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Abstract: SA-PO200

The Masked Parathyroid Adenoma in CKD: Is It Overlooked?

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Author

  • Atari, Mohammad, The University of Mississippi Medical Center, Jackson, Mississippi, United States
Introduction

Primary hyperparathyroidism (PHPT) is the leading cause of hypercalcemia in the outpatient setting, most commonly resulting from a solitary adenoma. PHPT is associated with hypercalciuria, kidney stones, chronic kidney disease (CKD), and/or nephrocalcinosis. On the other hand, CKD is associated with bone and mineral homeostasis abnormalities. PHPT can be masked or unmasked in certain conditions.

Case Description

Case 1: An 80-year-old female patient with multiple myeloma and CKD IV secondary to membranous nephropathy presented for follow-up. Calcitriol was resumed six months before this visit due to high parathyroid hormone (PTH) at 866 pg/mL and adjusted later due to a rise in serum calcium to 11.2-11.6 mg/dL. However, calcium continued to rise reaching 12.1 mg/dL and PTH increased to 1172 pg/mL. Phosphorus was normal. The findings prompted further evaluation; sestamibi scan revealed a large hyperfunctioning parathyroid adenoma in the mid-upper right lobe with concomitant mild hyperplasia on left.

Case 2: A 60-year-old female patient with a history of nonischemic cardiomyopathy, atrial fibrillation, obstructive sleep apnea, and progressive CKD of unclear etiology presented for follow up. Labs showed worsening creatinine secondary to loop diuretic-induced hypovolemia with concomitant hypophosphatemia of 1.8 mg/dL, hypokalemia, and hypomagnesemia. Serum calcium was normal at 9.8 mg/dL. Furosemide was held and hydration was recommended, PTH was 360 pg/mL, and repeated labs showed calcium of 10.7 mg/dL and phosphorus of 4.3 mg/dL with improvement in serum creatinine. Sestamibi scan showed a hyperfunctioning adenoma in the inferior left lobe.

Discussion

Masked PHPT has been described in the setting of hypothyroidism and hypovitaminosis D secondary to malabsorption or malnutrition. Vitamin D replacement and thiazide therapy have been reported to unmask PHPT. Here we describe unmasking two cases of parathyroid adenoma-induced PHPT in CKD, one case was unmasked by starting calcitriol, and the other was unmasked by stopping furosemide. These cases emphasize the importance of carefully interpreting mineral metabolism parameters in CKD populations where PHPT can be subclinical, normocalcemic, and masked by vitamin D deficiency. Normocalcemic PHPT cannot be easily differentiated from secondary hyperparathyroidism in CKD patients, requiring high clinical suspicion and imaging studies to establish the diagnosis.