Localization of the Renal Excretion of the Tritiated Digoxin

Doherty, JamesE.; Ferrell, Chris; Towbin, Eugene J.

doi:10.1097/00000441-196909000-00005

Cited by 27 publications

(3 citation statements)

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“…These experiments showed an actual fall in tritiated digoxin in an area beginning in the proximal tubule and extending through the mid-point of the distal tubular area. This reabsorption pattern was accentuated when expressed as the digoxin/creatinine clearance ratio (Doherty et al 1969a). …”

Section: Reabsorption Of Digoxin By the Renal Tubular Cellmentioning

confidence: 99%

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Clinical Pharmacokinetic Significance of the Renal Tubular Secretion of Digoxin

Koren

1987

Clinical Pharmacokinetics

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Tubular secretion appears to be a major route of the renal elimination of digoxin. Secretion of the drug by the tubules is modulated by renal blood flow, by a number of commonly coadministered drugs (e.g. quinidine, spironolactone, verapamil, amiodarone), and by age. The maximal transport capacity does not appear to be achieved with clinically relevant concentrations. The tubular transport of digoxin does not appear to be associated with the anionic or cationic transport systems, nor the Na+/K+-ATPase receptor. Further studies are needed to elucidate the exact mechanisms involved in the transtubular movement of the glycoside.

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Section: Reabsorption Of Digoxin By the Renal Tubular Cellmentioning

confidence: 99%

“…Using the stop flow technique, Doherty et al (1969a) demonstrated reabsorption of tritiated digoxin in the dog. In this procedure, the urine flow is completely arrested by occlusion of the ureters and there is enough time for detection of maximal effects of secretion and reabsorption.…”

Section: Reabsorption Of Digoxin By the Renal Tubular Cellmentioning

confidence: 99%

Clinical Pharmacokinetic Significance of the Renal Tubular Secretion of Digoxin

Koren

1987

Clinical Pharmacokinetics

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“…However, renal clearance of the intact drug accounts for the majority of total digoxin clearance. Both tubular reabsorption and secretion of digoxin have been demonstrated (Bloom et al, 1966;Doherty et aL, 1969;Marcus, 1972;Roman and Kauker, 1976;Steiness, 1974;Waldorff et aL, 1978), Steiness (I 974) has shown that digoxin serum concentrations may rise when tubular secretion is blocked by concurrent administration of spironolactone. In patients with hypokaIaemia, active renal tubular secretion of digoxin is reduced (Steiness, 1978), Conversely, tubular secretion is enhanced by potassium supplementation.…”

Section: J 3 2 Effect On Eliminationmentioning

confidence: 99%

Disease-related Alterations in Cardiac Glycoside Disposition

Ochs¹,

Greenblatt

Bodem

et al. 1982

Clinical Pharmacokinetics

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The eJJects of diseases involving the kidney, gastrointestinal tract, thyroid, and cardiovascular system on the disposition of cardiac glycosides are reviewed.The glycosides ouabain and digoxin are cleared predominantly by renal excretion of the intact drugs. Not surprisingly, total clearance (if these two compounds is reduced in patients with reduced creatinine clearance. Similarly, steady-state serum concentrations of digoxin at any given dose become higher as renal function declines. However, individual variability is considerable, thereby limiting the utility (if dosage schemes based on nomograms or equations. A further complication is Ihal tissue distribution (if digoxin is altered in renal inSI!fficiency, so that serum concentrations take on u different meaning in patients with renal failure. In the ca.~e (if digitoxin, renal clearance accounts for only part of the total clearance. A clear relationship between creatinine clearance and total digitoxin clearance has not yet been established. However, digitoxin protein binding is reduced in renal insufficiency, requiring a change in the clinical interpretation (if total (free plus bound) digitoxin serum concentrations in such patients. Although digoxin absorption may be impaired in patients with serious malabsorption syndromes, most studies have demonstrated normal or near normal absorption despite gastrointestinal disease or extensive ablative surgery. Hepatic cirrhosis does not alter the pharmacokinetics of digoxin, but is associated with impaired demethylation of ~-methyldigoxin (medigoxin). Although hepatic biotran~formation accounts for a substantialfraction (if the total clearance of digitoxin, disappearance (if digitoxin from the plasma is, if anything, more rapid in patients with liver disease as opposed to healthy controls.Clearance (if both digitoxin and digoxin varies in direct relation to thyroid function; clearance is increased and the ha(f-l!fe shortened in thyrotoxicosis, and the reverse is truefor hypothyroidism. This may be explained by parallel changes in creatinine clearance, but further studies are needed to d~fine the mechanism (if alterations in glycoside clearance in relation to thyroid function.Continuing re.finement of analytical and pharmacokinetic techniques will lead to rapid progress in research in this area, and a need for continuing re-evaluation of the state of the art.

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Furosemide-Induced Forced Diuresis in Digoxin Intoxication

Rotmensch¹

1978

Arch Intern Med

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Localization of the Renal Excretion of the Tritiated Digoxin

Cited by 27 publications

References 0 publications

Clinical Pharmacokinetic Significance of the Renal Tubular Secretion of Digoxin

Clinical Pharmacokinetic Significance of the Renal Tubular Secretion of Digoxin

Disease-related Alterations in Cardiac Glycoside Disposition

Furosemide-Induced Forced Diuresis in Digoxin Intoxication

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