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hypoaldosteronism/arginine

Krækjan er vistuð á klemmuspjaldið
GreinarKlínískar rannsóknirEinkaleyfi
5 niðurstöður
The first child of consanguineous parents presented with failure to thrive and feeding problems at age 6 weeks. Important laboratory findings were low plasma sodium and elevated potassium and renin. Salt wasting was caused by an enzymatic defect in the terminal aldosterone biosynthesis. The

Hyponatremia and antidiuresis syndrome.

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Antidiuretic hormone (ADH), or arginine vasopressin (AVP), is primarily regulated through plasma osmolarity, as well as non-osmotic stimuli including blood volume and stress. Links between water-electrolyte and carbohydrate metabolism have also been recently demonstrated. AVP acts via the

Amino acid substitution R384P in aldosterone synthase causes corticosterone methyloxidase type I deficiency.

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Corticosterone methyloxidase type I (CMO-I) deficiency is an autosomal recessively inherited disorder causing congenital hypoaldosteronism due to defects in aldosterone synthase (P450aldo), the enzyme that converts 11-deoxycorticosterone to corticosterone, 18-hydroxycorticosterone, and aldosterone.
In two from 3 hyperkalemic patients with chronic glomerulonephritis associated with suppressed aldosterone production ("selective hypoaldosteronism") fractional free water excretion increased and urine osmolality decreased during sodium (Na) restriction. In one of the patients with severe renal

Hyperkalemia in patients infected with the human immunodeficiency virus: involvement of a systemic mechanism.

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BACKGROUND The appearance of hyperkalemia has been described in human immunodeficiency virus (HIV)-positive patients treated with drugs with amiloride-like properties. Recent in vitro data suggest that individuals infected with HIV have alterations in transcellular K+ transport. METHODS With the
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