SUN-184 Pseudohypoaldosteronism Presenting with Salt Wasting Crisis
نویسندگان
چکیده
منابع مشابه
Autosomal Dominant Pseudohypoaldosteronism Type 1 in an Infant with Salt Wasting Crisis Associated with Urinary Tract Infection and Obstructive Uropathy
Type 1 pseudohypoaldosteronism (PHA1) is a salt wasting syndrome caused by renal resistance to aldosterone. Primary renal PHA1 or autosomal dominant PHA1 is caused by mutations in mineralocorticoids receptor gene (NR3C2), while secondary PHA1 is frequently associated with urinary tract infection (UTI) and/or urinary tract malformations (UTM). We report a 14-day-old male infant presenting with s...
متن کاملA mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism.
Aldosterone-dependent epithelial sodium transport in the distal nephron is mediated by the absorption of sodium through the highly selective, amiloride-sensitive epithelial sodium channel (ENaC) made of three homologous subunits (alpha, beta, and gamma). In human, autosomal recessive mutations of alpha, beta, or gammaENaC subunits cause pseudohypoaldosteronism type 1 (PHA-1), a renal salt-wasti...
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Background: The existence and prevalence of cerebral salt wasting and its differentiation from syndrome of inappropriate antidiuretic hormone have been controversial. This controversy stems from overlapping clinical and laboratory findings and an inability to assess the volume status of these patients. Objectives:To present a case of a cerebral salt wasting syndrome secondary to a bacterial men...
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متن کاملAldosterone in cerebral salt wasting.
ALTHOUGH recent studies of patients with cerebral and pulmonary salt wasting have implicated "inappropriate"' anti-diuretic hormone secretion as the basic defect, the norinality of aldosterone responsiveness has not been firmly established.'-' This paper reports a patient with cerebral salt wasting and hyponatremia in whom bal anee studies suggested normal aldosterone response and inappropriate...
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ژورنال
عنوان ژورنال: Journal of the Endocrine Society
سال: 2020
ISSN: 2472-1972
DOI: 10.1210/jendso/bvaa046.1456