A Randomized Controlled Trial of Fludrocortisone for the Treatment of Hyperkalemia in Hemodialysis Patients

Kaisar, M; Wiggins, Kathryn J.; Sturtevant, Joanne M.; Hawley, Carmel M.; Campbell, Scott; Isbel, Nicole M.; Mudge, David W.; Bofinger, Andrew; Petrie, James J.B.; Johnson, David W.

doi:10.1053/j.ajkd.2006.01.014

Cited by 30 publications

(31 citation statements)

References 9 publications

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“…[18][19][20] One study, published in 2003, was included in the prior review. 21 Therefore, we included in this updated review 5 new studies, [22][23][24][25][26] along with the 11 studies 21,[27][28][29][30][31][32][33][34][35][36] reviewed by Mahoney and associates 14 (Appendix 1, available at www .cmaj .ca /cgi /content /full /cmaj .100461 /DC1).…”

Section: Resultsmentioning

confidence: 99%

“…In a study of patients undergoing long-term hemodialysis who had predialysis hyperkalemia, fludrocortisone at a dose of 0.1 mg/day did not result in a significant decrease in serum potassium at three months, even after adjustment for number of hours of dialysis per week 25 (Appendix 5). There were no reported adverse effects with this drug, although its use would be limited to long-term management of hyperkalemia.…”

Section: Fludrocortisonementioning

confidence: 99%

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Management of patients with acute hyperkalemia

Elliott¹,

Ronksley²,

Clase³

et al. 2010

Canadian Medical Association Journal

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A 72-year-old man presents to his family physician for follow-up of hypertension, reporting fatigue and generalized weakness. His medical history also includes peptic ulcer disease, type 2 diabetes mellitus and chronic kidney disease. The estimated glomerular filtration rate is 30 mL/min per 1.73 m 2 . His medications include metformin, lansoprazole, acetylsalicylic acid, hydrochlorothiazide and ramipril, the dose of which was increased two weeks earlier to address suboptimal blood pressure control. Blood work at the time of the current presentation shows that the serum potassium level is 6.7 (normal range 3.3-5.1) mmol/L from a nonhemolyzed sample. The patient's family physician refers him to the emergency department urgently. In the emergency department, the patient is hemodynamically stable, with blood pressure 124/70 mm Hg and heart rate 80 beats/min (regular). Repeat testing shows a potassium level of 6.9 mmol/L, and electrocardiography shows sinus rhythm with peaked T waves, prolonged PR interval (240 milliseconds) and a narrow QRS interval. This patient requires urgent treatment of hyperkalemia. What therapeutic options are available, and what is the evidence supporting their use? H yperkalemia is a common disorder, occurring both in the outpatient setting and in up to 10% of patients who have been admitted to hospital. [1][2][3][4] Underlying renal insufficiency and use of medications that disrupt potassium balance, such as angiotensin-converting enzyme inhibitors and potassium-sparing diuretics, are welldescribed risk factors. [4][5][6][7] Although mild hyperkalemia is often asymptomatic and easily treated, acute, severe hyperkalemia that is left untreated can result in fatal cardiac arrhythmias. [8][9][10] In addition to discontinuation of precipitants, steps in the management of acute hyperkalemia include protecting the heart from arrhythmias by administering calcium-based salts, 11 shifting potassium into the cells and enhancing elimination of potassium. Several treatment options have been proposed, particularly for shifting potassium into the cells, with differing onset and duration of action. 12 In addition, available studies conflict with respect to the efficacy of the various treatment options, which has led to differences in recommendations among practitioners and institutions. 5,13The level of potassium at which treatment should be initiated has not been established by evidence. However, we recommend initiating nonpharmacologic steps for management at levels above 5.5 mmol/L, with pharmacologic interventions as outlined in this review being instituted at levels of 6.0 mmol/L or greater.Given uncertainties regarding the optimal management of this condition, we undertook a review of randomized controlled trials of therapies for the management of acute hyperkalemia in the adult population. MethodsFor the current review, we updated a previously published systematic review on this topic, 14 using a similar search strategy and similar criteria for selecting studies for inclusion. We identified all po...

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Section: Resultsmentioning

confidence: 99%

Section: Fludrocortisonementioning

confidence: 99%

Management of patients with acute hyperkalemia

Elliott¹,

Ronksley²,

Clase³

et al. 2010

Canadian Medical Association Journal

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“…Overall, these findings suggest that extrarenal potassium homeostasis was responsible for the different levels of extracellular potassium between the groups. Some animal and human studies support the role of aldosterone in extrarenal potassium handling through gastrointestinal secretion or transcellular shifts (24)(25)(26)(27), but a trial in anephric patients failed to identify a significant effect of exogenous mineralocorticoid on extracellular potassium (28). Angiotensin II may have varying effects on distal renal potassium channels, but effects of ARB on these channels in other tissues and extrarenal potassium homeostasis are unknown (29).…”

Section: Discussionmentioning

confidence: 99%

Potassium Handling with Dual Renin-Angiotensin System Inhibition in Diabetic Nephropathy

Buren

Adams‐Huet

Nguyen³

et al. 2014

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are the cornerstones of pharmacologic therapy in diabetic nephropathy. Mineralocorticoid receptor blockers reduce proteinuria as single agents or add-on therapy to other renin-angiotensin-aldosterone system-inhibiting drugs in these patients. The long-term benefits and ultimate role of mineralocorticoid receptor blockers in diabetic nephropathy remain unknown. A clinical trial previously showed that the kalemic effect of spironolactone is higher than losartan when added to lisinopril in patients with diabetic nephropathy. The purpose of this study was to investigate if renal potassium handling was primarily responsible for that observation.Design, setting, participants, & measurements In a blinded, randomized, three-arm placebo-controlled clinical trial, 80 participants with diabetic nephropathy taking lisinopril (80 mg) were randomized to spironolactone (25 mg daily), losartan (100 mg daily), or placebo (trial dates from July of 2003 to December of 2006). Serum potassium, aldosterone, and 24-hour urine sodium, potassium, and creatinine were measured over 48 weeks. Differences were analyzed with repeated measures mixed models.Results Mean follow-up serum potassium was 5.0 mEq/L for spironolactone, 4.7 mEq/L for losartan (P=0.05 versus spironolactone), and 4.5 mEq/L for placebo (P,0.001 versus spironolactone; P=0.03 versus losartan). The difference in serum potassium was 0.23 mEq/L for losartan versus placebo (P=0.02), 0.43 mEq/L for spironolactone versus placebo (P,0.001), and 0.2 mEq/L for spironolactone versus losartan (P=0.05). Serum and urine potassium excretion and secretion rates were similar between groups throughout the study.Conclusion Spironolactone raised serum potassium more than losartan in patients with diabetic nephropathy receiving lisinopril, despite similar renal sodium and potassium excretion. This finding suggests that extrarenal potassium homeostasis contributes to hyperkalemia in these patients. A better understanding of extrarenal potassium homeostasis will provide an opportunity to use this drug more safely in patients with diabetic nephropathy as well as other patient populations.

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“…Recently, Kaisar et al [15] demonstrated that FCA treatment of hyperkalaemic haemodialysis patients did not achieve a clinically important decrease in serum potassium levels. In this study, between treatment and control groups, serum potassium levels were not significantly different after 3 months of therapy.…”

Section: Discussionmentioning

confidence: 99%

Effect of fludrocortisone acetate on reducing serum potassium levels in patients with end-stage renal disease undergoing haemodialysis

Kim

Chung

Yoon

et al. 2007

Nephrology Dialysis Transplantation

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Background. 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. Methods. Prospectively, 21 HD patients with hyperkalaemia were enrolled in this study. Patients were divided into two groups, including FCA (0.1 mg/d, n ¼ 13) administration or no treatment (control, n ¼ 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 ¼ 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 ¼ 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. Conclusions. 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.

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A Randomized Controlled Trial of Fludrocortisone for the Treatment of Hyperkalemia in Hemodialysis Patients

Cited by 30 publications

References 9 publications

Management of patients with acute hyperkalemia

Management of patients with acute hyperkalemia

Potassium Handling with Dual Renin-Angiotensin System Inhibition in Diabetic Nephropathy

Effect of fludrocortisone acetate on reducing serum potassium levels in patients with end-stage renal disease undergoing haemodialysis

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