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Kidney Week

Abstract: SA-PO997

The Great Masquerader: Persistent Hypercalcemia in a Multiple Myeloma Patient

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Shirley, Kayla, University of South Florida, Tampa, Florida, United States
  • Verma, Sean, University of South Florida, Tampa, Florida, United States
  • Bassil, Claude, University of South Florida, Tampa, Florida, United States
Background

Hypercalcemia is a commonly encountered electrolyte abnormality in multiple myeloma patients. We present a case of persistent hypercalcemia which was not fully explained by underlying multiple myeloma and did not respond to initial treatment, thus, alerting a concomitant disease process and new diagnosis.

Methods

A 60-year-old woman with lambda light chain multiple myeloma, CKD secondary to biopsy proven chronic tubular injury secondary to lambda light chain proximal tubulopathy, type 2 diabetes mellitus, and hypertension was found to have acute on chronic renal failure with creatinine of 3.5 mg/dl (baseline 2.8 mg/dl) and hypercalcemia with corrected calcium of 13.3 mg/dl on routine labs. The patient was previously treated with bortezomib, dexamethasone, and cyclophosphamide, followed by autologous hematopoietic stem cell transplant with appropriate response and was not currently receiving chemotherapy. Hypercalcemia was previously attributed to underlying multiple myeloma and tertiary hyperparathyroidism, however, responded incompletely to treatment with intravenous fluids and pamidronate. She underwent additional workup, with intact parathyroid hormone of 319.5 pg/ml, 25-hydroxy vitamin D of 10.8 ng/ml, and elevated 1, 25-dihydroxy vitamin D level of 109 pg/m. Parathyroid hormone related peptide was within normal limits. PET/CT revealed hypermetabolic supraclavicular, mediastinal, and hilar lymphadenopathy. Left supraclavicular lymph nodes were biopsied, revealing rare small lymphocytes, rare epithelioid cells and multinucleated giant cells, suggesting a granulomatous process. Angiotensin converting enzyme was 46 U/L. The patient was diagnosed with sarcoidosis and treated with prednisone with improvement in hypercalcemia and creatinine.

Conclusion

Hypercalcemia in patients with granulomatous disorders is driven primarily by elevated calcitriol concentrations, which serve to increase calcium absorption from the gut and resorption from bone. Treatment of hypercalcemia in this setting involves not only treating the underlying disease process, but reducing dietary calcium and vitamin D supplementation. While in multiple myeloma patients, hypercalcemia is likely related to underlying disease, the nephrologist should rule out less common etiologies in cases poorly responsive to traditional therapy.