Diuretic-induced severe hyponatremia. Review and analysis of 129 reported patients

Chest. 1993 Feb;103(2):601-6. doi: 10.1378/chest.103.2.601.


Thiazides were responsible for severe diuretic-induced hyponatremia (serum sodium level < 115 mEq/L) in 94 percent of 129 cases reported in the literature between 1962 and 1990. The hyponatremia developed within 14 days in most of the patients receiving thiazides but in none of the patients who were treated with furosemide. Diuretic-induced hyponatremia was four times more common in women than in men. Advanced age was not associated with a higher tendency for hyponatremia. In the majority of the patients who received thiazides, excess antidiuretic hormone activity, hypokalemia, and excess water intake were accompanying findings which, singly or together, appeared to contribute to the development of hyponatremia. In 12 patients, mortality was directly related to hyponatremia. Rapid average correction of hyponatremia and a relatively high total correction (over 20 mEq/L) in the first 24 h were significantly associated with higher mortality or demyelinating syndrome. The presence of neurologic signs is an indication for active sodium replacement. The onset of thiazide-induced hyponatremia may in some cases occur within 1 day and therefore needs to be corrected rapidly, but within a total elevation of 20 mEq/L in the first 24 h. Where the onset is judged to have been slow (over several days), the level should be corrected at a slow rate, up to a total of 12 to 15 mEq/L in 24 h.

Publication types

  • Review

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Benzothiadiazines*
  • Diuretics
  • Female
  • Humans
  • Hyponatremia / chemically induced*
  • Hyponatremia / diagnosis
  • Male
  • Middle Aged
  • Risk Factors
  • Sodium Chloride Symporter Inhibitors / adverse effects*


  • Benzothiadiazines
  • Diuretics
  • Sodium Chloride Symporter Inhibitors