During a routine follow-up appointment, a 38-year-old female reports a one-month history of progressive muscle weakness and fatigue. Her past medical history is significant for Sjögren syndrome and multiple episodes of calcium phosphate nephrolithiasis. Vital signs show a blood pressure of 118/76 mm Hg and a heart rate of 84/min. Physical examination reveals dry oral mucosa and 4/5 motor strength in the proximal muscles of the upper and lower extremities.
Laboratory evaluation reveals the following:
| Test | Result |
|---|---|
| Serum sodium | 139 mEq/L |
| Serum potassium | 2.9 mEq/L |
| Serum chloride | 115 mEq/L |
| Serum bicarbonate | 14 mEq/L |
| Blood urea nitrogen | 12 mg/dL |
| Serum creatinine | 0.9 mg/dL |
| Urine sodium | 48 mEq/L |
| Urine potassium | 22 mEq/L |
| Urine chloride | 45 mEq/L |
Based on these findings, what is this patient's calculated urine anion gap in mEq/L?
Answer: 25 mEq/L
Answer
25
The patient presents with a normal anion gap metabolic acidosis (serum anion gap = mEq/L). To differentiate the etiology of the acidosis, the urine anion gap (UAG) is calculated using the formula . Substituting the provided urine electrolytes yields mEq/L. A positive UAG indicates that the kidneys are failing to adequately excrete ammonium () to buffer the acid load, pointing toward a renal origin for the acidosis. Specifically, a positive UAG combined with hypokalemia, a history of autoimmune disease (Sjögren syndrome), and recurrent nephrolithiasis is highly characteristic of distal (Type 1) renal tubular acidosis.
Step-by-Step Solution
Key Concept
The urine anion gap () differentiates the etiologies of a normal anion gap metabolic acidosis. A positive UAG implies a renal etiology (e.g., renal tubular acidosis), while a negative UAG points to a gastrointestinal etiology (e.g., severe diarrhea).