Search results
Results from the WOW.Com Content Network
Cerebral salt-wasting syndrome (CSWS), also written cerebral salt wasting syndrome, is a rare endocrine condition featuring a low blood sodium concentration and dehydration in response to injury (trauma) or the presence of tumors in or surrounding the brain. In this condition, the kidney is functioning normally but excreting excessive sodium. [1]
Hypokalemia which is recurrent or resistant to treatment may be amenable to a potassium-sparing diuretic, such as amiloride, triamterene, spironolactone, or eplerenone. Concomitant hypomagnesemia will inhibit potassium replacement, as magnesium is a cofactor for potassium uptake.
The thiazides and potassium-sparing diuretics are considered to be calcium-sparing diuretics. [6] The thiazides cause a net decrease in calcium lost in urine. [7] The potassium-sparing diuretics cause a net increase in calcium lost in urine, but the increase is much smaller than the increase associated with other diuretic classes. [7]
Potassium-sparing diuretics or antikaliuretics [1] refer to drugs that cause diuresis without causing potassium loss in the urine. [2] They are typically used as an adjunct in management of hypertension , cirrhosis , and congestive heart failure . [ 3 ]
Low potassium is caused by increased excretion of potassium, decreased consumption of potassium rich foods, movement of potassium into the cells, or certain endocrine diseases. [3] Excretion is the most common cause of hypokalemia and can be caused by diuretic use, metabolic acidosis , diabetic ketoacidosis , hyperaldosteronism , and renal ...
Hypoaldosteronism may result in high blood potassium and is the cause of 'type 4 renal tubular acidosis', sometimes referred to as hyperkalemic RTA or tubular hyperkalemia. However, the acidosis, if present, is often mild. It can also cause urinary sodium wasting, leading to volume depletion and hypotension. [citation needed]
Get AOL Mail for FREE! Manage your email like never before with travel, photo & document views. Personalize your inbox with themes & tabs. You've Got Mail!
Alternatively, one could differentiate between the two syndromes by administering a potassium-sparing diuretic. Patients with Liddle's syndrome will only respond to a diuretic that binds the ENaC channel, whereas those with AME will respond to a diuretic that binds to ENaC or the mineralcorticoid receptor. [9]