beta-acetyldigoxin and Acute-Kidney-Injury

This study was performed to get more informations on the renal and extracorporeal elimination of digoxin. The first part of this study demonstrated that a radioimmunoassay for digoxin or a specific tritium label of digoxin is necessary to measure renal digoxin clearances. Randomly labeled 3H-digoxin may loose its label and thus give incoherent results. A comparison of digoxin and inulin clearances in patients demonstrates glomerular filtration as the major renal excretion pathway of digoxin, but a major fraction of the glycoside is excreted by tubular secretion. Opposite to digoxin, beta-methyl-digoxin undergoes less tubular secretion but eventually additional tubular reabsorption. The insertion of digoxin and quinidine may be a further prove for the existence of a tubular secretion of digoxin. While the renal clearance of digoxin is significantly bigger than the renal clearance of creatinine, additional quinidine therapy reduces the renal clearance of digoxin to the one of creatinine. We studied the renal excretion mechanism of digoxin additionally in an animal model of acute prerenal failure. After a 33% reduction of renal arterial pressure glomerular filtrate dropped 68%. Under these circumstances the renal excretion mechanism of digoxin measured as the digoxin to inulin clearance ratio did not change. We evaluated the efficiency of hemodialysis, hemofiltration and hemoperfusion to eliminate digoxin. Although digoxin is eliminated by all three methods, even the most effective, hemoperfusion, can reduce total body content of digoxin less than 3%. Thus we conclude that all these methods have no indication in the treatment of digoxin intoxications.

Topics: Acetyldigoxins; Acute Kidney Injury; Animals; Digoxin; Dogs; Humans; Inulin; Medigoxin; Renal Dialysis