Low Urinary Potassium Research Articles

Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis

Hypokalemia and hypophosphatemia are commonly encountered during paralysis in patients with thyrotoxic periodic paralysis (TPP) and may contribute to neuromuscular manifestations. Potassium and phosphate supplements have been recommended to hasten recovery and prevent cardiopulmonary complications. However, this recommendation has not yet proven efficacious. Hyperadrenergic activity has been implicated in the pathogenesis of TPP. We tested whether nonselective β-blockers could terminate neuromuscular symptoms rapidly while reducing an intracellular shift of potassium and phosphate. We describe two patients who had an acute attack of TPP with characteristic hypokalemia and hypophosphatemia associated with low urinary potassium and phosphate excretion. After oral propranolol, 3 mg/kg, serum potassium and phosphate concentrations increased promptly in 2 hours in both patients, and there was complete amelioration of paralysis. No rebound hyperkalemia or hyperphosphatemia was detected. Given their efficacy in this pilot study, they should be considered as a first-line therapy for TPP.

Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxic periodic paralysis

Hypokalemia and hypophosphatemia are commonly encountered during paralysis in patients with thyrotoxic periodic paralysis (TPP) and may contribute to neuromuscular manifestations. Potassium and phosphate supplements have been recommended to hasten recovery and prevent cardiopulmonary complications. However, this recommendation has not yet proven efficacious. Hyperadrenergic activity has been implicated in the pathogenesis of TPP. We tested whether nonselective β-blockers could terminate neuromuscular symptoms rapidly while reducing an intracellular shift of potassium and phosphate. We describe two patients who had an acute attack of TPP with characteristic hypokalemia and hypophosphatemia associated with low urinary potassium and phosphate excretion. After oral propranolol, 3 mg/kg, serum potassium and phosphate concentrations increased promptly in 2 hours in both patients, and there was complete amelioration of paralysis. No rebound hyperkalemia or hyperphosphatemia was detected. Given their efficacy in this pilot study, they should be considered as a first-line therapy for TPP.

Sodium chloride deficiency in cystic fibrosis patients.

Sodium chloride deficiency (SCD) was observed within the 1st year of life in 12 of 46 cystic fibrosis (CF) patients between July 1989 and September 1992. All patients showed sweating, loss of appetite, fever, vomiting, irritation, dehydration, weakness, and cyanosis during an attack. Mean plasma sodium, potassium and chloride levels were 122.9 (range 106-135), 2.5 (range 1.6-3.5), and 73.3 (range 60-90) mEq/l respectively. Alkalosis and elevated plasma renin activity were detected in all patients. Of the patients, 50% showed microscopic haematuria, and hypercalciuria was detected in two out of four patients. Low urinary sodium and high urinary potassium were observed in the four examined patients. Increased creatinine, BUN and uric acid values returned to normal with treatment. All the patients were treated initially with intravenous fluids and electrolyte solutions. All patients were less than 7 months of age during the first attack, five received only breast milk and the others breast milk with formula milk. Their oral salt supplement was 2-4 mEq/kg per day, which is recommended for CF patients, but could be deficient in excessively sweating infants. The genotype of these patients might be cause of high salt losses. F508 is the most common mutation with the frequency of 38% in our CF patients with SCD, but the frequency of unknown mutations is high (54%).

Laxative Abuse as a Cause for Ammonium Urate Renal Calculi

Nine women with laxative abuse and predominantly ammonium urate renal calculi underwent metabolic studies to identify common chemical abnormalities and determine pathophysiology. The 24-hour urine studies demonstrated marked decreases in volume (902cm.3), sodium (28 mEq.), citrate (116mg.) and potassium (21 mEq.). A significant elevation in ammonium urate supersaturation was found compared to control subjects when studied by the computer model EQUIL 2. Of the patients 7 had 1 or more urine specimens positive for phenolphthalein. Gastrointestinal loss of fluid and electrolytes allowed for chronic extracellular volume depletion. Intracellular acidosis was present as judged by low urinary citrate and potassium. The fact that the ion product for ammonium urate is increased significantly compared to controls reflects the stated pathophysiological changes. Laxative abuse should be suspected whenever a woman has an ammonium urate renal calculus in sterile urine. (J. Urol., 143: 244–247, 1990).

Suppression of adrenal mineralocorticoid production in prehypertensive young adult men.

We assessed the renin-aldosterone axis in response to treadmill exercise and adrenal steroidogenesis after graded ACTH infusions in two groups, each composed of nine young adult men from Bourbon County, Kentucky, from the upper and lower deciles of the blood pressure distribution. Those from the upper decile with relatively higher blood pressures, termed prehypertensive, had significantly lower plasma aldosterone and 18-hydroxycorticosterone concentrations after graded ACTH than those with relatively lower pressures, and had significantly lower urinary potassium excretions. Renin and aldosterone responses to exercise were also significantly blunted in the prehypertensive subjects. No differences were found in plasma cortisol, deoxycortisol, deoxycorticosterone, corticosterone, or dehydroepiandrosterone sulfate, although dehydroepiandrosterone was higher at one infusion rate in prehypertensives. These findings suggest that the adrenal mineralocorticoid pathway and the renin-aldosterone axis are suppressed in prehypertensive young males perhaps as an appropriate feedback response to their higher blood pressures.

Dietary effects on blood pressure.

Low density potassium intake, particularly among black hypertensive patients, appears to contribute significantly to this disease and its major sequellae. The high sodium intake of industrialized societies and the epidemic prevalence of hypertension must be considered in the light of a relatively greater urinary potassium excretion as compared to a low-sodium diet with a lower urinary potassium excretion. There is no reason to assume that weight reduction per se is the major contributor to lowering of elevated blood pressure levels although claims to this effect have been made. In general, a high-caloric diet is loaded with sodium while a low-energy diet has a drastically reduced sodium content. The hypothesis that a higher dietary linoleic acid intake via increased prostaglandin synthesis may lead to natriuresis and a drop in blood pressure levels is an interesting development which needs more testing.

Hyperkalemia, hypertension and systemic acidosis without renal failure associated with a tubular defect in potassium excretion

A twenty-one year old man is described who has what appears to be a unique renal tubular defect in potassium excretion, associated with persistent hyperkalemia (up to 8.2 mEq. per L.), hypertension, systemic acidosis and slightly impaired renal excretion of acid. Renal failure was absent; glomerular filtration rate, maximal tubular secretion of p-aminohippurate, maximal urinary concentrating ability and urinary amino acid excretion pattern were all normal, as was the appearance of renal tissue at biopsy. Clearance of p-aminohippurate and phenolsulfonphthalein excretion were somewhat reduced. A balance study showed a positive potassium balance of 142 mEq. in four days, associated with low urinary potassium excretion and rising serum potassium levels; sodium balance was normal. Red cell electrolyte content was normal, as were salivary and sweat potassium concentrations. Sodium sulfate infusion combined with a carbonic anhydrase inhibitor, which markedly increased potassium excretion in control subjects, had little effect on the patient's potassium excretion, except when accentuated by prior salt depletion and 9α-fluorohydrocortisone administration. Adrenal insufficiency was excluded as a cause for hyperkalemia and there was no evidence of impaired tubular response to mineralocorticoids, since sodium metabolism was normal. The hypertension, associated with blood pressures up to 140 mm. Hg diastolic, responded well to treatment with sodium polystyrene sulfonate (Resonium ® A) and chlorothiazide, which also controlled the hyperkalemia. Diastolic blood pressures correlated significantly with serum potassium levels. Endocrine causes for hypertension were excluded. Presser responses to cold, smoking, norepinephrine and angiotensin were in the range reported in patients with hypertension of other causes. Chromosome studies were normal, but absent incisor teeth in the patient and in his brother, and a family history of mental illness raised the possibility of a genetic basis for his metabolic disorder.