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Abstract: TH-PO173

PTH Independent Hypercalcemia, Easily Missed Diagnosis: Case Report of Vitamin A Toxicity

Session Information

  • CKD-MBD: Targets and Outcomes
    November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical


  • Malik, Uzma, Westchester Medical Center, Valhalla, New York, United States
  • Sridhar, Abhinaya, Westchester Medical Center, Valhalla, New York, United States
  • Gupta, Sanjeev, Westchester Medical Center, Valhalla, New York, United States
  • Chugh, Savneek S., Westchester Medical Center, Valhalla, New York, United States
  • Mittal, Amol, Westchester Medical Center, Valhalla, New York, United States
  • Kore, Shruti, Westchester Medical Center, Valhalla, New York, United States

The first step in the evaluation of hypercalcemia is establishing the role of PTH in its pathogenesis. There are many causes of PTH independent hypercalcemia; Vitamin A toxicity is a rare cause of PTH-independent hypercalcemia.

Case Description

51 years old male with history of well controlled diabetes, HIV with a suppressed viral load and CKD stage 2 was found to have hypercalcemia at a routine nephrology clinic visit.
Patient reported no symptoms of hypercalcemia or decreased urine output. He also denied any weight loss, night sweats, decreased appetite. His vital signs and physical exam were unremarkable. Routine blood work was notable for hypercalcemia 10.5 mg/dL. Repeat testing 2 months later showed persistent hypercalcemia to 10.8 mg/dL. Initial work up revealed 25OH vitamin d 34; PTH 30pg/ml and phosphorus 3.3 mg/dL suggestive of PTH-independent hypercalcemia. Urinalysis was notable for 2+ glucose, no proteinuria. Urine protein to creatinine ratio was 62 mg/g. Given unclear cause of PTH independent hypercalcemia at this time, Vitamin A level was checked which was elevated to 94.6 mg/dL. However, patient denied excessive intake of vitamin A containing food. Patient was encouraged to hydrate well and was provided list of food items high in vitamin A and advised to avoid them. Repeat testing 3 months later showed Cr 1.34, Ca 9.9 and Vitamin A levels within normal limits.


The tolerable upper daily intake level of vitamin A is approximately 3,000 μg RAE. However, Vitamin A toxicity can occur at what is considered to be “safe doses” (700 to 900 μg RAE) from dietary sources and supplementation. The mechanism of vitamin A-induced hypercalcemia is poorly understood. It is hypothesized to be secondary to increased osteoclastic activity, suppression of osteoblastic activity, and hormonal dysregulation of calcium homeostasis of parathyroid hormone and vitamin D. In setting of hypercalcemia and suppressed PTH, Vitamin A toxicity should be considered in the diagnostic workup along with malignancy, bone metastasis, vitamin D toxicity, granulomatous disease and immobility. A thorough dietary history and serum retinol levels should be checked. Treatment involves withdrawal of vitamin A sources and supportive care.