# A novel idiopathic transient tubulopathy associated with exercise-induced-seizures: A case report

## TL;DR

A 26-year-old man experienced exercise-induced seizures linked to a rare kidney issue, with recovery after correcting electrolyte imbalances.

## Contribution

First reported case linking exercise-induced seizures to transient renal tubulopathy without structural or genetic causes.

## Key findings

- Exercise-induced seizures were associated with marked urinary losses of sodium, potassium, and chloride.
- Clinical recovery occurred after normalization of phosphate and uric acid levels.
- Spot urinary electrolyte analysis is recommended for diagnosing unexplained exertion-related seizures.

## Abstract

•First case of exercise-induced seizures linked to transient renal tubulopathy.•Marked urinary sodium, potassium, and chloride loss without structural abnormality.•Genetic, autoimmune, and toxic causes excluded by comprehensive analyses.•Full clinical recovery after normalization of phosphate and uric acid levels.•Spot urinary electrolytes recommended in unexplained exertion-related seizures.

First case of exercise-induced seizures linked to transient renal tubulopathy.

Marked urinary sodium, potassium, and chloride loss without structural abnormality.

Genetic, autoimmune, and toxic causes excluded by comprehensive analyses.

Full clinical recovery after normalization of phosphate and uric acid levels.

Spot urinary electrolytes recommended in unexplained exertion-related seizures.

Although exercise is generally considered beneficial for individuals with epilepsy, rare cases of exercise-induced seizures have been reported. Physical activity influences renal hemodynamics and electrolyte handling, both essential for neurological stability. Disruptions in renal compensatory mechanisms may contribute to seizure susceptibility during exertion. We describe a 26-year-old male patient with exercise-induced seizures over a period of four months, occurring during high-intensity activity, preceded by visual aura and followed by tonic-clonic episodes. Laboratory workup revealed persistent hypophosphatemia (nadir 1.4 mg/dL) and hyperuricemia (up to 15.8 mg/dL). Brain imaging and EEG were unremarkable, and extensive metabolic, autoimmune, toxicological, and genetic investigations ruled out structural, infectious, and hereditary epileptic causes. Spot urine analysis, obtained in the absence of recent exercise, revealed markedly elevated urinary losses of sodium (UNa 207.1 mEq/L), potassium (UK > 100 mEq/L), and chloride (UCl 281.8 mEq/L) suggesting a renal tubular defect. The patient’s condition stabilized with antiseizure medication and electrolyte supplementation therapy, and he remained seizure-free for five years following normalization of serum phosphate and uric acid levels. The absence of identifiable structural or genetic pathology, combined with spontaneous clinical resolution, suggests a reversible functional disorder. In patients with normal neurological and cardiac evaluations, renal electrolyte disturbances should be considered in the differential diagnosis of exercise-related seizures. Spot urinary electrolyte analysis can be a valuable diagnostic tool in atypical cases, particularly when neuroimaging and interictal findings are unremarkable.