Metabolism of the diuretic bumetanide in healthy subjects and patients with renal impairment

Howlett, M. R.; Skellern, G.G.; Auld, William; Murdoch, W. R.

doi:10.1007/bf00278586

Cited by 1 publication

(1 citation statement)

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“…The remaining 50% is metabolized in the liver in several steps, and only small amounts of these metabolites are secreted into the urine [14], Only 25% of torasemide is secreted un changed into the urine; the remainder is me tabolized in the liver [15], Three metabolites have been characterized. Metabolites M 1 and M3 have diuretic potential, M3 more than M l; the main metabolite, M5, has no diuretic properties.…”

Section: Metabolismmentioning

confidence: 99%

Comparative Pharmacokinetics and Pharmacodynamics of Loop Diuretics in Renal Failure

et al. 1994

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Loop diuretics increase the fractional excretion of volume, sodium, potassium, chloride and calcium in all stages of renal failure, and their potency is directly correlated with these excretory activities. Tubular secretion of loop diuretics in renal failure is impaired both by reduced renal blood flow and by reduced activity of the tubular carrier system. For these reasons, high concentrations of diuretics in the peritubular capillaries are necessary to guarantee delivery of sufficient drug to their site of action in the ascending limb of the loop of Henle. Piretanide and furosemide have a constant extrarenal elimination and thus accumulate in renal failure. Decreased renal excretion of bumetanide is compensated by hepatic elimination and hence bumetanide does not accumulate. Elimination of torasemide is also independent of its renal excretion. Thus in renal failure, torasemide is the only loop diuretic in which the plasma concentration is strictly dose dependent. Loop diuretics follow a number of different metabolic pathways, but this may not be clinically relevant.

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Section: Metabolismmentioning

confidence: 99%