A 48-year-old HIV-positive man on tenofovir alafenamide (TAF)-based ART for 3 years develops weakness, bone pain, and polyuria. Labs: Na 136, K 2.9, Cl 112, HCO3 14 mEq/L, phosphate 1.8 mg/dL, uric acid 2.1 mg/dL, glucose 85 mg/dL (urine glucose positive). Urine shows glycosuria, aminoaciduria, and phosphaturia. The underlying tubular syndrome is:

• A Distal renal tubular acidosis (Type 1 RTA)
• B Fanconi syndrome (proximal tubular dysfunction) ✓
• C Nephrogenic diabetes insipidus
• D Pseudohypoaldosteronism type II (Gordon syndrome)

Explanation

Fanconi syndrome is generalized proximal tubular dysfunction with wasting of phosphate, glucose (glycosuria with normoglycemia), uric acid, amino acids, bicarbonate, and potassium — the complete picture seen here. The older tenofovir disoproxil fumarate (TDF) was a well-known cause; TAF has much lower risk but can occasionally cause Fanconi syndrome. Normal anion gap metabolic acidosis with low bicarbonate reflects proximal RTA (part of Fanconi). Distal RTA does not cause phosphaturia or glycosuria; NDI causes polyuria/polydipsia without the metabolic abnormalities.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.