A 69-year-old man presents to the physician for fatigue and bone pain. His workup shows that he is anemic with the presence of an M-protein in the serum and urine, and he is diagnosed with multiple myeloma. Some of his other laboratory values are shown below.
An arterial blood gas shows that he has a pH of 7.3 and a PaCO2 of 35 mmHg. He has urine studies performed, which are significant for glucosuria, a urine pH of 7.8 after bicarbonate infusion, and a fractional excretion of bicarbonate of 25%.
Which of the following best represents the acid/base abnormality in this patient?
A. Anion gap metabolic acidosis with a compensatory respiratory alkalosisNonanion gap metabolic acidosis with a compensatory respiratory alkalosis. This question is a good reminder to read the question and skim the answer choices first before going on to read the vignette. In this case, the diagnosis of multiple myeloma and proximal (type 2) renal tubular acidosis (presenting with the Fanconi syndrome, which is a syndrome of proximal tubule dysfunction with a decrease in the reabsorption of bicarbonate, phosphate, amino acids, and glucose) are not important for answering the question, which happens often on the shelf examination. (A, C) From the laboratory values, the calculated anion gap is 10, ruling out an anion gap metabolic acidosis. The pH, bicarbonate, and PaCO2 are all low, indicating a metabolic acidosis. To compensate, patients will increase their ventilation to decrease the amount of CO2 in the blood, producing a compensatory respiratory alkalosis. To determine if the respiratory compensation is appropriate, Winter formula can be used: PaCO2 = (1.5 × HCO3) + 8 ± 2. (D) In the case above, the PaCO2 should be 30 to 36 mmHg, which fits with the actual value of 35 mmHg confirming that the compensation is appropriate. If the patient were overcompensating (e.g., PaCO2 28 mmHg), then a primary respiratory alkalosis would be present; if undercompensating (e.g., PaCO2 38 mmHg), then a primary respiratory acidosis would be present.
Briefly, monoclonal gammopathies are the most common cause of acquired type 2 renal tubular acidosis, which is caused by an inability of the proximal convoluted tubule to reabsorb important compounds (e.g., bicarbonate, glucose, phosphate, etc.). Patients will excrete bicarbonate in the urine, leading to a moderate nonanion gap metabolic acidosis. The diagnosis is confirmed by an inappropriately elevated urine pH in response to a bicarbonate infusion as well as an increased fractional excretion of bicarbonate >15%. Distal (type 1) renal tubular acidosis is caused by a failure to reabsorb bicarbonate in the distal convoluted tubule, leading to severe acidosis with a urine pH consistently >5.3. Type 4 renal tubular acidosis is a result of hypoaldosteronism and will produce a mild acidosis.