fludrocortisone-acetate and Hyperkalemia

Hyperkalaemia is a commonly encountered problem in dialysis patients with end-stage renal disease (ESRD). The aim of the present study was to assess the effect of fludrocortisone acetate (FCA) on reducing serum potassium levels in haemodialysis (HD) patients with hyperkalaemia.. Prospectively, 21 HD patients with hyperkalaemia were enrolled in this study. Patients were divided into two groups, including FCA (0.1 mg/d, n = 13) administration or no treatment (control, n = 8) for 10 months. No changes in dialysis or drug regimens were made during this period. Result. There were no significant differences in the baseline characteristics and biochemical parameters between the two groups (FCA therapy and control). At 10-months after FCA therapy, serum potassium levels were not significantly different between the treatment and control groups [median value (range): 5.2 (4.4-6.0) vs 5.8 (4.8-6.3) mEq/l, P = 0.121]. However, using the Wilcoxon signed ranks test, serum potassium levels were significantly lower at the end of the 10 month time period after FCA therapy compared with serum potassium levels of the pre-treatment period [5.2 (4.4-6.0) vs 6.1 (5.3-6.8), P = 0.01]. The biochemical values, including sodium, chloride, protein, albumin, blood nitrogen, creatinine, interdialytic weight change and blood pressure, did not show significant difference in comparisons between the two groups and pre-and post-FCA therapy period.. FCA therapy appears to slightly decrease serum potassium value in hyperkalaemic HD patients. However, these results are insufficient to explain the effectiveness of FCA. Therefore, potentially large-scale studies with increased dose concentrations are needed to minimize the positive potassium balance in hyperkalaemic HD patients.

Topics: Adult; Aged; Anti-Inflammatory Agents; Female; Fludrocortisone; Humans; Hyperkalemia; Kidney Failure, Chronic; Male; Middle Aged; Potassium; Renal Dialysis; Sodium-Potassium-Exchanging ATPase; Weight Gain

It is known that some patients with primary aldosteronism show postoperative hyperkalemia, which is due to inability of the adrenal gland to secrete sufficient amounts of aldosterone. However, hyperkalemia is generally neither severe nor prolonged, in which replacement therapy with mineralocorticoid is seldom necessary. We report a case of a 46-year-old woman with an aldosterone-producing adenoma associated with severe postoperative hyperkalemia. After unilateral adrenalectomy, the patient showed episodes of severe hyperkalemia for four months, which required not only cation-exchange resin, but also mineralocorticoid replacement. Plasma aldosterone concentration (PAC) was low, although PAC was increased after rapid ACTH test. Histological examination indicated the presence of adrenocortical tumor and paradoxical hyperplasia of zona glomerulosa in the adjacent adrenal. Immunohistochemistry demonstrated that the enzymes involved in aldosterone synthesis, such as cholesterol side chain cleavage (P-450scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), and 21-hydroxylase (P-450c21), or the enzyme involved in glucocorticoid synthesis, 11beta-hydroxylase (P-450c11beta), were expressed in the tumor, but they were completely absent in zona glomerulosa of the adjacent adrenal. These findings were consistent with the patterns of primary aldosteronism. Serum potassium level was gradually decreased with concomitant increase in PAC. These results suggest that severe postoperative hyperkalemia of the present case was attributable to severe suppression of aldosterone synthesis in the adjacent and contralateral adrenal, which resulted in slow recovery of aldosterone secretion. It is plausible that aldosterone synthesis of adjacent and contralateral adrenal glands is severely impaired in some cases with primary aldosteronism, as glucocorticoid synthesis in Cushing syndrome.

Topics: Adenoma; Adrenal Gland Neoplasms; Adrenalectomy; Aldosterone; Female; Fludrocortisone; Humans; Hyperaldosteronism; Hyperkalemia; Immunoenzyme Techniques; Middle Aged; Potassium; Steroid Hydroxylases