Abstract: TH-PO1161
Pseudohypervitaminosis D in Multiple Myeloma
Session Information
- Onconephrology: Emerging Biomarkers, Preclinical Models, Clinical Challenges, and Therapeutic Strategies
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Elmahi, Mahmoud, Stony Brook University Hospital, Stony Brook, New York, United States
- Ali, Selma, Stony Brook University Hospital, Stony Brook, New York, United States
- Khan, Sobia, Stony Brook University Hospital, Stony Brook, New York, United States
Introduction
Immunoassay based measurement of 25-hydroxyvitamin D [25(OH)D] is a cornerstone of non-PTH mediated hypercalcemia workup. Circulating monoclonal immunoglobulins can disrupt antibody analyte binding in these assays, generating spuriously elevated results. This phenomenon of pseudohypervitaminosis D is underrecognized and carries significant risk of diagnostic misdirection, particularly in nephrology practice where hypercalcemia and acute kidney injury (AKI) may herald multiple myeloma (MM).
Case Description
A 73 year old male with CKD stage III and diabetes mellitus presented with slurred speech, gait instability, and subacute back pain. Laboratory evaluation revealed severe hypercalcemia (calcium 14.4 mg/dL), suppressed PTH (12.3 pg/mL), hypophosphatemia (1.0 mg/dL), and AKI (creatinine 2.6 mg/dL from baseline 1.3 mg/dL). Immunoassay 25(OH)D returned markedly elevated at >150 ng/mL despite no history of vitamin D supplementation. A widened protein gap (9.7 g/dL) prompted evaluation for paraproteinemia; serum and urine protein electrophoresis identified a monoclonal gammopathy confirmed as MM on bone marrow biopsy. The elevated 25(OH)D was attributed to presumed myeloma paraprotein immunoassay interference given the absence of supplementation exposure and confirmed paraproteinemia. Confirmatory liquid chromatography-tandem mass spectrometry (LC-MS/MS) testing was not obtainable prior to clinical deterioration. Bortezomib based therapy was initiated; however, the patient's condition continued to decline, and he died prior to reassessment of vitamin D levels or treatment response.
Discussion
Monoclonal immunoglobulins interfere with competitive immunoassays by non-specifically binding assay components, falsely displacing or mimicking the analyte signal. In this case, a 25(OH)D level >150 ng/mL without supplementation exposure should have raised concern for assay interference rather than true vitamin D toxicity. Key red flags include markedly elevated 25(OH)D without supplementation history, widened protein gap, and AKI in the context of hypercalcemia collectively forming a CRAB-adjacent presentation of MM. Confirmatory LC-MS/MS testing is not always clinically feasible, making prospective recognition of this pitfall essential. Misattributing hypercalcemia to vitamin D toxicity risks delaying diagnosis of MM and its nephrotoxic sequelae, including cast nephropathy and irreversible renal injury.