ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO695

Hypercalcemia Associated with Severe Tophaceous Gout

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Author

  • Gudlawar, Sirisha, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
Introduction

Refractory gout remains a persistent challenge leading to significant functional impairment. Hyperuricemia is strongly associated with chronic kidney disease. Severe hypercalcemia from gout is a rare phenomenon and we, herein present a case with chronic tophaceous gout presented with severe hypercalcemia leading to acute kidney injury (AKI).

Case Description

40-year-old male with history significant for chronic tophaceous Gout presented to the emergency department from clinic for further evaluation of hypercalcemia and AKI noted on the laboratory results. His symptoms were arthralgias and muscle weakness. Vital signs notable for blood pressure of 150/70 mmHg, Heart rate 92 beats per minute. Laboratory results significant for serum creatinine 3.80 mg/dL( baseline of 1.3 mg/dL), calcium 12.9 mg/dL, albumin 2.9 g/dL, corrected calcium is 13.4 mg/dL , ionized calcium 1.76 mmol/L, phosphorus 4.7 mg/dL, parathyroid hormone 11.1 pg/mL,Thyroid stimulating hormone is 3.58 ulU/mL, 25-hydroxy vitamin D 48.6 ng/mL,1-25, dihydroxy vitamin D was 85.9 ng/mL, uric acid is 11 mg/dL,PTHrP 3.3 pmol/L, work-up for myeloma was negative. X-Ray of the extremities showed multifocal partially calcified tophaceous gout. CT scan of the chest, abdomen and pelvis with no evidence of lymphadenopathy or granulomatous process. Biopsy of the skin lesions was consistent with Gout with calcifications. Given the above findings, it was thought to be secondary to increased production of 1,25 dihydroxy vitamin D( calcitriol) due to granulomatous inflammation caused by severe gout and he was treated with calcitonin x 3 doses, intravenous hydration and prednisone 40 mg daily. His calcium improved to 10 mg/dL, and was discharged home.

Discussion

The most common cause of hypercalcemia is primary hyperparathyroidism, however in the hospital setting it is malignancy. Chronic tophaceous gout results in granulomatous inflammation leading to increased production of calcitriol resulting in hypercalcemia. This is extremely rare and our case illustrates the importance of understanding the pathophysiology for hypercalcemia in chronic gout. Treatment includes primarily corticosteroids.