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- W2001978360 abstract "Investigations into the mechanism of hyperkalemia following renal transplantation. Hyperkalemia was observed in 23 of 75 patients in the first three months following renal transplantation. The hyperkalemia was unrelated to rejection, renal failure, oliguria, or acidosis. Six patients (four with hyperkalemia and two with normal serum potassium) were studied to evaluate the role of the renin-angiotensin-aldosterone system and/or impairment of renal tubular potassium handling in this syndrome. Following equilibration on a normal dietary intake, patients were placed on a low sodium diet and were given furosemide. All patients achieved sodium and potassium balance during both periods, but at the expense of significant hyperkalemia (5.3 to 5.7 mEq/liter) in the four patients with preexisting hyperkalemia. Plasma aldosterone concentration and urinary aldosterone excretion rates in the hyperkalemic patients were 8.4 ± 0.6 ng/dl and 2.8 ± 1.1 µg/day, respectively, on a control diet, and they rose appropriately to 15.4 ± 1.9 ng/dl and 20.3 ± 1.4 µg/day with sodium restriction. Subsequent administration of exogenous mineralocorticoid, 9-α fluorohydrocortisone (Florinef), 1 mg/day, while the sodium intake was high, failed to increase urinary potassium excretion. Neither furosemide nor acetazolamide plus sodium bicarbonate administration produced a consistent increase in potassium excretion despite a significant natriuresis. In contrast, hydrochlorothiazide increased urinary potassium excretion in three patients from 34 ± 8 mEq/day to 54 ± 5 mEq/day, and serum potassium concentrations fell to normal in all. Three patients, restudied when the serum potassium concentrations were normal, had kaliuretic responses to 9-α fluorohydrocortisone and furosemide. These data demonstrate a reversible defect in urinary potassium excretion following renal transplantation. The impaired response to mineralocorticoids suggests that this defect is related to an abnormality of renal tubular function. The mechanism of correction with thiazides in unknown. Etude des mecanismes de l'hyperkaliemie consecutive a la transplantation renale. Une hyperkaliemie a ete observee chez 23 parmi 75 malades dans les trois premiers mois consecutifs a une transplantation renale. L'hyperkaliemie n'etait pas en rapport avec un rejet, une insuffisance renale, une oligurie ou une acidose. Six malades (quatre atteints d'hyperkaliemie et deux dont le potassium plasmatique etait normal) ont ete etudies afin d'evaluer le role du systeme renine-angiotensine-aldosterone et/ou l'alteration du comportement tubulaire vis-a-vis du potassium dans ce syndrome. Apres une periode d'equilibration avec une alimentation normale les sujets ont recu un regime pauvre en sodium et de la furosemide. Tous le sujets ont atteint un etat stationnaire au cours des deux periodes, mais au prix d'une hyperkaliemie significative (5,3 a 5,7 mEq/liter) chez les quatre d'entre eux qui avaient une hyperkaliemie anterieure. La concentration plasmatique d'aldosterone et les debits d'excretion urinaire d'aldosterone chez les quatre sujets hyperkaliemiques etaient de 8,4 ±0,6 ng/dl et 2,8 ± 1,1 µg/jour respectivement avec le regime de la periode controle et ont augmente de facon adequate a 15,4 ± 1,9 ng/dl et 20,3 ± l,4µg/jour au cours de la restriction de sodium. L'administration ulterieure de mineralo-corticoides exogenes, 9 α-fluorohydrocortisone (Florinef) 1 mg/jour, alors que l'apport de sodium etait eleve n'a pas augmente l'excretion urinaire de potassium. Ni l'administration de furosemide ni celle d'acetazolamide associee a du bicarbonate n'ont produit une augmentation importante de l'excretion du potassium malgre une natriurese significative. L'hydrochlorothiazide, au contraire, a augmente l'excretion urinaire de potassium chez trois sujets de 34 ± 8 mEq/jour a 54 ± 5 mEq/jour et le potassium plasmatique est revenu a la normale chez tous. Trois sujets, etudies a nouveau alors que leur potassium plasmatique etait revenu a la normale, avaient une reponse kaliuretique a la 9-α-fluoro-hydrocortisone et a la furosemide. Ces resultats montrent une alteration reversible de l'excretion urinaire du potassium apres transplantation renale. L'anomalie de reponse aux mineralo-corticoides suggere que cette alteration est liee a une anomalie du fonctionnement tubulaire. Le mecanisme de la correction par les thiazides n'est pas connu." @default.
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- W2001978360 title "Investigations into the mechanisms of hyperkalemia following renal transplantation" @default.
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