Lazar G S, Feinstein D I
Arch Intern Med. 1981 Apr;141(5):655-6.
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, of 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-lambda) and a urine M component (lambda light chains). Multiple myeloma should be considered in the differential diagnosis of conditions of patients who have a renal tubular acidification defect.