MON-514 Bone Density Yo-yo In A Patient With Severe Hypercalciuria

INTRODUCTION: Idiopathic hypercalciuria is an important secondary etiology of osteoporosis (OP). Treatment of hypercalciuria with diuretics such as thiazides or amiloride (A) can result in significant improvement in bone mineral density (BMD) when combined with targeted therapies for OP. Here we present a case of severe idiopathic hypercalciuria on denosumab (D) and amiloride (A), who underwent decline in BMD after stopping D. However when D was resumed and a second drug, chlorthalidone (CTH) was added to A for persistent hypercalciuria, BMD in the hip increased significantly more than the increase previously seen with a combination of D and A alone. CASE REPORT: 65 year old female who initially presented at 55 years of age for evaluation of osteoporosis. She had previously tried different oral bisphosphonates with significant gastrointestinal side effects. At presentation, initial workup revealed significant hypercalciuria. She was recommended CTH for hypercalciuria, and zoledronic acid was recommended. She did not follow through with either and came back a few years later. BMD in 2012 declined significantly with L1-L4 T score of -3.7 (9.8% decrease) and mean total hip mean T score of -2.1 (6.6% decrease) from 2008 bone density. Workup at the time showed persistent hypercalciuria with 24- hr urinary calcium of 488mg. She agreed to start D for OP and CTH for hypercalciuria. Urinary calcium improved to 279 mg/24 hr. A year later, CTH was changed to A due to severe hypokalemia. BMD continued to increase progressively and after 3 years of therapy, BMD showed a 12.8% increase in bone density at the lumbar spine and a 5% increase in total hip. She continued D for another year and decided to stop D due to concern about side effects. A was continued for hypercalciuria. Follow up BMD a year later (off D for only 6 months) showed decline in BMD by 11.8% at the spine and 4.2% at total hip. 24- hr urinary calcium on A was noted to be significantly high again at 552 mg/24 hrs. She was restarted on D every 6 months. A was continued and CTH was added due to severe hypercalciuria. Follow up BMD a year later on the regimen of D, A and CTH showed a very significant increase in bone density again (9.4% at the spine and 10.4% at the femur), with a much greater increase in hip BMD than previously seen with 3 years of D. 24 hour urinary calcium had also decreased significantly to 189 mg/24 hrs, lower than had ever been documented previously. CONCLUSION: Patients with osteoporosis and idiopathic hypercalciuria are managed with thiazides or amiloride as anti-calciuric agent in addition to anti-resorptive agents. Although D is a potent anti-resorptive and improved BMD, this case highlights the need to evaluate for secondary causes of osteoporosis and pursue their treatment sometimes with dual agents to optimize bone density response to anti-resorptive agents.