Abstract: TH-PO0231
PTH-Independent Hypercalcemia After Kidney Transplantation Caused by Redistribution from Soft-Tissue Calcifications
Session Information
- Bone and Mineral Metabolism: Clinical Reports and Practice
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Geranpayeh, Tanya, Baylor University Medical Center at Dallas, Dallas, Texas, United States
- Maalouf, Naim M., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Borda Sanchez, Gustavo Alfonso, Baylor University Medical Center at Dallas, Dallas, Texas, United States
- Akinfolarin, Akinwande A., Baylor University Medical Center at Dallas, Dallas, Texas, United States
- Canan, Arzu, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Introduction
PTH-independent hypercalcemia (PIHC) may be caused by a variety of etiologies. We report a case of PIHC in a kidney transplant recipient with extensive soft tissue calcifications in whom persistent hypercalcemia resolved after gradual decrease in calcifications evidenced by CT-scan.
Case Description
A 21-year-old man with end stage renal disease due to vesicoureteral reflux since early childhood underwent combined heart-lung-kidney transplant due to significant metastatic calcifications in the heart, lungs, and other tissues. He underwent subtotal parathyroidectomy (PTX) 4 months post-transplantation due to persistent hypercalcemia despite maximum dose cinacalcet. Post-PTX, PTH level dropped and remained low, but serum calcium remained elevated. Further work-up was notable for low serum PTHrP, normal 25-OH-Vit D and 1,25-OH2-Vit D levels, and ruled out multiple myeloma, adrenal insufficiency, and other common PIHC causes. Serum calcium remained elevated for approximately two years post-transplantation despite multiple measures including anti-resorptive therapy, before eventually normalizing with no specific intervention. The patient endorsed regression of hard calcified tissue in his elbows and under skin starting within weeks post-transplantation, and this was confirmed by serial chest CT scans performed over subsequent years, using dedicated software to measure calcification volume and mass (Table)
Discussion
We report a case of hypercalcemia after kidney transplantation which persisted despite PTX. Decline in serum calcium was observed in parallel with a decrease in subcutaneous soft tissue calcifications clinically and diaphragmatic calcifications on imaging. We propose that PIHC was caused by mobilization of calcium from calcified tissues to the bloodstream.
| Test, units | pre-TX | 4 months post-TX | 6 months post-TX | 9 months post-TX | 1 year post-TX | 2 years post-TX | 3 years post-TX | 5 years post-TX |
| eGFR, ml/min/1.73 m2 | 7 | 52 | 48 | 31 | 31 | 26 | 30 | 22 |
| Serum calcium, mg/dl | 12 | 14.6 | 12 | 11.4 | 11.9 | 10.5 | 10.1 | 8.9 |
| Serum Phosphorus, mg/dl | 6 | 3 | 2.7 | 4 | 3.3 | 3.3 | 2.8 | 3.9 |
| Serum 25-OH-vit D, ng/ml | 53.9 | ND | 24 | 27 | 26 | 19 | 45 | 18 |
| Serum 1,25-OH2-vit D, Pg/ml | 32 | 8.2 | <8 | <8 | ND | ND | ND | ND |
| Serum PTH, Pg/ml | 144.4 | 89.4 | 17 | 28 | 18 | ND | ND | ND |
| Diaphragmatic calcification volume, mm3 | ND | 4381 | ND | ND | 5813 | 4046 | 4030 | 3020 |
| Diaphragmatic calcification mass, mg | ND | 851 | ND | ND | 1088 | 801 | 779 | 543 |
Tx: Transplantation, PTX: Parathyroidectomy