Potassium Chloride Supplementation Research Articles

Effects of chlorthalidone on serum and total body potassium in hypertensive patients.

Total body potassium has been estimated in 26 hypertensive patients who were hypokalaemic as a result of long-term chlorthalidone treatment (mean 20.5 months), while they were on chlorthalidone and 4 weeks after this had been discontinued. The mean difference amounted to only 95 mEq (not significant). In 6 additional patients not previously treated with chlorthalidone, serial total body potassium estimations revealed a mean potassium deficiency of 245 mEq after 33 days and of 106 mEq after 100 days. These results suggest that the mechanism causing the initial potassium loss is partly reversed or compensated later on. In patients with uncomplicated hypertension, no significant potassium deficiency was detected during long-term treatment. Eighteen of our patients received 39 mEq potassium chloride supplements daily for 4 weeks; this caused a mean rise in serum potassium from 3.23 mEq/l to 3.38 mEq/l (not significant). Total body potassium did not change at all. We conclude that potassium chloride supplements are not an effective treatment of hypokalaemia in this condition. Correction of the extracellular pH by ammonium chloride in 6 patients on chlorthalidone, who demonstrated a slight metabolic alkalosis, gave rise to a mean increase in plasma potassium from 2.78 mEq/l to 2.96 mEq/l (not significant). The hypokalaemia in hypertensive patients on long-term chlorthalidone treatment cannot be explained by either a potassium deficiency or the change in extracellular pH.

Hypomagnesemia as a Cause Of Persistent Hypokalemia

<h3>To the Editor.—</h3> We wish to call to the attention of your readers the documented but little-appreciated importance of hypomagnesemia as a cause of persistent hypokalemia. <h3>Report of a Case.—</h3> A 40-year-old healthy woman was admitted to our burn and trauma unit after sustaining 65% total body burns. She was treated in the conventional manner but progressive dehydration and hypokalemia developed during four weeks of hospitalization. A medical consultation was requested when her serum electrolyte values were as follows: Na+, 180 mEq/liter; K+, 2.0 mEq/liter; Cl-, 128 mEq/liter; and CO₂, 26 mEq/liter. A diagnosis of secondary hyperaldosteronism was made and intravenous fluids were increased to obtain a positive free water balance. During the next four days, serum Na+ value gradually fell to 147 mEq/liter, but serum K+ remained at 2.0 mEq/liter in spite of massive supplementation of potassium chloride (25 to 40 mEq/hr intravenously). Urinary K+ values demonstrated that

Clinical Evaluation of a New Sugar‐Coated Potassium Chloride Supplement

The Journal of Clinical PharmacologyVolume 14, Issue 11 p. 624-629 Clinical Evaluation of a New Sugar-Coated Potassium Chloride Supplement JAMES C. HUTCHISON M.D., Corresponding Author JAMES C. HUTCHISON M.D. Abington, Penn. Dr. Hutchison is Director, Hypertension Research, Abington Memorial Hospital, Abington, Penn.1930 Keith Road, Abington, Penn. 19001.Search for more papers by this author JAMES C. HUTCHISON M.D., Corresponding Author JAMES C. HUTCHISON M.D. Abington, Penn. Dr. Hutchison is Director, Hypertension Research, Abington Memorial Hospital, Abington, Penn.1930 Keith Road, Abington, Penn. 19001.Search for more papers by this author First published: November‐December 1974 https://doi.org/10.1002/j.1552-4604.1974.tb01383.xCitations: 3 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume14, Issue11November‐December 1974Pages 624-629 RelatedInformation

Congenital nephropathy and chronic diarrhoea with hypokalemic alkalosis.

Long-term observation and laboratory investigations of a female infant with chronic diarrhoea, hypokalemia, alkalosis and hypochloremia are presented. Diarrhoea with hypokalemic alkalosis persisted despite large-scale potassium chloride supplementation. An intravenous pyelogram showed duplication of the right pelvis and fetal lobate kidneys. She was normotensive. Plasma renin activity was increased. A permanent loss of electrolytes through urinary and digestive tracts was observed. Renal biopsy revealed the presence of fetal-like glomeruli, hyperplasia of juxtaglomerular apparatus and thickening of arterial walls. Hypertrophy and hyperplasia of the zona glomerulosa of adrenal cortex were present. It is supposed that a case presenting with co-existence of electrolytes disturbances on digestive and urinary tracts stands between congenital chloride diarrhoea and Bartter's syndrome, being an unknown kind of congenital hypokalemia.

Premenstrual tension: Symptoms and weight changes related to potassium therapy

With the use of patients with and without evidence of premenstrual tension, a study was done in which comparison of weight changes and symptoms were evaluated during control menstrual cycles, menstrual cycles when a placebo (glucose) was taken, and menstrual cycles when a diuretic (potassium chloride) was taken. It was found that the clinician can make a verifiable diagnosis of premenstrual tension. While the symptoms of this entity could not be correlated with premenstrual weight gain, they could be with lability of weight during the 5 days preceding menses. In fact, in all of the cycles (control, placebo, and diuretic-treated), there was found to be a highly significant gain in weight in the 5 days premenses. The use of oral potassium chloride supplements in gelatine capsules had no effect on symptoms reported by patients with premenstrual tension.

Treatment of arterial hypertensive disease with diuretics. I. Effects on blood pressure of bendroflumethiazide, potassium chloride, and spironolactone.

Pilot studies with bendroflumethiazide, a recently introduced benzothiadiazine diuretic, 1,2 suggested superior antihypertensive qualities. Long-term effects on outpatients were studied and compared to placebo, reserpine, and other benzothiadiazine derivatives. Our observations suggested that bendroflumethiazide, given singly, often proved unusually effective. We postulated a separate group of sensitive patients and a therapy-induced bimodal redistribution of blood pressure was sought. Blood pressure responsiveness was also statistically related to various other clinical parameters including dietary sodium intake. The depressor effect of low-potassium diets, 3 the stimulation of aldosterone by potassium, 4,5 and the results of animal experiments 6,7 made it pertinent to test the blood pressure influence of potassium chloride supplementation. Overproduction of aldosterone, whatever its cause, might contribute to the refractoriness of high blood pressure to diuretic therapy. This prompted a trial of combination therapy of bendroflumethiazide with spironolactone in 17 patients with severe hypertension, inadequately controlled by bendroflumethiazide therapy alone.

Antiphlogistic property of desoxycorticosterone after partial hepatectomy, adrenalectomy, force-feeding and KC1 ingestion in the rat.

Desoxycorticosterone (DOC) has been shown to be antiphlogistic in tho rat after both local and systemic administration. When given systeniically, it is, in addition, thymolytic and catabolic. It was found that these new properties of DOC are greatly augmented after removal of 70% of the liver. The efficient inactivation of the steroid by the liver may explain why high doses must be given in intact animals. The present investigations also indicate that the antiphlogistic and catabolic properties of DOC are specific and not due to stress reaction consequent to metabolic disturbances of the hormone. Actually, the effect observed was not modified by adrenalectomy, force-feeding or potassium chloride supplements. The difference in activity between DOC and cortisol appears to be mainly in degree, the former being much weaker.

Observations on a case of primary aldosteronism

Another case of primary aldosteronism is recorded. This patient differs from others reported in that there was no chemical evidence of extracellular alkalosis and the excretion of mineralocorticoids in the urine was normal or only slightly elevated. The biological decay time of radioactive sodium was forty days before surgery and ten days after removal of the adenoma, both tests being performed with high sodium ingestion. High intake of extra sodium chloride produced edema and headaches. Headache is considered to be a presenting complaint in these patients along with hypertension, spells of muscle weakness, polydipsia and polyuria. The symptoms and the hypertension and electrolyte disturbances were relieved by removal of a benign adrenal cortical adenoma. It is suggested that a patient with primary aldosteronism should be given adrenocorticotropin and supplemental potassium chloride for about three to five days preoperatively to remove some of the extra sodium and to correct some of the potassium deficit.