Impaired water excretion following diuretic therapy

Abstract

Water excretion in normal subjects during water loading was impaired after the administration of the short‐acting diuretics, mannitol, quinethazone, furosemide, and ethacrynic acid. Correlation between antidiuresis and body‐fluid‐volume depletion was established. Minimum contraction of body‐fluid volume is postulated as the cause of the antidiuresis. It is postulated that free water formation in the urine is regulated by several intra‐ and extrarenal factors; the role of the antidiuretic hormone is uncertain.

Diuretic-Induced Hyponatremia

“…There are several differences in presentation as compared with thiazide-induced hyponatremia: the indication is more often heart failure than hypertension [6], the duration of therapy is usually longer [6,22], and the serum blood urea nitrogen and uric acid levels tend to be higher [22]. In some of these cases it is likely that diuretic-induced volume depletion reduces the ability to excrete water by the mechanisms previously discussed [19,47]. In other cases, water excretion may be impaired by the underlying disease (e.g., heart failure).…”