# Biotin-Induced Proximal Renal Tubular Acidosis in an Adolescent Female: Report of a Rare Case With Rechallenge Confirmation

**Authors:** Qazi Tauseef Ahmad, Abdul Haseeb, Wajib Ullah, Muzzamil Samad, Ammara Afridi

PMC · DOI: 10.7759/cureus.103396 · 2026-02-10

## TL;DR

A teenage girl developed kidney-related acidosis from high-dose biotin supplements, confirmed by symptom recurrence upon re-exposure.

## Contribution

This is the first reported case of biotin-induced proximal RTA confirmed by rechallenge.

## Key findings

- Biotin supplementation caused hypokalemia and metabolic acidosis in a previously healthy adolescent.
- Symptoms resolved upon discontinuation and recurred upon re-exposure to biotin.
- The patient's condition was sustained with fluid and potassium therapy after avoiding biotin.

## Abstract

Proximal renal tubular acidosis (RTA) results from impaired bicarbonate reabsorption in the proximal renal tubule, leading to a normal anion gap metabolic acidosis and electrolyte abnormalities. We report the case of a 16-year-old previously healthy female who presented with recurrent episodes of hypotension, dizziness, and generalized weakness over one month. Laboratory evaluation demonstrated severe hypokalemia, hyperchloremic metabolic acidosis with a normal anion gap, and glucosuria in the absence of hyperglycemia, with preserved renal function. Extensive evaluation for endocrine and autoimmune causes was unrevealing. A detailed review of medications and supplements identified recent initiation of high-dose biotin supplementation (2,500 µg daily) for cosmetic purposes. A strong temporal association was noted between biotin exposure and symptom onset, with rapid clinical and biochemical improvement following discontinuation. Two months later, inadvertent re-exposure to biotin resulted in recurrence of symptoms and laboratory abnormalities, which again resolved promptly after cessation of the supplement. The patient was managed with intravenous fluids, potassium supplementation, and avoidance of biotin, leading to sustained resolution of symptoms. At one-month follow-up, she remained asymptomatic with normal electrolyte levels and preserved renal function. This case identifies biotin as a rare, reversible cause of proximal RTA and underscores the importance of obtaining a thorough supplement history when evaluating patients with otherwise unexplained metabolic acidosis.

## Linked entities

- **Chemicals:** biotin (PubChem CID 171548)
- **Diseases:** proximal renal tubular acidosis (MONDO:0008369), metabolic acidosis (MONDO:0000440), hypokalemia (MONDO:0003019)

## Full-text entities

- **Diseases:** Proximal Renal Tubular Acidosis (MESH:D000141), electrolyte (MESH:D014883), hyperglycemia (MESH:D006943), hypotension (MESH:D007022), glucosuria (MESH:D006030), dizziness (MESH:D004244), hyperchloremic metabolic acidosis (MESH:D000138), hypokalemia (MESH:D007008), weakness (MESH:D018908)
- **Chemicals:** bicarbonate (MESH:D001639), potassium (MESH:D011188), Biotin (MESH:D001710)
- **Species:** Homo sapiens (human, species) [taxon 9606]

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Source: https://tomesphere.com/paper/PMC12983043