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Furosemide pharmacokinetics and pharmacodynamics in renal transplantation
Author(s) -
Gehr Todd W B,
Sica Domenic A,
Brater D Craig,
Davis Judy,
Fakhry Itaf
Publication year - 1988
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1988.71
Subject(s) - furosemide , aldosterone , plasma renin activity , transplantation , natriuresis , pharmacodynamics , pharmacokinetics , endocrinology , medicine , excretion , kidney transplantation , renal physiology , kidney , renal function , pharmacology , renin–angiotensin system , blood pressure
Furosemide was administered intravenously to four patients who had undergone renal transplantation in the past and four creatinine clearance—matched control subjects. Both patients who had undergone renal transplant and control subjects displayed similar pharmacokinetic and pharmacodynamic behavior, as assessed by drug delivery to the urine and sodium excretion, respectively. Despite similar degrees of natriuresis, patients who had undergone renal transplantation demonstrated a clear defect in urine potassium excretion. This defect in potassium excretion was not related to altered responsiveness of the renin‐angiotensin‐aldosterone axis because plasma renin activity increased in a normal fashion after furosemide in both control and transplant subjects. Although the plasma aldosterone response to increases in plasma renin activity was sluggish in patients undergoing renal transplantation, normal increases in plasma aldosterone levels were achieved in both groups, suggesting that there may be an intrinsic defect in distal tubular potassium secretion that can be unmasked by furosemide. Clinical Pharmacology and Therapeutics (1988) 43, 547–553; doi: 10.1038/clpt.1988.71