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Results for “Potassium Deficiency”

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PubMed1986

Guidelines for rational diuretic use in the elderly.

The elderly not only have lower body stores of potassium, but also tend to eat a diet relatively low in potassium content. Loss of muscle strength, constipation and mental apathy are all features of potassium deficiency. In addition, serious arrhythmias have been attributed to hypokalaemia and must therefore be prevented. While potassium supplements may replete body potassium stores, they often require large amounts and may still be ineffective in preventing diuretic-induced hypokalaemia. Thus, several guidelines for the rational and safe use of diuretics in the elderly have been proposed including in addition to potassium supplementation, the determination of dietary and total body potassium sources, dosage of the diuretic and intensity of the diuresis, and the relationship between potassium and calcium and magnesium.

Aged↗

PubMed1983

Role of the medullary collecting duct in potassium conservation.

A capacity for both net potassium absorption and net potassium secretion has been demonstrated in the inner medullary collecting duct. The quantitative importance, however, of the inner medullary collecting duct in the regulation of urinary potassium in potassium deficiency, however has not been established. To assess the contribution of this segment to potassium conservation, microcatherization studies were performed in male Sprague-Dawley rats maintained either on a control diet or on a potassium free diet for 72 h. In control animals approximately 15% of the filtered load of potassium was excreted. Analysis of tubule fluid along the inner medullary collecting duct failed to demonstrate evidence of net potassium movement. Administration of a potassium free diet resulted in a marked reduction in potassium excretion to 0.3% of the filtered load. In contrast to control the inner medullary collecting duct of experimental animals absorbed nearly 90% of the amount of potassium entering this segment, since fractional delivery to the terminal portion of the nephron was about 2%. These data indicate that the inner medullary collecting duct makes a significant contribution to maximal renal conservation of potassium, since previous studies have shown that only 5 to 10% of filtered potassium is present in the late distal tubule of surface nephrons in animals on a low potassium intake.

Animals↗

PubMed1984

Intra-/extracellular shifts of potassium after the administration of Mg in patients with cardiovascular diseases.

Body potassium status is often dosed on serum potassium determinations. However, this parameter is not an adequate guide to the body potassium status, unless several factors are taken into consideration, e.g. acid-base balance and serum creatinine level. Muscle magnesium content is another factor, probably operative through its activation of Na-K-ATPase, which produces the energy necessary for the active transport of potassium into the cell. Magnesium has a membrane-stabilizing effect as well, diminishing the outward movement of potassium from the cell. In case of magnesium deficiency, potassium cannot be transported into the cell in sufficient amounts and the result is an imbalance between the intra- and the extracellular potassium concentration, which in turn may lead to cardiac dysrhythmias.

Cardiovascular Diseases↗

PubMed1976

The role of potassium in the control of ammonium excretion during starvation.

Administration of KC1 0.5 mmol/kg/day to subjects undergoin prolonged starvation reduced daily urinary ammonium and beta-hydroxybutyrate excretion by one-third. These changes were accompanied by an improvement in potassium balance and an increased rate of chloride excretion. A similar fall in ammonium excretion occurred in a second group of subjects after administration of KHCO3 0.5 mmol/kg/day. Ketone body and bicarbonate excretion remained unchanged in this group while potassium balance improved. In both the first and second groups urine pH fell significantly as the rate of excretion of urinary buffer (ammonium) decreased. When the dose of KHCO3 was increased to 1.5-2.0 mmol/kg/day in fasting subjects, the urine was alkalinized, and ammonium excretion fell to negligible levels, resulting in nitrogen sparing of 2.0 g/day. The results indicate that one-half of the increase in ammonium excretion observed in starvation is due to potassium deficiency. Nitrogen wastage caused by losses of urinary ammonium during starvation can be virtually eliminated by potassium supplementation and urinary alkalinization. The decrease in beta-hydroxybutyrate excretion after potassium chloride administration was not caused by a fall in the rate of nonionic diffusion of this organic acid related to the reduction in urine pH. The reason for the fall in beta-hydroxybutyrate excretion is not apparent, though it was associated with an increase in chloride excretion.

Acid-Base Equilibrium↗

PubMed1987

Effect of acute potassium depletion and thiazide treatment on blood glucose in the normal rat.

The effect of potassium depletion and a thiazide diuretic on glucose metabolism was investigated in male rats. Potassium depletion was induced by potassium-deficient diet and ion-exchange resin by stomach tube for 5 days. Plasma and muscle potassium was reduced by 30% (P less than 0.001), and fasting blood glucose concentration was elevated by 20% (P greater than 0.025) by potassium depletion. Hydroflumethiazide 10 mg/kg given orally once daily for 8 days produced no further alteration in any parameter. We conclude that acute potassium depletion in the rat may increase fasting blood glucose concentration, whereas addition of short-term thiazide treatment does not seem to potentiate this effect.

Animals↗

PubMed1992

[Apropos of a rare cause of torsades de pointe: hypokalemia caused by dietary deficiency].

The authors report a case of wave burst arrhythmia in a young immigrant woman of Laotian origin aged 32. The main cause of the arrhythmia was related to potassium deficiency of dietary origin. Some contributory factors may have had a promoting effect: theophylline treatment, beta-mimetics and adrenaline (epinephrine). This case can therefore be related to the cases of wave burst arrhythmia and hypokalemia previously reported in anorexic subjects. This case suggests that special attention should be paid to the diet of some ethnic groups who have been displaced by economic causes. Their very unusual dietary habits may induce or aggravate hypokalemia, which may also be promoted in some cases by drugs. Some treatments should therefore be introduced with caution in this context due to the potential risk of inducing severe arrhythmia.

Adult↗

PubMed1982

Periodic paralysis and the sodium-potassium pump.

Analysis of the pathophysiology of hypokalemic paralysis, as it occurs in barium poisoning, chronic potassium deficiency, and thyrotoxicosis, suggests that these disorders may have a similar mechanism. An increased ratio of muscle sodium permeability to potassium permeability reduces the ionic diffusion potential, while the resting membrane potential is sustained by an increase of Na-K pump electrogenesis. The result is that potassium entry (the sum of active and passive influx) exceeds potassium efflux; this causes a large shift of extracellular potassium into muscle until the Na-K pump turns off, leading to depolarization and paralysis. The primary defect in familial hypokalemic periodic paralysis, as in the example of barium poisoning, may be a marked reduction of muscle permeability to potassium.

Animals↗

PubMed1983

Variation in the potassium needs of chickens selected genetically for variation in blood uric acid concentrations.

Two strains of sex-linked dwarf chickens that have been selected genetically for divergence in plasma uric acid concentrations were found to differ in their requirements for potassium. The rates of growth of chicks from both strains were similar when nutritionally adequate levels of potassium were provided. However, the growth of chicks having normal plasma uric acid concentrations was significantly poorer than that of hyperuricemic chicks when the chicks received potassium-deficient diets, and the retention of dietary potassium was less in the former group. There were no consistent strain differences in response to sodium deficiency. Because the two strains previously were found to differ in the renal tubular transport of uric acid, the strain difference in potassium requirement may reflect an association of potassium with uric acid excretion.

Animals↗

PubMed1984

[Changes in total body potassium and ion distribution compartments in general surgery and intensive care patients].

Measurements of total body potassium in a whole body counter revealed significant total body potassium depletion in patients suffering from high output enteric fistulas, short bowel syndrome and Crohn's disease. The clinical importance of this finding is derived from the fact that the degree of potassium depletion was found to be related to mortality, and that the introduction of an infusional regimen for preparation for surgery in Crohn's disease which effected intracellular potassium refilling resulted in a decreased surgical mortality and complication rate. In conclusion specific nutritional support as an essential measure in preparing such patients for elective surgery is particularly recommended. Significant cellular potassium depletion was also found in critically ill patients dying from sepsis. In contrast to the aforementioned diseases with malnutrition, where an increased fecal loss of potassium is the most likely cause of potassium deficiency, a different mechanism for cellular potassium loss is suggested in this condition from additional indicator dilution studies. Rather here the finding of increased distribution volumes for ions physiologically predominantly restricted to the extracellular space (82Br and 24Na) indicates a change of cell membran permeability suggestive of so called sick cell syndrome.

Adult↗

PubMed1975

A correlated study of kidney function and ultrastructure in potassium-depleted rats.

In order to provide an ultrastructural description of kaliopenic nephropathy in rats, potassium deficiency uncomplicated by chloride depletion or extracellular fluid volume expansion was induced by dietary means alone. After 12 days, serum and muscle analyses demonstrated severe potassium depletion, while urine concentrating ability was markedly impaired. Although micropuncture techniques demonstrated that net fluid transport in proximal tubules was normal, the epithelial cells showed the following morphological alterations: electron-lucent vacuoles and lysosome-like dense bodies were numerous, focal cytoplasmic degradation was present, and intercellular spaces were dilated in many proximal tubules. Medullary cell droplets were characterized by fusion, massive enlargement with sequestration of cytoplasmic components such as ribosomes, and occasional extrusion through ruptured plasma membranes--features not previously reported.

Animals↗

PubMed2005

[Aldosterone and magnesium].

Magnesium ion (Mg) directly inhibits aldosterone production in rat adrenal glomerulosa cells, while potassium ion directly stimulates aldosterone production. It is reported that Mg shows antihypertensive effect in patients with essential hypertension. Secondary hyperaldosteronism induced by diuretic treatment in patients with congestive heart failure accelerates potassium and magnesium ions' excretion in urine. Diuretic-induced falls in potassium and magnesium ions and aldosterone-induced cardiac fibrosis and remodelling are associated with fatal ventricular arrhythmia. Aldosterone antagonists, such as spironolactone and eplerenone, correct not only potassium deficiency but also magnesium deficiency induced by diuretics. Mg supplementation also may be useful procedure to correct potassium and magnesium deficiency, because Mg itself inhibits aldosterone release from the adrenal glands.

Aldosterone↗

PubMed1990

Potassium raises cytochrome P-45011 beta mRNA level in zona glomerulosa of rat adrenals.

During potassium repletion of potassium-deficient rats, a marked rise in the adrenal zona glomerulosa content of cytochrome P-45011 beta mRNA preceded an extensive increase in corticosterone methyl oxidation (CMO) 1 and 2. Potassium intake did not substantially affect zona glomerulosa cytochrome P-450SCC or zona fasciculata-reticularis cytochrome P-45011 beta mRNA levels. We had previously shown that the induction of CMO 1 and 2 in the zona glomerulosa of potassium-repleted rats was associated with the appearance of a second form of cytochrome P-45011 beta with a lower molecular weight (49,000) than the major form of the enzyme (51,000). On the basis of the present observations, mRNAs encoding the two forms of the enzyme would be homologous and of similar length. Potassium intake thus controls the biosynthesis of the 49 kDa enzyme most likely at the level of transcription or, alternatively, by influencing mRNA stability.

Animals↗

PubMed1984

Copper response to rheumatoid arthritis.

Rheumatoid arthritis can be divided into two syndromes, one a potassium deficiency, the other an inappropriate copper requirement seriously affecting the elastin tissues through reduced lysyl oxidase cross linking. The malfunction in copper may arise from the steroids which regulate potassium, which reduces those steroids, and through that, increases the copper response to the needs of the immune system. It is a mechanism which may have evolved to help fight potassium wasting infections.

Animals↗

PubMed1977

Formation of renal medullary lysosomes during potassium depletion nephropathy.

The biochemical correlates of droplet formation in renal inner medullary cells of potassium-deficient rats were studied. An increase in the activities of five hydrolytic enzymes typical of lysosomes was associated with an increase in the number and size of droplets observed during progressive potassium depletion. Acid phosphatase activity increased 7-fold whereas beta-glucuronidase, beta-galactosidase, cathepsin, and acid DNase increased 2- to 4-fold in medullary homogenates at 25 days of depletion. Following potassium repletion the activities returned to normal at a rate dependent upon the duration of potassium depletion. The decreases in enzyme activities were associated with a concomitant rapid disappearance of the droplets from medullary cells. Protein synthesis for new droplet enzyme formation was studied by measuring the rate of [14C]leucine incorporation into protein in medullary slices. The rate increased at 1 day of depletion and reached a maximum which was 139 per cent higher than control after 7 days of depletion. In droplets isolated from medullary tissue during progressive potassium depletion the rate of protein labeling with [14C]leucine and acid phosphatase specific activity increased in parallel. When droplet proteins were separated by gel electrophoresis, acid phosphatase activity was detected in a protein band which had been labeled with [14C]leucine, thereby suggesting new enzyme protein formation. The increase in enzyme and protein synthesis and a previously demonstrated increase in phospholipid synthesis and membrane formation indicate that potassium depletion induces specific alterations in renal inner medullary cell metabolism which result in increased lysosome formation.

Acid Phosphatase↗

PubMed1993

Renal vascular induction of TGF-beta 2 and renin by potassium depletion.

Recently, we have found that transforming growth factor (TGF)-beta 2 and renin are abundantly expressed in the juxtaglomerular apparatus (JGA) of dehydrated mice. Since potassium (K+) depletion also stimulates renin and induces hypertrophy of the JGA, we examined the ability of this maneuver to stimulate TGF-beta isoforms and renin in renovascular tissue and the JGA of young rats. Sprague-Dawley rats (50 +/- 5 g) were fed either a control diet or a potassium-deficient diet (< 0.05% K+) for 7, 16, or 21 days. As a control for TGF-beta and renin stimulation, an additional group of animals was fed a normal diet but was water deprived for three days. Potassium-depleted animals experienced severe growth retardation but kidney weight increased significantly. Potassium depletion induced both TGF-beta 2 and renin immunoreactivity in renal arterioles and the JGA but had no effect on TGF-beta 1 and TGF-beta 3 isoforms. To determine the role of circulating angiotensin II in the stimulation of TGF-beta 2 by potassium depletion, a group of potassium-depleted rats received enalapril (100 mg/liter) in the drinking water. The addition of converting enzyme inhibitor increased both the intensity of TGF-beta 2 and renin staining as well as the number of cells positively stained. Our results demonstrate that K+ depletion induces TGF-beta 2 and renin in renal arterioles and in the JGA. Furthermore, circulating angiotensin II is not responsible for the increase in the local expression of TGF-beta 2. These findings suggest that TGF-beta 2 may be an important mediator of JGA hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Kwashiorkor revisited: the pathogenesis of oedema in kwashiorkor and its significance.

Cicely Williams, in her original description of kwashiorkor, implied that deficiency of protein in the baby's food could be a main cause of the syndrome. The hallmark of kwashiorkor is oedema. According to the 'classical' theory, an inadequate intake of protein leads to a low plasma albumin concentration, which in turn causes oedema. This theory has been contested from several points of view: that hypoalbuminaemia is not the major factor determining the presence of oedema, and that there is no real evidence of dietary protein deficiency. The resolution of this question is of some importance from the point of view of public health diagnosis and prevention. A crucial point in the argument is the pathogenesis of oedema, which is discussed in some detail. Although it is clearly multifactorial, with electrolyte disturbances--potassium deficiency and sodium retention--playing an important role, it is contended that the classical theory is essentially correct. On the dietary side, recent experimental work supports the earlier view that the development of oedema depends on a relative deficiency of protein with a relative excess of energy. Comparisons of intakes with requirements are unconvincing in view of uncertainty about the validity of the estimates of children's needs for protein.

Adult↗

PubMed1972

Pathophysiology of intense physical conditioning in a hot climate. I. Mechanisms of potassium depletion.

Serial estimations of exchangeable (42)K showed that six volunteer subjects undergoing intensive physical conditioning in a hot climate sustained a mean deficit of 517 mEq. This deficit occurred despite a daily potassium intake of 100 mEq. Simultaneous values for lean body mass rose suggesting that potassium deficiency was not the result of catabolism. Although sweating was the major avenue by which the deficit occurred, daily excretion of potassium into the urine when each subject was maximally deficient ranged from 46 to 75 mEq and thus was inappropriately high for potassium-depleted subjects. Despite high intakes of sodium and excretion of corresponding quantities into the urine, Na/K ratios in sweat were low thus indicating unsuppressed activity of aldosterone on sweat glands. Moreover, excretion and secretion of aldosterone and in many instances, plasma renin activity, appeared to be high with respect to sodium intake. These findings suggest that intense physical work in the heat stimulates higher production of aldosterone than would occur in nonexercising subjects on similar sodium intakes. Similar to the phenomenon of mineralocorticoid escape, such overproduction of aldosterone in the presence of conditions permitting excretion of sodium into the urine could facilitate continued excretion of potassium by the kidney despite serious potassium depletion. As a consequence, the kidney played a role in the genesis of potassium depletion in these subjects. In contrast to subjects undergoing conditioning in the summer months, potassium depletion did not occur in 16 subjects during identical training under cooler environmental conditions.

Acclimatization↗

PubMed1979

Measurement of total-body 40potassium in patients with urate calculi.

Fifty-eight patients with urate calculi and 31 patients with other (non-urate) calculi were examined for total-body potassium by means of a total-body counter. The patients with urate calculosis were found to differ significantly in their total-body K from patients with other calculi as well as from normal subjects. The results indicate that total-body potassium deficiency is one of the factors causing urate calculosis.

Body Composition↗