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SEVERAL reports attesting to the efficacy of cation-exchange resins as therapeutic adjuncts in the management of congestive cardiac failure1 2 3 4 5 6 7 8 9 suggest their use in other clinical states associated with fluid retention. The resins are not absorbed from the gastrointestinal tract; when taken by mouth they act by binding sodium, thus preventing its absorption and resulting in excretion of the bound sodium in the stool.1 , 3 , 10 As sodium is bound, other cations, — for example, NH3+ or H+,—are released and are presumably available for absorption. Clinical evidence of toxicity has been meager, with the exception of the development of hypokalemia in some cases. . . .
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Gabuzda et al. (1952) studied this question.
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