated by the lower phosphorus levels observed in this cohort.