NDT Advance Access originally published online on January 25, 2007
Nephrology Dialysis Transplantation 2007 22(4):1150-1155; doi:10.1093/ndt/gfl752
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No impact of hyperkalaemia with renin–angiotensin system blockades in maintenance haemodialysis patients
Department of Internal Medicine, Hanyang University Guri Hospital, Guri, Republic of Korea
Correspondence and offprint requests to: Ho-Jung Kim, MD, Division of Nephrology, Department of Internal Medicine, Hanyang University Guri Hospital, 249-1, Gyomoon-dong, Guri, Gyeonggi, 471-701, Republic of Korea Email: kimhj{at}hanyang.ac.kr
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Abstract |
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Background. Renin–angiotensin system (RAS) blockades, angiotensin converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are well accepted for the cardiorenal-protective benefits added to antihypertensive effects in chronic kidney diseases (CKD), but associated with an increased risk of hyperkalaemia. However, few studies have investigated the effect of RAS blockades on serum potassium in dialysis patients.
Methods. Hyperkalaemia associated with RAS blockades by ACEI and/or ARB was evaluated in 69 patients on maintenance haemodialysis, who underwent a three-period crossover study in four groups (no exposure to RAS blockades, ACEI or ARB alone and ACEI plus ARB treatments), lasting one month in each period.
Results. Sixty-two patients completed this prospective 3-month study, and no one stopped the study because of the development of hyperkalaemia and/or complications. Mean serum K was similar among the four periods (no exposure, 5.54 ± 0.67 mmol/l; ACEI alone, 5.54 ± 0.75 mmol/l; ARB alone, 5.50 ± 0.66 mmol/l; ACEI + ARB combination, 5.42 ± 0.66 mmol/l) and was also equal when compared between the two groups with and without exposure to RAS blockades (5.48 ± 0.68 vs 5.54 ± 0.67 mmol/l, P = NS). The incidence of severe hyperkalaemic episodes (>6.0 mmol/l) upon monthly predialysis serum K determination was 25.8% with no exposure to RAS blockades, 29.8% for ACEI alone, 19.6% for ARB alone and 17.7% for ACEI + ARB combination without statistically significant differences among the four periods (P = NS). Among covariables, the degree of Kt/V, intakes of other medications interfering with potassium homeostasis and diabetes mellitus did not result in any significant hyperkalaemic changes during the 3-month study period except anuric patients compared with non-anuric patients (5.58 ± 0.69 vs 5.19 ± 0.65 mmol/l, P < 0.001).
Conclusion. Neither monotherapy (ACEI or ARB) nor combination therapy (ACEI plus ARB) is associated with the additional risk of hyperkalaemia in patients on maintenance haemodialysis. However, those patients with anuria on RAS blockades warrant the cautious monitoring of serum K to prevent hyperkalaemia.
Keywords: angiotensin-converting enzyme inhibitor; angiotensin II receptor blocker; haemodialysis; hyperkalaemia
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Introduction |
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Serious hyperkalaemia is common in patients with end-stage renal disease (ESRD), and is observed in about 10% of haemodialysis patients [1]. One group of investigators reported that hyperkalaemia, besides congestive heart failure, was the most common indication requiring interventional extra-haemodialysis in an emergency department for ESRD patients on maintenance haemodialysis [2].
Therefore, the prevention of life-threatening hyperkalaemia is one of the main goals of haemodialysis. Aside from dietary indiscretion, there are few known major risk factors for the development of hyperkalaemia in maintenance haemodialysis patients, such as prolonged fasting, hyperglycaemia and medications that might affect potassium homeostasis. Medications generally produce hyperkalaemia either by causing redistribution of potassium or by impairing renal potassium excretion [3].
Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) are thought to have greater cardio-protective effects than other groups of antihypertensive drugs in haemodialysis patients as well as in the general population [4,5]. Therefore, the use of ACEIs or ARBs is often recommended as a first line of treatment in the majority of patients on maintenance haemodialysis [6]. However, patients with chronic renal disease are at increased risk of hyperkalaemia, and ACEIs can exacerbate the hyperkalaemia. This increase in serum potassium necessitated the discontinuation of ACEI in 1.2–1.6% of subjects in clinical trials [7]. Therefore, hyperkalaemia limits the use of ACEIs in a patient population that could otherwise derive significant benefit. Knowledge of ACEI and ARB influences on serum potassium concentrations results from clinical trials that compare an ACE inhibitor with an ARB on renal function in people with heart failure. These trials demonstrated a significantly lower incidence of hyperkalaemia in patients randomly assigned to an ARB treatment compared with those undergoing ACEI treatment [8,9].
In contrast with those patients before the start of maintenance haemodialysis, renin–angiotensin system (RAS) blockades are not likely to have major effects on the serum potassium levels in patients on maintenance dialysis because the removal of potassium is achieved mainly by haemodialysis and renal excretion plays a minor role in those patients. Because only few studies have investigated the effect of ACEIs and ARBs on serum potassium in patients on maintenance dialysis [10,11], the risk of hyperkalaemia from ACEI and ARB in haemodialysis patients is unclear.
The purposes of this study were to evaluate the incidence and severity of hyperkalaemia due to ACEI and/or ARB, and to evaluate the difference between monotherapy (ACEI or ARB) and combination therapy (ACEI + ARB) on hyperkalaemia.
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Subjects and methods |
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Patients selection and data collection
Between January and August 2003, we performed a prospective crossover study involving adult patients with ESRD. All patients with a history of hypertension undergoing haemodialysis treatment at Hanyang University Guri Hospital and two local dialysis centres (Centre A and B, Guri, Korea), three times per week for a minimum of 2 months, were eligible to participate. A history of hypertension was defined as a current use of antihypertensive medications or as systolic blood pressure
140 mmHg and/or diastolic blood pressure 90 mmHg. The exclusion criteria included (i) serious concomitant illnesses or medical diseases such as uncontrolled hypertension, unstable angina, congestive heart failure, acute myocardial infarction within six months or cancer, (ii) history of recurrent hypotension during dialysis, (iii) known allergy to or intolerable adverse effects from ACEI or ARB and (iv) history of admission with life-threatening hyperkalaemia and severe recurrent hyperkalaemia (serum K > 6.0 mmol/l) due to poor dietary compliance despite repeated dietary counseling.
All patients gave their written informed consent before enrolment in our study. This study was approved by the Institutional Review Board of Hanyang University Guri Hospital. Age, sex, duration of dialysis, cause of ESRD and the presence of diabetes mellitus were recorded from the chart of each patient. The use of ACEI or ARB was determined by chart review. The use of other medications including cation-exchange resins during the 3-month study period was also recorded. Patients were asked to estimate their residual urine output (anuria was defined as a daily urine output 
100 ml). Participants were given dietary counselling by a renal dietician and were requested to maintain their regular diets containing 60 mmol of potassium per day and low sodium (<100 mmol/day) throughout the entire study. The patients developing hyperkalaemia (>5.5 mmol/l) during the study were examined further for their compliance to diets and medications with additional counselling. In addition, subsequent predialysis potassium measurements were followed until it became 5.5 mmol/l. Among them, patients with mild hyperkalaemia (5.6–6.0 mmol/l) were carefully observed while being treated with a low potassium diet (<0.5 mmol/kg), but severe hyperkalaemia (>6.0 mmol/l) was treated with cation-exchange resins as needed to reduce potassium level (<6.0 mmol/l).
Study design
If started before the initiation of this study, medications that might affect serum potassium concentration [ß-blockers, ß-agonists, diuretics, NSAIDs (Non-steroidal anti-inflammatory drugs), and digoxin] were maintained during the study period. The haemodialysis schedules of all patients were unchanged during the study period. As a part of their routine care, all patients had a monthly midweek (Wednesday for patients receiving dialysis on a Monday–Wednesday–Friday schedule, or Thursday for patients on a Tuesday–Thursday–Saturday schedule) predialysis arterial blood sample taken to measure serum potassium. Blood samples were collected before the start of the study and monthly for 3 months. The potassium concentration of the dialysis solution (2 mmol/l) was not changed during the study period. The Kt/V, urine output (ml/day), dry weight and predialysis blood pressure were recorded each month. The target blood pressure during the study was 140/90 mmHg. The main ACEI and ARB used as RAS blockades were moexipril and irbesartan with recommended standard dose, respectively. However, if ACEIs or ARBs had been administered previously, these medications were maintained. Throughout the study period, other antihypertensive agents were added or deleted to maintain the target blood pressure in predialysis blood pressure measurements (<140/90 mmHg) as required.
This study was a prospective, three-period crossover design lasting 1 month in each period over 3 months. Depending on the RAS blockade (ACEI or ARB) intake at the beginning, enroled patients were classified into (i) no exposure to RAS blockades, (ii) ACEI alone, (iii) ARB alone and (iv) ACEI plus ARB combination therapy. The no-exposure patients to RAS blockades at the beginning were randomized into either ACEI or ARB for the first month. One subgroup treated with ACEI for the first month was given ARB for the next month in addition to ACEI, and then both drugs were discontinued for the last month. The second subgroup treated with ARB for the first month was given ACEI in addition to ARB for the next month and then both drugs were discontinued for the last month. Patients who were treated with ACEI-alone (ACEI monotherapy) were administered ARB additionally for the first month, then ARB alone for the next month and then discontinued ARB for the last month. Patients treated with ARB-alone (ARB monotherapy) were administered ACEI additionally for 1 month, then ACEI alone for the next month and then ACEI was discontinued for the last month. Patients who had been treated with ACEI and ARB (combination therapy) discontinued ARB for one month, then received ARB alone for the next month and finally discontinued both agents for the last month (Figure 1).
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During the 3-month study period, those with no exposure to any RAS blockades are designated as the no exposure group, those on ACEI alone as the ACEI (monotherapy) group, those on ARB alone as the ARB (monotherapy) group and those on both ACEI plus ARB as the ACEI + ARB (combination) group.
Statistical analysis
All data were analysed using SPSS version 11.5 for Windows. All continuous variables were expressed as mean ± SD unless otherwise stated. Differences of mean serum potassium level between different groups were compared by Kruskal–Wallis test or one-way ANOVA test. Mann–Whitney U-test or Student t-test was used for comparison of the mean serum potassium level between two groups. Repeated measures analysis of variance (RM ANOVA) test was performed to compare serum potassium level between different groups and within subjects during the study periods. Comparison of the incidence of hyperkalaemia according to contributing factors that might affect potassium homeostasis was evaluated by the chi-square test. Statistical significance was set at P < 0.05.
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Results |
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A total of 69 patients were enroled in this study. In the Hanyang University Guri Hospital, dialysis centre A and dialysis centre B, 20, 33 and 16 patients were enroled, respectively. Seven patients discontinued and 62 patients completed the study. Of the seven patients who did not complete the study, two discontinued because of non-compliance, four patients because of dry cough and one patient because of recurrent hypotension. The demographic information of the patients is listed in Table 1.
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The mean serum potassium levels during the periods of no exposure (n = 93), ACEI monotherapy (n = 47), ARB monotherapy (n = 46) and ACEI + ARB combination (n = 62) were 5.54 ± 0.67 mmol/l, 5.54 ± 0.75 mmol/l, 5.50 ± 0.66 mmol/l and 5.42 ±0.66 mmol/l, respectively. There were no statistically significant differences between the four periods (P = 0.684) (Figure 2). The mean serum potassium level of the ACEI or ARB monotherapy period was 5.52 ± 0.70 mmol/l. When classified by no exposure and exposure to RAS blockade, the mean serum potassium level during the no-exposure period (n = 93) was 5.54 ± 0.67 mmol/l and during the exposure period (n = 155) was 5.48 ± 0.68 mmol/l (P = 0.471). The relative risk of hyperkalaemia (serum K
5.5 mmol/l) during the ACEI monotherapy period was 1.031 [95% confidence interval (CI); 0.739–1.437], 0.886 for the ARB monotherapy period (95% CI; 0.610–1.283) and 0.750 for the ACEI + ARB combination period (95% CI; 0.518–1.086), respectively.
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Serum potassium levels between four groups and those within subjects in the subsequent study periods did not show significant differences. The mean serum potassium values at the baseline, first month, second month and third month are as follows: (i) values on no-exposure subgroup to RAS blockades at the beginning with addition of ACEI at the first month (n = 16) were 5.69 ± 0.80 mmol/l, 5.45 ± 0.84 mmol/l, 5.54 ± 0.76 mmol/l and 5.56 ± 0.48 mmol/l respectively; (ii) values on no-exposure subgroup to RAS blockades with addition of ARB at the first month (n = 15) were 5.51 ± 0.62 mmol/l, 5.59 ± 0.77 mmol/l, 5.32 ± 0.31 mmol/l and 5.65 ± 0.61 mmol/l, respectively; (iii) values on ACEI-alone at the beginning (n = 14) were 5.60 ± 0.78 mmol/l, 5.61 ± 0.64 mmol/l, 5.49 ± 0.55 mmol/l and 5.50 ± 0.74 mmol/l, respectively; (iv) values on ARB alone at the beginning (n = 11) were 5.36 ± 0.73 mmol/l, 5.16 ± 0.73 mmol/l, 5.51 ± 0.65 mmol/l and 5.30 ± 0.88 mmol/l, respectively; and (v) values on ACEI + ARB combination at the beginning (n = 6) were 5.32 ± 0.92 mmol/l, 5.72 ± 0.71 mmol/l, 5.53 ± 0.59 mmol/l and 5.50 ± 0.58 mmol/l, respectively.
The incidences of hyperkalaemia (serum K >5.5 mmol/l) were 51.6% in the no-exposure group, 53.1% in the ACEI group, 45.7% in the ARB group, 49.5% in either ACEI or ARB group and 38.7% in the ACEI + ARB combination group, respectively, without statistically significant differences among groups. The incidence of severe hyperkalaemia (serum K >6.0 mmol/l) was 25.8% in the no-exposure group to RAS blockades, 29.8% in the ACEI group, 19.6% in the ARB group, 24.7% on either ACEI or ARB group and 17.7% in the ACEI + ARB combination group, respectively; differences did not reach statistical significance among these groups (Table 2). Fifty two episodes of severe hyperkalaemia occurred (>6.0 mmol/l) during the study period (3 months), and subsequent potassium levels were <6.0 mmol/l in all patients within 2 weeks, but five in the no-exposure group to any RAS blockades, seven in the ACEI group, six in the ARB group and six in the ACEI + ARB combination group hyperkalaemia persisted longer than 2 weeks. However, at the end of each 1-month study period, continuous treatment of the cation-exchange resin was required only in two in the no-exposure group to any RAS blockades, three in the ACEI group, three in the ARB group and two in the ACEI + ARB combination group, respectively.
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Intakes of other medications interfering with potassium homeostasis such as ß-blockers, diuretics, digoxin and NSAIDs did not affect serum potassium significantly during the 3-month study period. However, serum potassium levels in the anuric group were higher than those in non-anuric group (5.58 ± 0.69 mmol/l vs 5.19 ± 0.65 mmol/l, P < 0.001), whereas serum potassium levels in the diabetic group were similar to non-diabetic group (5.36 ± 0.75 mmol/l vs 5.56 ± 0.68 mmol/l, P = 0.121) (Table 3). Also, the degree of Kt/V did not affect serum potassium level during the study period (Kt/V < 1.2 (n = 9) vs
1.2 (n = 53); 5.36 ± 0.68 mmol/l vs 5.54 ± 0.65 mmol/l, P = 0.352).
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Discussion |
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TopAbstractIntroductionSubjects and methodsResultsDiscussionAcknowledgementsReferences |
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In this study, the incidence of hyperkalaemia and severe hyperkalaemia as well as the mean serum potassium level in maintenance haemodialysis patients were similar with or without exposure to RAS blockades (Table 2). Also, there was no difference in mean potassium levels among four groups, i.e. no exposure to any RAS blockades, ACEI monotherapy, ARB monotherapy and ACEI plus ARB combined therapy, during the 3-month study period (Figure 2). Furthermore, serum potassium levels were not different between four groups, either at the beginning of the study or in the subsequent monthly predialysis serum potassium measurements throughout the following crossover study periods. As a result, in our prospective study of patients receiving maintenance haemodialysis, the use of an ACEI or an ARB did not result in increased risk of hyperkalaemia.
One study found that the use of ACEIs or ARBs significantly increased serum potassium from the baseline values in patients on maintenance dialysis [10]. The authors suggested that interference with the RAS in patients on maintenance dialysis might impair intestinal potassium excretion or block tissue potassium redistribution. The authors claimed that aldosterone plays an important role in increasing potassium excretion via the intestinal tracts and in potassium redistribution in many cell types. In patients with chronic renal failure, gut elimination of potassium is shown to be increased, and appears to be mediated by increased colonic secretion of potassium [12]. The enhancement of colonic secretion of potassium was shown to be mediated by an upregulation of angiotensin II subtype 1 receptors according to an animal model [13]. Another study suggested that enhanced colonic secretion in patients with ESRD is mediated by aldosterone [12]. In either case, RAS blockades in chronic renal failure would interfere with potassium homeostasis. However, increased fecal potassium excretion as an extrarenal adaptation of potassium homeostasis in chronic renal failure has not been convincingly demonstrated [14]. Furthermore, recent studies have shown that a high dose of the non-selective aldosterone antagonist, spironolactone does not produce hyperkalaemia in chronic haemodialysis patients [15,16].
Similarly, our study showed that the risk of hyperkalaemia among ESRD patients on maintenance haemodialysis was not greater in those taking either ACEI, ARB or both of ACEI and ARB than those not taking either agent. Therefore, although the degree of Kt/V did not influence serum potassium level during the study period in our study, inadequate haemodialysis in addition to poor dietary compliance could be still considered as the main cause of hyperkalaemia because the regulation of potassium homeostasis mainly depends on dialysis in ESRD patients on maintenance haemodialysis [17]. Besides high dietary potassium intake, there are other obvious factors to induce hyperkalaemia on stable patients on maintenance haemodialysis without ongoing hypercatabolic state, severe metabolic acidosis and reduction in the dialysis clearance are: (i) drugs used concomitantly that interfere potassium homeostasis, (ii) hypoaldosteronism and (iii) reduction in residual renal function [18]. But, in this study, those drugs such as ß-blockers, diuretics, digoxin and NSAIDs did not affect serum potassium levels significantly during the 3-month study period. Also, serum K was similar between our maintenance haemodialysis patients with diabetes mellitus, well known as a cause of hyporeninaemic hypoaldosteronism [19], and those with non-diabetic diseases. However, as expected, the anuric group revealed significantly higher serum K compared with non-anuric group with residual renal function, though it might suggest minimal renal function (Table 3).
However, our study had several limitations: (i) The potassium content of the patients’ food could not be measured. Although all patients were prescribed a similar diet containing the same amount of potassium (60 mmol/day), some patients may not have followed the diet accurately. (ii) This study did not include washout periods. Therefore, drugs from previous periods might have influenced subsequent periods. (iii) This study used standard doses of ACEIs and ARBs. In one study, no increase in serum potassium was noted following 1 month of treatment with a low dose of ARB, but serum potassium increased following an additional month of therapy at higher doses of ARB [20]. Therefore, a further study with higher doses of ACEI and ARB may be needed to determine the development of hyperkalaemia in maintenance haemodialysis patients.
In conclusion, the use of ACEI or ARB is not associated with a higher incidence of hyperkalaemia in patients on maintenance haemodialysis. However, the subgroup with anuria on RAS blockades needs cautious observation for the risk of hyperkalaemia. Therefore, as long as the appropriate dietary potassium restriction and adequate haemodialysis are well maintained in addition to careful attention for the development of hyperkalaemia in those patients with anuria, we suggest that ACEI and ARB, either alone or in combination can be administered without additional risks of hyperkalaemia in patients on maintenance haemodialysis.
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Acknowledgements |
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The authors thank Dr Man S. Oh, Downstate Medical Centre, State University of New York, Brooklyn, NY, USA, for comments and critical reading of the manuscript.
Conflict of interest statement. None declared.
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References |
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Accepted in revised form: 16.11.06
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