Abstract: FR-PO0863
Waldenström Macroglobulinemia Unmasked by Pseudohyponatremia and Hyperviscosity Syndrome
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Khater, Abdarrhman, Stony Brook Medicine, Stony Brook, New York, United States
- Ali, Selma, Stony Brook Medicine, Stony Brook, New York, United States
- Sheikh, Fatima Danish, Stony Brook Medicine, Stony Brook, New York, United States
Introduction
Waldenström's macroglobulinemia (WM) is a rare IgM secreting lymphoplasmacytic lymphoma whose nephrologic manifestations are frequently missed. Circulating IgM macroglobulins displace plasma water, producing pseudohyponatremia- a paraprotein artifact that mimics true dysnatremia and delays diagnosis. Recognizing this alongside osmolar gap elevation and a widened protein gap can be the first step toward identifying an otherwise occult hematologic malignancy.
Case Description
An 84-year-old male with hypertension, atrial fibrillation and hyperthyroidism presented with right eye pain, hemorrhagic chemosis, retinal hemorrhages and blurred vision. Labs were notable for a sodium of 126 mEq/L against a measured osmolality of 306 mOsm/kg yielding an osmolar gap of 43 unexplained by glucose or triglycerides (185 mg/dL). TSH and morning cortisol were normal. A protein gap of 5.3 (total protein 8.0, albumin 2.7 g/dL) raised immediate concern. Serum viscosity was 13.7 cP; SPEP showed a monoclonal gamma peak and IFE confirmed IgM kappa paraprotein with serum IgM of 4,810 mg/dL, establishing WM. After emergent Quinton catheter placement, two plasmapheresis sessions reduced IgM to 1,470 mg/dL and sodium normalized to 143 mEq/L without any sodium directed therapy. MYD88 mutation analysis and bone marrow biopsy are pending; Zanubrutinib is planned.
Discussion
The osmolar gap here was not toxin or renal failure rather it was IgM. That distinction matters because the reflex to treat a sodium of 126 instinctively invites fluid restriction, the exact opposite of what hyperviscosity demands . In hyperviscosity syndrome, prompt IV hydration is a cornerstone of acute management which is directly at odds with the standard approach to hyponatremia. Restricting fluids in this setting would have further concentrated an already critically viscous paraprotein load, worsening sludging, end-organ hypoperfusion, and the very ocular and neurologic injury the patient presented with. Excluding hypothyroidism, adrenal insufficiency, and hypertriglyceridemia left the protein gap as the critical redirect. The parallel normalization of sodium with IgM clearance post-plasmapheresis closed the argument mechanistically - this was never a sodium problem.
Conclusion Hyperosmolar hyponatremia with protein gap may reveal WM; recognizing the pattern enables timely plasmapheresis over sodium correction.