hypoaldosteronism/uppköst

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A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism.

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A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism, presenting severe hyponatremia, is described. A 57-year-old man complaining of nausea, vomiting and fatigability was admitted to our hospital because of hyponatremia (114 mEq/I). The low levels of serum cortisol and urinary

Congenital hypoaldosteronism associated with nails hypothrophy - case report and review of the literature.

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We report 15 years follow-up of a girl born with nails hypothrophy and primary hypoaldosteronism. The failure to thrive, troubles with feeding and vomiting were observed since the first weeks of life. The results of the laboratory examination confirmed isolated hypoaldosteronism. The growth velocity

Molecular genetic studies in a case series of isolated hypoaldosteronism due to biosynthesis defects or aldosterone resistance.

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OBJECTIVE Hypoaldosteronism is associated with either insufficient aldosterone production or aldosterone resistance (pseudohypoaldosteronism). Patients with aldosterone defects typically present with similar symptoms and findings, which include failure to thrive, vomiting, hyponatremia, hyperkalemia

Primary hypoaldosteronism in a dog with pituitary and adrenal T-cell lymphoma.

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A 7-year-old mixed breed dog was presented with a 2-week history of vomiting, diarrhoea, weakness and loss of appetite. Initial laboratory tests revealed hyponatraemia and hyperkalaemia consistent with hypoadrenocorticism. Basal plasma cortisol and adrenocorticotropic hormone concentrations were not

Hypokalemia, normal blood pressure, and hyperreninemia with hypoaldosteronism.

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The etiology of persistent hypokalemia and renal potassium loss was investigated in three children. Each had normal blood pressure but low plasma aldosterone values in relation to elevated plasma renin activity. None had a history of licorice abuse, laxative or diuretic use, persistent vomiting or

Aldosterone synthase deficiency type II: an unusual presentation of the first Greek case reported with confirmed genetic analysis

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Objective: Aldosterone synthase deficiency (ASD) is a rare, autosomal recessive inherited disease with an overall clinical phenotype of failure to thrive, vomiting, severe dehydration, hyperkalemia, and hyponatremia. Mutations in the

Salt losing nephropathy simulating congenital adrenal hyperplasia in an infant.

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Pseudo-hypoaldosteronism occurring predominately in male infants has been reported in association with a spectrum of urologic diseases including obstructive uropathy. This is thought to reflect tubule unresponsiveness to aldosterone. We report a case, which was misdiagnosed as a case of congenital

Diagnosis and treatment of a child with the syndrome of apparent mineralocorticoid excess type 1.

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We report the case of a 16-month-old boy who presented with chronic vomiting, failure to thrive, arterial hypertension and medullary nephrocalcinosis. Laboratory results revealed hypokalaemia, metabolic alkalosis, increased urinary potassium excretion and a hyporeninaemic hypoaldosteronism.

Restoration of Epithelial Sodium Channel Function by Synthetic Peptides in Pseudohypoaldosteronism Type 1B Mutants.

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The synthetically produced cyclic peptides solnatide (a.k.a. TIP or AP301) and its congener AP318, whose molecular structures mimic the lectin-like domain of human tumor necrosis factor (TNF), have been shown to activate the epithelial sodium channel (ENaC) in various cell- and animal-based studies.

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