A patient with heart failure has been managed with digoxin and furosemide and is doing well by all measures, for 3 years. He develops acute rheumatoid arthritis and is placed on rather large doses of a very efficacious nonsteroidal anti-inflammatory drug—one that inhibits both cyclooxygenase pathways (COX-1 and -2). Which of the following is the most likely outcome of adding the NSAID?
ExplanationAn important element in the renal responses to furosemide is the maintenance of adequate renal blood flow. That is, to a degree, prostaglandin-mediated. NSAIDs, such as the hypothetical one described here, inhibit prostaglandin synthesis. That, in turn, antagonizes the desired effects of the loop diuretic, leading to less fluid and salt elimination: edema, weight gain, and other markers of heart failure are likely to develop as a result. Hyperchloremic alkalosis (a) is incorrect, in part, because chronic or acute excessive effects of loop diuretics are characterized by hypochloremic metabolic alkalosis. Regardless, NSAIDs are not likely to potentiate the effects of these diuretics. “Dramatic increases of furosemide’s K-sparing effects (b)” is incorrect. Recall that loop diuretics are K-wasting. Digoxin is eliminated by renal excretion. If we accept the notion that loop diuretics may increase the excretion of digoxin, then we should accept the likely possibility that NSAID-induced reductions of diuretic action should reduce the glycoside’s renal loss, not increase it