Changes in total body potassium during long-term thiazide treatment: Effects of potassium supplements on total body and serum potassium in hypertensive patients with thiazide treatment

2011 ◽  
Vol 3 (01) ◽  
pp. 142-147 ◽  
Author(s):  
Yutaka Doi ◽  
Waturu Aoi ◽  
Shin Suzuki ◽  
Shinji Seto ◽  
Koreaki Baba ◽  
...  
Keyword(s):  
Serum Potassium ◽  
Treatment Effects ◽  
Total Body Potassium ◽  
Hypertensive Patients ◽  
Total Body

Total Body Potassium in Long-Term Lasix Therapy

1974 ◽  
Vol 19 (1_suppl) ◽  
pp. 40-44 ◽  
Author(s):  
H. J. Dargie ◽  
A. C. Kennedy ◽  
D. M. Ward ◽  
K. Boddy ◽  
Priscilla C. King
Keyword(s):  
Total Body Potassium ◽  
Total Body

scholarly journals Fluctuations in plasma potassium in patients on dialysis

2019 ◽  
Vol 34 (Supplement_3) ◽  
pp. iii19-iii25
Author(s):  
Csaba P Kovesdy
Keyword(s):  
Potassium Concentration ◽  
Plasma Potassium ◽  
Total Body Potassium ◽  
Potassium Balance ◽  
Increased Risk ◽  
Total Body ◽  
Stage Renal Disease ◽  
End Stage ◽  
The Impact

Abstract Plasma potassium concentration is maintained in a narrow range to avoid deleterious electrophysiologic consequences of both abnormally low and high levels. This is achieved by redundant physiologic mechanisms, with the kidneys playing a central role in maintaining both short-term plasma potassium stability and long-term total body potassium balance. In patients with end-stage renal disease, the lack of kidney function reduces the body’s ability to maintain normal physiologic potassium balance. Routine thrice-weekly dialysis therapy achieves long-term total body potassium mass balance, but the intermittent nature of dialytic therapy can result in wide fluctuations in plasma potassium concentration and consequently contribute to an increased risk of arrhythmogenicity. Various dialytic and nondialytic interventions can reduce the magnitude of these fluctuations, but the impact of such interventions on clinical outcomes remains unclear.

Effects of amiloride on plasma and total body potassium, blood pressure, and the renin-angiotensin-aldosterone system in thiazide-treated hypertensive patients

1983 ◽  
Vol 34 (4) ◽  
pp. 448-453 ◽  
Author(s):  
Ulrik Gerner Svendsen ◽  
Hans Ibsen ◽  
Sten Rasmussen ◽  
Arne Leth ◽  
Meta Damkjær Nielsen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Total Body Potassium ◽  
Renin Angiotensin Aldosterone System ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Total Body

Total Body Potassium in Patients Receiving Chlorthalidone and Metoprolol for Hypertension

1983 ◽  
Vol 28 (2) ◽  
pp. 172-175 ◽  
Author(s):  
J. M. B. Gray ◽  
D. H. Lawson ◽  
K. Boddy ◽  
W. East
Keyword(s):  
Blood Cell ◽  
Plasma Potassium ◽  
Fixed Dose ◽  
Average Period ◽  
Total Body Potassium ◽  
Total Blood ◽  
Hypertensive Patients ◽  
Dose Combination ◽  
Β Blocker ◽  
Total Body

Measurements of potassium status were reviewed in 23 hypertensive patients receiving metoprolol either alone or in combination with chlorthalidone or chlorthalidone plus potassium over an average period of nine months. There was no statistically significant change in plasma potassium, total blood cell or total body groups developed hypokalaemia (serum potassium <3.0mmol/l) in the absence of significant falls in total blood cell or total body potassium. Thus the use of chlorthalidone plus potassium did not provide adequate prophylaxis against hypokalaemia even in metoprolol recipients. The study confirms that monitoring parameters of potassium handling is still necessary in β-blocker recipients who also receive diuretics alone or in a fixed-dose combination with potassium.

Increase of Total Body Potassium and Decrease of Exchangeable Sodium after Long-Term Treatment with a β-Receptor-Blocking Agent (Prindolol) in Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 551s-554s
Author(s):  
H. M. Brecht ◽  
E. Werner ◽  
W. Schoeppe
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Term Treatment ◽  
Renin Activity ◽  
Exchangeable Sodium ◽  
Total Body Potassium ◽  
Long Term Treatment ◽  
Total Body

1. The effect of long-term treatment with prindolol on blood pressure, total body potassium (Kt), exchangeable sodium (Nae) and plasma renin activity was investigated in twelve patients with essential hypertension. 2. Systolic and diastolic pressures were significantly reduced from 164/112 to 127/90 mmHg under basal conditions. 3. Before treatment Na. in patients with essential hypertension was significantly higher than in normotensive individuals. After an average of 16 weeks on prindolol Nae in patients with essential hypertension was significantly decreased, despite an average increase in body weight of 2 kg in the patients. 4. In contrast to the decrease in Nae, Kt was found to be significantly increased after long-term treatment with prindolol. Kt values of patients before and after prindolol, however, did not differ significantly from the corresponding sex- and age-dependent normal values. 5. Plasma renin activity was slightly diminished under basal and orthostatic conditions; the stimulatory effect of orthostasis was not abolished but reduced by prindolol. 6. It is suggested that the changes in sodium balance contribute to the anti-hypertensive effect of prindolol in patients with essential hypertension.

Hyperkalemia

1996 ◽  
Vol 17 (3) ◽  
pp. 106-106
Author(s):  
Kenneth B. Roberts
Keyword(s):  
Interstitial Nephritis ◽  
Serum Potassium ◽  
Heart Muscle ◽  
Potassium Concentration ◽  
Chronic Glomerulonephritis ◽  
Total Body Potassium ◽  
Common Cause ◽  
Serum Potassium Concentration ◽  
Life Threatening ◽  
Total Body

Potassium is the major intracellular cation; only a very small fraction of total body potassium is in the intravascular space. Increased potassium concentration in serum is infrequent in pediatrics, but it can be life-threatening because of its effect on membrane potentials, particularly of heart muscle. The serum potassium concentration is affected primarily by the kidney. Potassium is filtered by the glomerulus, then reabsorbed and secreted by the tubule. Processes that interfere with filtration or secretion (eg, acute on chronic glomerulonephritis, interstitial nephritis) may cause hyperkalemia; processes that interfere with reabsorption may cause hypokalemia. The most common cause of an increased serum potassium is "pseudohyperkalemia" due to hemolysis or to tissue hypoxia distal to the placement of a tourniquet.

scholarly journals Total Body Potassium in Long-Term Frusemide Therapy: Is Potassium Supplementation Necessary?

BMJ ◽  
1974 ◽  
Vol 4 (5940) ◽  
pp. 316-319 ◽  
Author(s):  
H. J. Dargie ◽  
K. Boddy ◽  
A. C. Kennedy ◽  
P. C. King ◽  
P. R. Read ◽  
...  
Keyword(s):  
Total Body Potassium ◽  
Potassium Supplementation ◽  
Total Body

Effects of Chlorthalidone on Serum and Total Body Potassium in Hypertensive Patients

2009 ◽  
Vol 200 (1-6) ◽  
pp. 37-45 ◽  
Author(s):  
M. P. Leemhuis ◽  
K. J. Damme ◽  
A. Struyvenberg
Keyword(s):  
Total Body Potassium ◽  
Hypertensive Patients ◽  
Total Body

Total body potassium and serum potassium among eating disorder patients

1995 ◽  
Vol 18 (3) ◽  
pp. 269-276 ◽  
Author(s):  
Pauline S. Powers ◽  
Ian B. Tyson ◽  
Beth A. Stevens ◽  
Albert V. Heal
Keyword(s):  
Eating Disorder ◽  
Serum Potassium ◽  
Total Body Potassium ◽  
Total Body

Relation of Arterial Pressure with Body Sodium, Body Potassium and Plasma Potassium in Essential Hypertension

1982 ◽  
Vol 63 (3) ◽  
pp. 257-270 ◽  
Author(s):  
C. Beretta-Piccoli ◽  
D. L. Davies ◽  
K. Boddy ◽  
J. J. Brown ◽  
A. M. M. Cumming ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Arterial Pressure ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Total Body Potassium ◽  
Hypertensive Patients ◽  
Body Sodium ◽  
Low Renin Hypertension ◽  
Total Body

1. Exchangeable sodium (NaE), plasma electrolytes and arterial pressure were measured in 121 normal subjects and 91 patients with untreated essential hypertension (diastolic >100 mmHg), 21 of whom had low-renin hypertension. Plasma concentrations of renin, angiotensin II and aldosterone were measured in all hypertensive patients, total body sodium, total body potassium and exchangeable potassium (KE) in some patients. 2. Mean NaE was not different in normal and hypertensive subjects provided the two groups were matched for leanness index. In the subgroup of young hypertensive patients aged 35 years or less mean NaE was below normal. NaE was not related to arterial pressure in normal subjects but in hypertensive patients there were positive and significant correlations of arterial pressure with NaE and with total body sodium. 3. NaE and total body sodium increased with age in hypertensive but not in normal subjects. Partial regression analysis suggested that the correlation of NaE with arterial pressure was not explained by an influence of age. 4. Mean NaE was not increased and mean KE was not decreased in patients with low-renin hypertension. 5. Plasma potassium concentration, KE and total body potassium correlated inversely and significantly with blood pressure in hypertensive patients. These correlations were more marked in young than in old patients. 6. Multiple regression analysis showed that the combination of NaE and plasma potassium concentration ‘explained’ more of the variation of systolic blood pressure in hypertensive patients than it did in normal subjects. Plasma potassium concentration ‘explained’ more of the variation in young hypertensives and NaE ‘explained’ more in older patients. 7. Our findings suggest that changes of plasma and body potassium are important in the earlier stages of essential hypertension and that changes of body sodium become important later.

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