Abstract: TH-PO182
Calcium Chaos: When Siliconoma Steals the Show
Session Information
- CKD-MBD: Clinical
October 24, 2024 | 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
- De la Pena, Anna Valeria, Rutgers Health, Newark, New Jersey, United States
- Garcia, Celine, Rutgers Health, Newark, New Jersey, United States
- Savani, Priya A., Rutgers Health, Newark, New Jersey, United States
- Tajamal, Maryam, Rutgers Health, Newark, New Jersey, United States
- Kumar, Akshay, Rutgers Health, Newark, New Jersey, United States
- Haddad, Danny, Jersey City Medical Center, Jersey City, New Jersey, United States
Introduction
Kidney damage resulting from silicone implants is a rarely reported phenomenon. Rare complications from wound dehiscence can trigger an autoimmune response eliciting cascade of reactions causing hypercalcemia and nephrocalcinosis. We report a case of hypercalcemia-induced CKD following silicone buttock augmentation.
Case Description
A 52-year-old transgender woman with a past medical history of asthma, hypertension, and silicone injection in the glutes presented to the ED with polyuria, polydipsia, and constipation. Bloodwork showed calcium of 16 mg/dL, BUN 38 mg/dL, and creatinine 2.03 mg/dL. Further work-up revealed low PTH 6.3 pg/mL, low PTHrP 16 pg/mL, low 25-hydroxyvitamin D 15 ng/mL, and elevated 1,25-dihydroxyvitamin D 66 pg/mL. The patient was treated with IV fluids, zoledronic acid, and calcitonin for 5 days and discharged on alendronate 70 mg weekly.
Four months later, she was hospitalized with symptomatic hypercalcemia and was managed similarly. Further work-up revealing a negative SPEP and immunofixation, and elevated LDH 234 U/L, elevated ACE levels 162.9 U/L, suggesting granulomatous disease. A CT of the abdomen/pelvis showed infiltration throughout the bilateral gluteal subcutaneous fat with scattered calcified granulomas. A bone scan showed diffuse radionuclide accumulation in the buttocks corresponding with soft tissue attenuation and scattered calcifications. Over the next two years of receiving denosumab 120 mg monthly, hypercalcemia persisted, leading to recurrent nephrolitiasis and hydronephrosis, which further compromised kidney function. Calcium levels began to stabilize by the third year of treatment. Unfortunately, this improvement coincided with the patient progressing to CKD stage 4.
Discussion
This case underscores the importance of considering rare causes like siliconoma in cases of recurrent hypercalcemia. Siliconoma, though difficult to treat and often leading to complications like CKD, can result from an immune reaction to silicone, causing hypercalcemia by increasing calcium absorption through the production of 1,25 Vitamin D3.(1) Normalization of calcium could be related to the development of secondary hyperparathyroidism due to advanced CKD compared to treatment response as observed in this case. Due to the challenge in removing extensive granulomas, the development of alternative management strategies is crucial.