Abstract: TH-PO181
Hypercalcemia Due to Elevated 1,25-Dihydroxyvitamin D in Severe Tophaceous Gout
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
- Ahmad, Madhia Bashir, Rutgers Health, Newark, New Jersey, United States
- Chaudhari, Harshad, Rutgers Health, Newark, New Jersey, United States
- Mahendrakar, Smita, Rutgers Health, Newark, New Jersey, United States
- Yudd, Michael, Rutgers Health, Newark, New Jersey, United States
Introduction
Granulomatous disorders, like sarcoidosis and tuberculosis, can cause hypercalcemia by increasing production of calcitriol through the activation of extrarenal 1-alpha-hydroxylase by macrophages in granuloma. Patients often are asymptomatic and have low parathyroid hormone (PTH) level and elevated 1,25 dihydroxyvitamin D levels. Severe tophaceous gout can cause granulomatous inflammation and is a rare cause of hypercalcemia.
Case Description
A 68-year-old male with severe tophaceous gout and possible seronegative rheumatoid arthritis resulting in extensive deformities presented with asymptomatic hypercalcemia 13.1 mg/dL and worsening kidney function. His laboratory testing notable for creatinine 2.6 mg/dL with baseline chronic kidney disease creatinine 2.0 mg/dL, low PTH, elevated serum 1,25-dihydroxyvitamin D and angiotensin converting enzyme (ACE) levels. Extensive workup ruled out sarcoidosis, malignancy, fungal infections, and tuberculosis. He had resection of his elbow tophi which showed many granulomas. Renal Biopsy consistent with ateriosclerosis disease .Aggressive treatment of his gout with steroids and urate lowering therapy febuxostat improved his hypercalcemia.
Discussion
Our patient presented with relatively long-standing hypercalcemia with minor symptoms. This occurred in the setting of severe tophaceous gout and probable seronegative rheumatoid arthritis.
In normal states, 25-hydroxyvitamin D is hydroxylated to the active 1,25-dihydroxyvitamin D in renal proximal tubular cells through the enzyme 1α-hydroxylase. In hypercalcemia this conversion is inhibited. Elevated 1,25-dihydroxyvitamin D in the setting of hypercalcemia as seen in this patient points to abnormal unregulated extrarenal conversion, typically found in granulomatous states and lymphomas.
Table 2 Review of the 6 cases found in the literature of hypercalcemia associated with tophaceous gout
| References | Age (Years) | Serum Calcium/Uric Acid (mg/dL) | Extensive Tophi | Granulomas in Tophi | Serum 1,25- Vitamin D | Serum ACE | ULT/ steroids | Reported cause of hypercalcemia |
| Rodriquez et al [6] | 42 | 14.5/14.0 | Yes | Yes | N | ND | Yes/Yes | Transient increase PTH-RP |
| Sachdeva et al [7] | 41 | 13.5/ND | Yes | Yes | Elevated | ND | Yes/Yes | Increased 1,25-Vitamin D |
| Gallegos-Bayas et al [10] | 75 | 14.0/10.4 | Yes | Yes | N | Yes | Yes/Yes | Increased 1,25-Vitamin D |
| Hasbani et al [11] | 62 | 11.7/11.3 | Yes | ND | ND | Yes | Yes/Yes | PTH independent |
| Lee et al [12] | 49 | 15.3/11.7 | Yes | ND | N | Normal | Yes/ No | Immobilization |
| Gudlawar, S American Society of Nephrology [13] | 40 | 13.4/11 | Yes | ND | Elevated | ND | Yes/Yes | Increased 1,25-Vitamin D |
ND = No Data; N = Normal; ACE = serum Angiotensin Converting Enzyme; ULT = Urate Lowering Therapy * when measured during hypercalcemia