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- W1991826103 endingPage "28" @default.
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- W1991826103 abstract "Recently many clinical syndromes have been described, characterized by renal tubular dysfunction as a major disturbance.1-7In some cases, tubular reabsorption of single substances is defective, e. g., water, glucose, amino acids, or phosphorus. In others, deficient reabsorption affects several materials, usually combinations of those enumerated. Loss of cation is rare as a primary or isolated defect in tubular absorption, although it is not uncommon in association with other absorptive defects.7Severe depletion of calcium and potassium has occurred on numerous occasions, but loss of sodium under similar circumstances is infrequent. Salt wasting is encountered chiefly in association with advanced renal disease,8,9with adrenal insufficiency,10,11and with prolonged administration of mercurial diuretics.12,13Excessive excretion of sodium due to an isolated tubular dysfunction has long been postulated, but it has only recently been reported for the first time.14 The purpose of this paper is to" @default.
- W1991826103 created "2016-06-24" @default.
- W1991826103 creator A5053307090 @default.
- W1991826103 creator A5053645267 @default.
- W1991826103 creator A5083293910 @default.
- W1991826103 date "1959-06-01" @default.
- W1991826103 modified "2023-10-16" @default.
- W1991826103 title "Pseudohypo-adrenalocorticism; renal sodium loss, hyponatremia, and hyperkalemia due to a renal tubular insensitivity to mineralocorticoids." @default.
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