The most likely diagnosis is type 1 (hypokalemic distal) renal tubular acidosis (RTA), which results from a defect in urine acidification in the distal tubule with impaired excretion of hydrogen ions, most commonly caused by decreased activity of the proton pump in distal tubular cells. Because of the inability to excrete hydrogen ions, patients develop a metabolic acidosis with compensatory hyperchloremia, resulting in a normal anion gap (8 mEq/L [8 mmol/L] in this patient) and the inability to acidify urine below a pH of 6.0, even after an acid load. The urine pH is therefore almost always inappropriately elevated for the degree of acidemia, and there is a positive urine anion gap. The same defects also cause potassium wasting, and the increased proximal resorption of citrate that occurs with metabolic acidosis leads to hypocitraturia and increased risk of calcium phosphate kidney stones and nephrocalcinosis. Type 1 (hypokalemic distal) RTA is associated with genetic causes, autoimmune disorders, nephrocalcinosis/hypercalciuria, dysproteinemias, drugs/toxins, and tubulointerstitial disease; this patient likely has sicca complex secondary to Sjögren syndrome and kidney involvement with interstitial nephritis.
Acetaminophen is associated with pyroglutamic acidosis (also known as 5-oxoprolinuria), which causes an increased anion gap metabolic acidosis and is less likely to cause a pure normal anion gap metabolic acidosis.
Type 2 (proximal) RTA involves a defect in regenerating bicarbonate in the proximal tubule and is characterized by a normal anion gap metabolic acidosis, hypokalemia, glycosuria (without hyperglycemia), low-molecular-weight proteinuria, and renal phosphate wasting. However, distal urine acidification mechanisms are intact, and the urine pH is usually less than 5.5 without alkali therapy. This patient's high urine pH, absence of glycosuria, and normal urinalysis are inconsistent with type 2 (proximal) RTA.
Type 4 (hyperkalemic distal) RTA is associated with a urine pH <5.5 and hyperkalemia as a result of hypoaldosteronism, neither of which is seen in this patient.