A 58-year-old woman comes to the office due to increasing fatigue and muscle cramps over the past 2 months. Medical history is significant for Sjögren syndrome. Blood pressure is 130/74 mm Hg, and pulse is 86/min. Physical examination shows enlarged parotid glands and dry oral mucosa. Laboratory results are as follows: Urine pH is 6.8. Which of the following is the most likely cause of this patient's acid-base imbalance?

Question

A 58-year-old woman comes to the office due to increasing fatigue and muscle cramps over the past 2 months.  Medical history is significant for Sjögren syndrome.  Blood pressure is 130/74 mm Hg, and pulse is 86/min.  Physical examination shows enlarged parotid glands and dry oral mucosa.  Laboratory results are as follows:  Urine pH is 6.8.  Which of the following is the most likely cause of this patient's acid-base imbalance?

Quizplus · Accepted Answer

Explanation: 11ec25c8_d305_c420_bc81_1513c5d02350_MD0003_00 This patient has primary metabolic acidosis, evidenced by pH <7.35 and serum bicarbonate (HCO₃⁻) <24 mEq/L. The normal anion gap of 10 mEq/L is consistent with nonanion gap metabolic acidosis (NAGMA), which results from loss of HCO₃⁻. This patient's NAGMA is likely due to type 1 renal tubular acidosis (RTA), a common complication of Sjögren syndrome. metabolic acidosis ₃ ⁻ normal ₃ ⁻ There are 3 major types of RTA, all of which cause NAGMA due to a net loss of HCO₃⁻. ₃ ⁻ Type 1 (distal) RTA results from impaired H⁺ excretion by alpha-intercalated cells in the distal tubule. Hypokalemia is typically present due to reduced K⁺ reabsorption, and urine pH >5.5 is expected due to markedly impaired capacity to acidify the urine. Type 2 (proximal) RTA results from impaired HCO₃⁻ reabsorption in the proximal tubule, and hypokalemia is usually present. Because distal tubular H⁺ excretion is able to somewhat compensate for the impaired proximal HCO₃⁻ reabsorption, urine pH is variable and often <5.5. Type 4 RTA results from reduced aldosterone activity, leading to impaired H⁺ and K⁺ excretion in the collecting duct. In contrast to type 1 and type 2 RTA, hyperkalemia is typical. The urine pH is usually <5.5. (Choice A) Impaired respiratory muscle function causes hypoventilation and primary respiratory acidosis, evidenced by pH <7.35 but elevated PaCO₂ (>40 mm Hg). This patient's low PaCO₂ represents compensatory respiratory alkalosis for primary metabolic acidosis. ₂ ₂ (Choices C and F) Increased gastrointestinal HCO₃⁻ loss (eg, severe diarrhea) is a common cause of NAGMA. Intracellular shift of HCO₃⁻ occurs with infusion of excess sodium chloride and leads to NAGMA. These and most other etiologies of acidosis occur with intact distal tubular H⁺ excretion; therefore, low urine pH (eg, <5.5) is expected as the kidneys are able to appropriately acidify the urine and excrete excess acid. In this patient, NAGMA is due to a net loss of HCO₃⁻ from RTA, not to gastrointestinal bicarbonate loss. ₃ ⁻ ₃ ⁻ ⁺ ₃ ⁻ (Choices D and E) Anion gap metabolic acidosis (AGMA) results from the accumulation of unmeasured acidic compounds that increase the anion gap. Increased ketoacid production is responsible for AGMA in severe insulin deficiency (ie, diabetic ketoacidosis), and increased lactic acid production causes AGMA during periods of poor organ and tissue perfusion (eg, sepsis). AGMA Educational objective: Renal tubular acidosis (RTA) involves a net loss of HCO₃⁻ and is a common cause of nonanion gap metabolic acidosis. Type 1 RTA results from impaired H⁺ excretion in the distal tubule and can be recognized by abnormally high urine pH (eg, >5.5) in the setting of acidosis. ₃ ⁻ ⁺ References: Hyperchloremic acidosis. (http://www.ncbi.nlm.nih.gov/pubmed/29493965)

A 58-Year-Old Woman Comes to the Office Due to Increasing