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April 1981

Distal Renal Tubular Acidosis in Multiple Myeloma

Author Affiliations

From the Division of Hematology, University of Southern California School of Medicine and Los Angeles County-University of Southern California Medical Center, Los Angeles.

Arch Intern Med. 1981;141(5):655-657. doi:10.1001/archinte.1981.00340050101022

• A patient with early multiple myeloma was initially seen with a severe hyperchloremic metabolic acidosis with a normal anion gap and a urine pH of 6.3. The patient did not have glucosuria, aminoaciduria, or phosphaturia. A bicarbonate loading test showed that the fractional excretion of bicarbonate was less than 5% and confirmed the hypothesis that the patient had a distal renal tubular acidification defect. The pathophysiologic mechanism that caused this defect is unknown, but it is associated with the presence of a serum M component (IgG-λ) and a urine M component (A light chains). Multiple myeloma should be considered in the differential diagnosis of conditions of patients who have a renal tubular acidification defect.

(Arch Intern Med 1981;141:655-657)

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