ECEESPE2025 Poster Presentations Bone and Mineral Metabolism (112 abstracts)
1University Hospital Würzburg, Department of Internal Medicine I, Division of Endocrinology and Diabetes, Würzburg, Germany; 2Funktionsbereich Endokrinologie und Stoffwechsel, I. Medizinische Klinik, Universitätsklinikum, Augsburg, Germany
JOINT3387
Background: Chronic hypoparathyroidism (hypoPT) is characterized by insufficient production of parathyroid hormone, resulting in hypocalcemia and hyperphosphatemia. This condition can lead to hypercalciuria, which is a common finding in patients with chronic hypoparathyroidism and can contribute to long-term renal complications such as nephrocalcinosis, kidney stones, and impaired renal function. Current guidelines suggest adjustment of calcium and active vitamin D and/or treatment with thiazide diuretics to reduce hypercalciuria. However, data regarding their efficacy is lacking.
Methods: We retrospectively analyzed urinary calcium excretion in 244 patients with chronic hypoparathyroidism from two different German centers (Wuerzburg n = 224, Augsburg n = 20) between 1999 and 2024 (median age 52 years [IQR 19-82], 75% female, 91% postsurgical hypoPT). A total of 1231 patient-years were recorded with a median of 4. 2 [IQR 1-24] visits per patient and a median follow-up of 5 [IQR 0-23] years.
Results: At baseline (first recorded visit), 39% (n = 95) of patients presented with hypercalciuria, whereas concomitant treatment with thiazide diuretics occurred only in 13% of patients. During time of data collection, thiazide treatment was initiated in 97 cases. The majority of patients received hydrochlorothiazide (73%) at a median daily dose of 22 mg [IQR 12. 5-50]. Initiation of thiazide treatment led to a significant reduction of urinary calcium excretion (-2. 31 mmol/d, P < 0. 001) at the next recorded visit. This effect was even more pronounced in case of hypercalciuria at treatment initiation (-3. 49 mmol/d, P < 0. 001, n = 68). Interestingly, higher thiazide doses did not lead to a greater reduction of urinary calcium and 70% of patients remained hypercalciuric despite initiation of thiazide treatment. Serum albumin-corrected calcium remained unchanged during treatment. Reduction of oral calcium supplementation by 833 mg/d (median) led to a significant decrease of urinary calcium (-1. 79 mmol/d, P < 0. 001 for the whole cohort, -2. 86 mmol/l, P < 0. 001 for hypercalciuric patients at baseline), whereas a reduction of calcitriol by 0. 5 µg/d decreased urinary calcium excretion by 2. 8 mmol/d at the following visit.
Conclusion: Hypercalciuria frequently occurs in patients with hypoPT. Thiazides, as well as dose reduction of calcium or active vitamin D significantly reduce urinary calcium excretion. However, even the combination of both approaches was still not sufficient to lower urinary calcium into the normal range.