Recently many clinical syndromes have been described, characterized by renal tubular dysfunction as a major disturbance.1-7 In 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.7 Severe 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,8,9 with adrenal insufficiency,10,11 and with prolonged administration of mercurial diuretics.12,13 Excessive 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
DONNELL GN, LITMAN N, ROLDAN M. Pseudohypo-Adrenalocorticism: Renal Sodium Loss, Hyponatremia, and Hyperkalemia Due to a Renal Tubular Insensitivity to Mineralocorticoids. AMA Am J Dis Child. 1959;97(6):813–828. doi:10.1001/archpedi.1959.02070010815008
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