Abstract: SA-PO0585
SGLT2 Inhibitor Use in Patients with CKD May Unmask Primary Hyperparathyroidism
Session Information
- Bones, Stones, and Mineral Metabolism: Research and Cases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Pang, Bo, Samuel S Stratton Department of Veterans Affairs Medical Center, Albany, New York, United States
- Gosmanov, Aidar R., Samuel S Stratton Department of Veterans Affairs Medical Center, Albany, New York, United States
- Gosmanova, Elvira O., Samuel S Stratton Department of Veterans Affairs Medical Center, Albany, New York, United States
Introduction
Evidence suggests that SGLT2i may influence serum phosphate (P), parathyroid hormone (PTH), and fracture risk; however, their effects on calcium homeostasis remain unclear. Three cases of hypercalcemia with unsuppressed PTH, indicative of primary hyperparathyroidism (PHPT), were observed 6 to 18 months after initiation of SGLT2i therapy in individuals with CKD.
Case Description
Individuals were followed in CKD clinic of the Stratton VAMC and were started on SGLT2i empagliflozin 12.5 mg daily for renoprotection. Time course of laboratory parameters is shown in Table. Of note, all also had mild erythrocytosis after initiation of empagliflozin and were found to have a heterogeneous hemochromatosis (HH) H63D gene mutation. Hypercalcemia resolved in one person after SGLT2i discontinuation for recurrent genital yeast infection. In two individuals 30mg daily cinacalcet controlled hypercalcemia.
Discussion
The case-series illustrates the development of mild persistent hypercalcemia with elevated PTH after the initiation of SGLT2i in patients who also had secondary erythrocytosis and heterozygous HH gene mutation. Renal function remained stable, and vitamin D and phosphorus levels were not suggestive of vitamin D deficiency or hyperphosphatemia-driven secondary hyperparathyroidism. None were taking thiazide diuretics. Therefore, unmasking and/or development of PHPT was the most likely diagnosis. It is unclear if erythrocytosis played a contributory role for the development of PHPT or it was a coincidental finding.
In patients with CKD, especially those with baseline high-normal calcium levels, SGLT2i therapy should be initiated with caution and followed by close monitoring of serum calcium. Underlying PHPT should be considered when hypercalcemia develops after SGLT2i initiation.
Timing of Laboratory Measurements Relative to SGLT2i Exposure
| Patient 1, 76-year-old male | Patient 2, 56-year-old male | Patient 3, 71-year-old male | ||||||||||||||
| Serum values | Ref range | SGLT2i start 7/2022 | 10/2022 | 1/2023 | 1/2025 | 4/2025, 3 mo after SGLT2i stopped | SGLT2i start 10/2022 | 2/2023 | 3/2024 | 11/2025 | 4/2026, 2 mo on cinacalcet | SGLT2i start 6/2022 | 3/2023 | 1/2024 | 10/2025 | 12/2025, 1 mo on cinacalcet |
| Ionized Ca, mmol/L | 1.15-1.32 | 1.28 | 1.36 | 1.39 | 1.3 | 1.31 | 1.30 | N/A | 1.34 | 1.38 | 1.21 | 1.29 | 1.36 | 1.41 | 1.47 | 1.32 |
| Ca, mg/dL | 8.3-10.6 | 9.5 | 10.4 | 10.8 | 10.7 | 10.2 | 9.8 | 10.5 | 10.9 | 10.0 | 9.1 | 9.5 | 10.4 | 10.9 | 11.2 | 10 |
| Albumin, g/dL | 3.4-4.5 | 3.4 | 3.8 | 3.7 | 3.5 | 3.5 | 4.4 | 4.3 | 4.2 | 3.9 | 3.8 | 3.5 | 3.5 | 3.5 | 3.5 | 3.6 |
| P, mg/dL | 2.5-4.5 | 3.4 | 3.8 | 4.0 | 3.6 | 3.4 | 3.2 | 3.5 | 3.4 | 2.6 | 3.2 | 2.7 | 3.3 | 3.4 | 3.2 | 3.1 |
| PTH, pg/mL | 14-72 | 98 | 57 | 68 | 174 | 283 | 101 | 87 | 80 | 61 | 62 | 94 | 100 | 193 | 148 | 160 |
| eGFR, ml/min/1.73m2 | >90 | 33 | 29 | 25 | 29 | 30 | 41 | 52 | 44 | 45 | 53 | 47 | 42 | 46 | 41 | 43 |
| Hemoglobin, g/dL | 13.5-17.0 | 16.8-17.6 | 18.6 | 20.0 | 18.7 | 17.1 | 16.5-17.7 | 17.6 | 17.6 | 17.7 | 17.6 | 11.4-12.4 | 16.9 | 18.2 | 17.6 | 17.4 |
Footnotes: Vitamin D-25(OH) levels were within target ranges in all persons at all timepoints. Ca, calcium; P, phosphate; PTH, parathyroid hormone; mo, month.