Hyponatremia: Diuretic‑Induced Renal Losses and Exercise‑Associated Dilutional Hyponatremia

Renal Causes – Diuretic‑Induced Hyponatremia

Thiazide diuretics are the most common iatrogenic cause of hypovolemic hyponatremia, producing simultaneous sodium loss and impaired renal diluting capacity. This effect results from inhibition of tubular sodium‑chloride transport, which limits delivery of filtrate to the diluting segments of the nephron. Clinical Nutrition (2018) 2
Thiazide therapy impairs tubular diluting mechanisms, reducing the kidney’s ability to excrete free water and predisposing patients to hyponatremia. The mechanism involves direct blockade of the Na⁺‑Cl⁻ cotransporter in the distal convoluted tubule, leading to a relative excess of water reabsorption. Clinical Nutrition (2018) 2

EAH is a dilutional hyponatremia that occurs when fluid intake during prolonged exercise (> 4 h) exceeds sodium losses through sweat, leading to a net positive water balance. The condition is most frequently reported in endurance athletes such as marathon runners. Sports Medicine (2015) [3][4]
Key risk factors for EAH include excessive fluid consumption beyond sweat losses, female sex, low body‑mass index, race duration longer than 4 hours, and transient alterations in renal function during exercise. These factors synergistically increase the likelihood of a positive water balance and impaired free‑water excretion. Sports Medicine (2015) [3][4]
Incidence of EAH in marathon participants ranges from 3 % to 22 %, with reported fatalities (six deaths) in the United States and United Kingdom linked to severe hyponatremia. This highlights the potential seriousness of the condition despite its relatively low overall frequency. Sports Medicine (2015) [3][4]