Mechanisms Contributing to Unresponsiveness to Mercurial

The ultimate failure of edematous cardiac patients to respond to mercurial diuretics is well established. 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 potentiation of mercurial diuresis in previously unresponsive patients by pre-treatment with ammonium chloride, resistance to mercurials has been attributed to chloride depletion (1, 2). However, acidotic potentiation of mercurial diuresis may persist after the elevated serum chloride level has returned to normal (3). Moreover, mercurial-resistant patients may not exhibit hypochloremia and some hypochloremic patients continue to have good mercurial diureses (2). Since organic mercurials act by decreasing renal tubular reabsorption of filtered electrolyte and water, any factor which increases such reabsorption will tend to antagonize the diuretic effect of mercurials. The present communication is an attempt to analyze mercurial resistance in cardiac patients in the light of the severely impaired renal excretion of salt and water, resulting from the changes in cardiovascular-renal hemodynamics, hormonal balance, and other mechanisms affecting renal tubular activity in congestive failure. One of these factors, decreased glomerular filtration rate, reduces the quantity of filtered sodium and chloride presented to the tubules. Recent studies have shown that whenever filtration is decreased without change in tubular function the resulting glomerulo-tubular imbalance is associ-