TY - JOUR
T1 - Investigations into the mechanisms of hyperkalemia following renal transplantation
AU - DeFronzo, R. A.
AU - Goldberg, M.
AU - Cooke, C. R.
AU - Barker, C.
AU - Grossman, R. A.
AU - Agus, Z. S.
N1 - Funding Information:
A preliminary report of this work appeared in the abstracts of the American Society of Nephrology, 1975, p. 100. This work was supported by a research grant from the National Heart and Lung Institute, HL-00340; an NIH Clinical Research Center Grant, NIH 5 MOl RR0004O; and by a training grant from the National Arthritis, Metabolic and Digestive Dis-eases, AM-05634. Dr. Agus was a Clinical In- vestigator of the Veteran's Administration. Ms. Do- rothy Senesky, Terry Liebsch, Freda Rappoport, and Sandra Markus performed the laboratory analyses. We acknowledge Ms. Cordelia Shute, R.N., and the staff of the Clinical Research Center of the Hospital of the University of Pennsylvania for the nursing care and assistance provided in studying these patients.
PY - 1977
Y1 - 1977
N2 - 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 is unknown.
AB - 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 is unknown.
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U2 - 10.1038/ki.1977.53
DO - 10.1038/ki.1977.53
M3 - Article
C2 - 330924
AN - SCOPUS:0017685325
SN - 0923-2508
VL - 11
SP - 357
EP - 365
JO - Research in Microbiology
JF - Research in Microbiology
IS - 5
ER -