Background: Osteoporosis is under-recognized in men and the incidence of secondary osteoporosis in men is high, between 50% and 80%. Idiopathic hypercalciuria (IH) is defined by excessive renal calcium excretion and is an important secondary cause of osteoporosis. Treatment of IH-associated osteoporosis with antiresorptive agents does not relieve the underlying pathology and treatment should instead focus on increasing calcium reabsorption via the distal convoluted tubule.
Aim: To increase awareness of IH as a highly treatable cause of secondary osteoporosis.
Methods: Retrospective analysis of three male patients with IH-associated osteoporosis treated with chlorthalidone, a thiazide-like diuretic, over 12-months.
Results: Three men (median age 59, range 48-60) were referred independently to an endocrinology clinic for assessment of osteoporosis and minimal trauma fracture. On baseline DEXA, median lumbar spine and femoral neck BMD were reduced, measuring 0.94 g/cm2 (T-score –2.3 SD) and 0.79 g/cm2 (T-score –2.2 SD) respectively. Baseline bone turnover was elevated based on plasma markers, with median P1NP 60 ug/L (range 45-105) and CTX 660 ng/L (range 504-678). Urine collection over 24-hours on two occasions confirmed hypercalciuria with median calcium excretion 9.2 mmol/day (normal range 2.5-7.5). Chlorthalidone 25 mg daily was prescribed with repeat urine collection performed after 6-weeks of treatment demonstrating normalization of 24-hour urine calcium excretion. On repeat DEXA following 12-months of chlorthalidone treatment, median lumbar spine and femoral neck BMD increased a median 8% (range 6-14) and 3% (range 2-9), respectively with concomitant median reduction in bone turnover marker P1NP by 50% (range 16-53) and CTX by 62% (range 19-68).
Conclusion: All men with unexplained osteoporosis should be screened for IH with a 24-hour urine calcium collection. Treatment of IH-associated osteoporosis with chlorthalidone results in marked improvement in bone density and may avert the need for treatment with potent antiresorptive agents like bisphosphonates or RANKL inhibitors.