Delayed digoxin toxicity following dis- continuance in acute renal failure

A dJgitalized 75-year-oldpatiem with postoperative renal failure demonstrated a rise in serum digoxin concentration, peaking at 3.4 nmol.L -j three days following discontinuance of the drug. This was accompanied by cardiac bradyarrhythrains. Although the serum digoxin concentration had already started to climb from a therapeutic level prior to the discontinuance of the drug, the unabated and subatantiat rise was consistent with a dramatic decrease in the apparent volume of distribution of digoxin accompanying acute renal failure. Serum digoxin levels were determined with fluorescence polarization immunoassay, which has an improved specifici~ when compared to the commonly used radioimmunoassays for digoxin. Digoxin is cleared from the body primarily through glomerular filtration and partially through active renal tubular secretionJ Following discontinuance of digoxin administration, the serum digoxin concentration (SDC) may be expected to decline at a rate which closely cot'rclatcs with creatinine clearance. This assumes that all other factors influencing the SDC are constant. A patient is reported in acute renal failure whose serial SDC measurements rose after digoxin was stopped, peaking on the third day with a concentration of 3.4nmol'L -~. The pathogenesis of the SDC rise, which was accompanied by cardiac arrhythmias consistent with digoxin toxicity, will be discussed.