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The ultimate failure of edematous cardiac pa- tients to respond to mercurial diuretics is well es- tablished. Although the older literature ascribed this to renal tubular accommodation to mercury, some patients have received mercurials for many years without manifesting such acquired tubular resistance. More recently, because of the potenti- ation of mercurial diuresis in previously unrespon- sive patients by pre-treatment with ammonium chloride, resistance to mercurials has been at- tributed to chloride depletion (1, 2). However, acidotic potentiation of mercurial diuresis may per- sist after the elevated serum chloride level has re- turned to normal (3). Moreover, mercurial-re- sistant patients may not exhibit hypochloremia and some hypochloremic patients continue to have good mercurial diureses (2).
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Weston et al. (1952) studied this question.
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