Antihypertensive Therapy and Its Effects on Potassium Homeostasis

Sica, Domenic A.

doi:10.1111/j.1524-6175.2006.05139.x

Cited by 34 publications

(15 citation statements)

References 38 publications

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“…It is possible that the effects of E 2 on potassium excretion might be altered in the setting of chronic cardio-renal disease. This point is highlighted by clinical studies, which report differential effects of antihypertensive therapies on potassium homeostasis in chronic kidney disease and heart failure (27,32). Furthermore, we did not observe any significant effects of ovariectomy on blood pressure and heart rate.…”

Section: Discussionsupporting

confidence: 59%

17β-Estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner

Ji¹,

Zheng²,

Falconetti³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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This study examined the effects of ovariectomy (OVX) and 17beta-estradiol (E(2)) replacement (OVX + E(2)) on renal function in Sprague-Dawley rats. OVX caused a 40% decrease in the fractional excretion of potassium (FE(K(+))) that was prevented by E(2) replacement [Sham, 24.2 +/- 2.9%; OVX, 14.5 +/- 2.1% (P < 0.05 vs. OVX + E(2)); and OVX + E(2), 26.2 +/- 2.7%; n = 7-11] and that corresponded to significant increases in plasma potassium [(in mmol/l): Sham, 3.15 +/- 0.087; OVX, 3.42 +/- 0.048 (P < 0.05 vs. OVX + E(2)); and OVX + E(2), 3.19 +/- 0.11; n = 7-11]. No effects of OVX were detected on plasma levels of sodium and aldosterone. Angiotensin II type 1 receptor (AT(1)R) densities in ovariectomized rats were 1.4-fold and 1.3-fold higher in glomerular [maximum binding capacity (B(max); in fmol/mg protein): Sham, 482 +/- 21; OVX, 666 +/- 20 (P < 0.05 vs. OVX + E(2)); and OVX + E(2), 504 +/- 26; n = 7-11] and proximal tubular [B(max) (in fmol/mg protein): Sham, 721 +/- 16; OVX, 741 +/- 24 (P< 0.05 vs. OVX + E(2)); and OVX + E(2), 569 +/- 23; n = 7-11] membranes compared with E(2) replete animals, respectively. Both the angiotensin-converting enzyme inhibitor captopril and the AT(1)R antagonist losartan prevented the OVX-induced decrease in the FE(K(+)) and the increase in renal AT(1)R densities, suggesting that E(2) deficiency reduces potassium excretion in an ANG II/AT(1)R-dependent manner. These findings may have implications for renal function in postmenopausal women as well as contribute to the reasons underlying the age-induced increase in susceptibility to hypertension-associated disease in women.

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Section: Discussionsupporting

confidence: 59%

17β-Estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner

Ji¹,

Zheng²,

Falconetti³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…CKD progression[ 14 ] and the use of RAS inhibitor combinations[ 19 ] were previously reported to be risk factors for hyperkalemia, which supports the validity of our study. In contrast, the use of NSAIDs[ 20 ], β-blockers[ 21 ], and potassium salt substitutes[ 22 ], which are known risk factors for hyperkalemia, were not associated with hyperkalemia in our study. The number of patients using these medications was limited, and this study might have lacked sufficient power for the detection of these risk factors.…”

Section: Discussioncontrasting

confidence: 79%

Incidence of and risk factors for newly diagnosed hyperkalemia after hospital discharge in non-dialysis-dependent CKD patients treated with RAS inhibitors

Saito¹,

Yamamoto²,

Nakajima³

et al. 2017

PLoS ONE

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IntroductionRenin-angiotensin system (RAS) inhibitors have been increasingly prescribed due to their beneficial effects on end-organ protection. Iatrogenic hyperkalemia is a well-known life-threatening complication of RAS inhibitor use in chronic kidney disease (CKD) patients. We hypothesized that CKD patients treated with RAS inhibitors frequently develop hyperkalemia after hospital discharge even if they were normokalemic during their hospitalization because their lifestyles change substantially after discharge. The present study aimed to examine the incidence of newly diagnosed hyperkalemia, the timing of hyperkalemia, and its risk factors in CKD patients treated with RAS inhibitors at the time of hospital discharge.MethodsWe retrospectively enrolled patients aged 20 years or older with CKD G3-5 (estimated glomerular filtration rate < 60 mL/min/1.73 m2) and who were treated with RAS inhibitors and discharged from St. Luke’s International Hospital between July 2011 and December 2015. Patients who were under maintenance dialysis or had hyperkalemic events before discharge were excluded. Data regarding the patients’ age, sex, CKD stage, diabetes mellitus status, malignancy status, combined use of RAS inhibitors, concurrent medication, and hyperkalemic events after discharge were extracted from the hospital database. Our primary outcome was hyperkalemia, defined as serum potassium ≥ 5.5 mEq/L. Multiple logistic regression and Kaplan-Meier analyses were performed to identify the risk factors for and the timing of hyperkalemia, respectively.ResultsAmong the 986 patients, 121 (12.3%) developed hyperkalemia after discharge. In the regression analysis, relative to CKD G3a, G3b [odds ratio (OR): 1.88, 95% confidence interval 1.20–2.97] and G4-5 (OR: 3.40, 1.99–5.81) were significantly associated with hyperkalemia. The use of RAS inhibitor combinations (OR: 1.92, 1.19–3.10), malignancy status (OR: 2.10, 1.14–3.86), and baseline serum potassium (OR: 1.91, 1.23–2.97) were also significantly associated with hyperkalemia. The Kaplan-Meier analysis showed that hyperkalemia was most frequent during the early period after discharge, particularly within one month.ConclusionHyperkalemia was frequent during the early period after discharge among previously normokalemic CKD patients who were treated with RAS inhibitors. Appropriate follow-up after discharge should be required for these patients, particularly those with advanced CKD or malignancy status, such as hematological malignancy or late-stage malignancy, and those who are treated with multiple RAS inhibitors.

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“…Potassium-sparing diuretics, despite not fully - are known to correct the fall in serum potassium by increasing serum potassium concentrations [35]. The impacts of beta blocker on potassium match those observed in earlier studies and are not of clinical importance [13, 36]. …”

Section: Discussionmentioning

confidence: 73%

Changes in selected metabolic parameters in patients over 65 receiving hydrochlorothiazide plus amiloride, atenolol or placebo in the MRC elderly trial

Damian

McNamee

Carr

2016

BMC Cardiovasc Disord

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BackgroundTreatment of hypertension reduces incidence of stroke, myocardial infarction and heart failure perhaps partly by controlling different metabolic parameters. There is limited information regarding the changes in potassium, sodium, weight, cholesterol and glucose levels in patients using anti-hypertensives. This study aimed to determine changes in potassium, sodium, glucose, cholesterol, weight, urea and urate levels in patients using anti-hypertensives. Furthermore, to describe these changes and differences between the atenolol, hydrochlorothiazide plus amiloride and placebo arms of the Medical Research Council (MRC) elderly randomised controlled trial.MethodsPatients were randomly allocated to one of the three treatment arms. Measurements were taken at baseline, end of year one and end of year two in 4396 subjects. Linear Mixed Models (LMM) were used to determine the longitudinal profiles of sodium, potassium, weight, cholesterol, glucose, urea and urate. Estimates of changes within groups and difference between groups were obtained.ResultsPatients randomised to receive hydrochlorothiazide + amiloride experienced a significantly greater mean reduction in potassium, sodium and weight compared to placebo at end of year one - mean differences in change −0.18 mmol/L, (95 % CI: −0.21, −0.15); −1.45 mmol/L, (95 % CI: −1.62, −1.29) and −0.46 kgs (95 % CI: −0.73, −0.20) respectively, and greater increases in cholesterol, urea and urate - mean differences in change 0.16 mmol/L, (95 % CI: 0.10,0.22); 0.77 mmol/L, (95 % CI: 0.68, 0.87) and 53.10 μmol/L, (95 % CI: 49.35, 56.85) respectively. Changes were in the same direction but smaller in the atenololarm except for potassium and weight (increases). No group differences in glucose were found.ConclusionResults were in line with expectation except for lack of change in glucose in the hydrochlorothiazide + amiloride arms.Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-016-0368-2) contains supplementary material, which is available to authorized users.

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Antihypertensive Therapy and Its Effects on Potassium Homeostasis

Cited by 34 publications

References 38 publications

17β-Estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner

17β-Estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner

Incidence of and risk factors for newly diagnosed hyperkalemia after hospital discharge in non-dialysis-dependent CKD patients treated with RAS inhibitors

Changes in selected metabolic parameters in patients over 65 receiving hydrochlorothiazide plus amiloride, atenolol or placebo in the MRC elderly trial

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