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Hypertensive hypokalemic disorders

Title
Hypertensive hypokalemic disorders
Authors
Kyu B.C.
Ewha Authors
최규복
SCOPUS Author ID
최규복scopus
Issue Date
2007
Journal Title
Electrolyte and Blood Pressure
ISSN
1738-5997JCR Link
Citation
vol. 5, no. 1, pp. 34 - 41
Indexed
SCOPUS; KCI scopus
Abstract
Hypokalemia is a common clinical problem. The kidney is responsible for long term potassium homoeostasis, as well as the serum potassium concentration. The main nephron site where K secretion is regulated is the cortical collecting duct, mainly via the effects of aldosterone. Aldosterone interacts with the mineralocorticoid receptor to increase sodium reabsorption and potassium secretion; the removal of cationic sodium makes the lumen relatively electronegative, thereby promoting passive potassium secretion from the tubular cell into the lumen through apical potassium channels. As a result, any condition that decreases the activity of renal potassium channels results in hyperkalemia (for example, amiloride intake or aldosterone deficiency) whereas their increased activity results in hypokalemia (for example, primary aldosteronism or Liddle's syndrome). The cause of hypokalemia can usually be determined from the history. If there is no apparent cause, the initial step is to see if hypokalemia is in associated with systemic hypertension or not. In the former group hypokalaemia is associated with a high mineralocorticoid effect or hyperactive sodium channel as in Liddle's syndrome. In hypertensive hypokalemic patients, measurement of the renin, aldosterone, and cortisol concentrations would be of help in differential diagnosis.
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의학전문대학원 > 의학과 > Journal papers
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