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Abstract: FR-PO662

Acid-Base Disturbances in Multiple Myeloma

Session Information

Category: Trainee Case Report

  • 902 Fluid and Electrolytes: Clinical

Authors

  • Patel, Amol M., Houston Methodist Hospital, Houston, Texas, United States
  • Lee, Benjamin J., Houston Kidney Consultants, Houston, Texas, United States
Introduction

Multiple myeloma (MM) can be associated with several acid/base abnormalities that may not be as frequently appreciated as other clinical manifestations such as renal insufficiency, anemia, hypercalcemia, lytic bone lesions.

Case Description

A 62-year-old man with relapsed IgA kappa monoclonal MM presented with confusion and malaise. Labs showed: serum bicarbonate 13 mEq/L, serum chloride 102 mEq/L, anion gap (AG) 19, albumin 1.6 g/dL. Beta-hydroxybutyrate and lactic acid were not elevated. Additional labs included: blood urea nitrogen 29 mg/dL, creatinine 1.1 mg/dL, eGFR 72 mL/min/1.73m2. Arterial blood gas demonstrated pH 7.50, pCO2 18 mmHg, pO2 95 mmHg. Head imaging and infectious work-up were unremarkable. Although renal function normalized with supportive care, symptoms did not improve and these acid/base abnormalities persisted.

Despite no history of liver disease and normal liver function tests, serum ammonia was elevated at 142 umol/L. MM-associated hyperammonemic encephalopathy leading to hyperventilation was felt to be the cause of his respiratory alkalosis. In addition, the elevated AG was attributed to presumed negatively charged IgA. Ultimately, plasma exchange was started, and he received carfilzomib, pomalidomide, and dexamethasone. His acid/base abnormalities subsided with treatment of his MM, and mental status returned to baseline.

Discussion

This case demonstrates unusual acid/base disturbances associated with MM. Respiratory alkalosis from hyperammonemic encephalopathy is thought to be due to excess ammonia production by myeloma cells.1 Several cases report failure with standard treatments for hyperammonemia but response to chemotherapy.2-3 Furthermore, inpatient mortality is reduced in patients who received MM-targeted therapy compared to those who did not.4

The AG metabolic acidosis is presumed due to negatively charged IgA immunoglobulins. An increased AG has been reported in up to 30% of patients with IgA monoclonal gammopathy, in contrast to a decreased AG that is more commonly seen in IgG gammopathy.5 Of note, however, the magnitude of AG elevation does not correlate with monoclonal protein concentration, and AG abnormalities are not a sensitive test for screening for monoclonal gammopathies.5

It is important for clinicians to recognize and understand these potential acid/base disturbances in MM, as early identification may expedite proper therapy.