Acute Hypercalcemic Renal Failure As A Presenting Manifestation Of Primary Hyperparathyroidism Due To Atypical Adenoma
Recommended Citation
Gomes KM, Davydov E, Lahiri SW. Acute Hypercalcemic Renal Failure As A Presenting Manifestation Of Primary Hyperparathyroidism Due To Atypical Adenoma. Journal of the Endocrine Society 2024; 8(Suppl 1):A187.
Document Type
Conference Proceeding
Publication Date
10-5-2024
Publication Title
Journal of the Endocrine Society
Abstract
Atypical parathyroid adenomas have uncertain malignant potential and are a rare cause of primary hyperparathyroidism. Compared to typical parathyroid adenomas, patients with atypical parathyroid adenomas have higher preoperative serum calcium and parathyroid hormone (PTH) levels. However pre-operative distinction between atypical parathyroid adenomas, typical adenomas and parathyroid carcinoma is challenging, and histological evaluation is needed for definitive diagnosis. A 59-year-old female with history of nephrolithiasis presented with syncope. Laboratory evaluation revealed a serum calcium of 21.3 mg/dL (8.2-10.2), creatinine of 2.35 mg/dL with GFR of 36 mL/min/1.723 m2, PTH of 3711 pg/mL (15-65), 25-hydroxy vitamin D of 12 ng/mL, phosphorus of 5.6 mg/ dL (2.5-4.5). She incidentally tested positive for COVID-19. CT abdomen/pelvis demonstrated bilateral obstructive renal calculi requiring stent placement. Despite treatment with intravenous normal saline, 4 mg of zoledronic acid, two doses of 300 units of calcitonin, and cinacalcet 30 mg twice daily, repeat calcium and creatinine were 17.9 mg/dL and 3.64 mg/dL, respectively, and hemodialysis was initiated. CT neck and chest identified a 2.0 x 2.3 x 3.8 cm hypodense nodule inferior to the left thyroid lobe. A parathyroid planar scan with SPECT/CT showed uptake within the hypodense nodule. Bone scan did not reveal any disease. The enlarged left parathyroid gland was removed. Intra-operatively, PTH decreased to 302 pg/mL. Pathological evaluation of the left inferior parathyroid gland revealed a 4.2 cm partially encapsulated hypercellular neoplasm weighing 7.3 grams with increased mitotic activity and focally thickened fibrotic capsule and no extracapsular or vascular invasion consistent with atypical parathyroid adenoma. On postop day 4, her calcium declined to 7.1 mg/dL and PTH was 383 pg/mL. Calcium supplementation was initiated due to concern for hungry bone syndrome. On postop day 14, calcium increased to 10.3 mg/ dL and supplementation was discontinued. Her calcium levels have remained normal without supplementation three months after surgery. Severe hypercalcemia causing renal failure is an uncommon manifestation of primary hyperparathyroidism. Preoperative differentiation of parathyroid carcinomas and parathyroid adenomas is difficult, but important since surgical management of these two distinct entities differs. Higher preoperative calcium and PTH levels and concomitant renal failure suggest parathyroid carcinoma. This case highlights the challenge of differentiating atypical parathyroid adenomas from parathyroid carcinoma since both conditions can present with severe hypercalcemia and renal failure. Further research on the risk of carcinoma and recurrence of hypercalcemia in atypical parathyroid adenoma is needed.
Volume
8
Issue
Suppl 1
First Page
A187