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PubMed1991

Blood and urinary aggregator and inhibitor composition in controls and renal-stone patients from northeastern Thailand.

Renal-stone disease (RSD) is common in the rural communities of northeastern Thailand. We report the biochemical composition of blood and urine in 25 healthy city dwellers (G1), 12 healthy village dwellers (G2) and 25 village dwellers who had RSD (G3). They were male with a range of ages between 20 and 50 years and were free of renal failure, urinary infection, urinary obstruction and systemic illness. The results showed that hypocitraturia, hypokalemia and hypokaliuria were more common in the latter 2 groups. The 24-h urinary citrate excretion correlated significantly with urinary potassium in G3 cases (r = 0.704, p = 0.0002). After potassium chloride supplementation, serum and urinary potassium increased remarkably (p less than 0.003 and p = 0.002, respectively), whereas urinary citrate remained unchanged. Our results suggest that the predominant abnormality in our RSD patients were hypocitraturia and potassium deficiency and that these may be related.

Adult↗

PubMedDate not supplied

[Activation of specific membrane mechanisms in the myocardium cells on early stages of ischemia].

Electron probe microanalysis was employed to determine the elemental concentration (K,Na,Cl) in a myocyte on cryosections of the papillary muscle of the isolated rat (Wistar) heart. Protocols of global ischemia and ischemic conditions under glucose-free anoxic perfusion were applied. It was shown that global ischemia induces potassium deficiency (94 +/- 2 mM) in the myocyte and an increase in the level of sodium (72 +/- 4 mM) and chlorine (42 +/- 1 mM) in the cytoplasm compared with intact cell (122 +/- 2; 36 +/- 1; 24 +/- 1 mM). Glucose-free anoxic perfusion leads to a smooth fall of potassium concentration in the cell up to 54 +/- 2 mM with the retention of intracellular sodium (40 +/- 1 mM) and chlorine (26 +/- 1 mM) level. The present finding suggest that, in early ischemia, specific membrane mechanisms of ion transport are activated. Among these are KNa channel, Hi(+)-Nao+ exchange, KATP channel, lactate transport from the cell, associated either with potassium efflux to the extracellular space or chlorine influx into the myocyte. It is assumed that Na/K-ATPase is also activated under ischemic conditions.

Animals↗

PubMedDate not supplied

Diminished diuretic and natriuretic response to furosemide in potassium-depleted rats.

Renal clearance and tubule microperfusion experiments were carried out to investigate the effects of chronic potassium depletion upon the renal response to furosemide. Rats kept on a potassium-deficient diet for 3 weeks developed hypokalemia, metabolic alkalosis, and decreased aldosterone levels. These rats responded to an oral administration of furosemide (32 mg/kg) with a blunted excretion rate of urine and sodium. Whereas furosemide increased fractional urine sodium excretion to 5.2% in control rats, the corresponding rate in potassium-depleted rats was 2.8%. The urinary excretion of furosemide was also significantly reduced during potassium depletion from 3.06 mg/kg in control rats to 0.97 mg/kg in potassium-depleted rats. In separate experiments, loops of Henle were pump-perfused with furosemide-containing solutions in control and potassium-depleted rats. No major modification of the inhibitory effects of furosemide on sodium transport was observed when the potassium concentration of the perfusion fluid was kept at the low levels expected in hypokalemic rats. Metabolic alkalosis unaccompanied by potassium deprivation did not decrease the diuretic response to furosemide. These experiments indicate that potassium deprivation reduces the diuretic effects of furosemide by mechanisms including diminished furosemide delivery to its tubule site of action.

Animals↗

PubMed1981

Serum potassium concentration in acidemic states.

It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH4Cl-or CaCl2-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias per se, should not be expected to be accompanied by elevations of serum potassium concentration. Moreover, the classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe potassium deficiency, may not be universally valid in patients with uncomplicated organic acidemias.

Acidosis↗

PubMed2006

Hypokalemic paralysis and osteomalacia secondary to renal tubular acidosis in a case with primary Sjögren's syndrome.

A 39-year-old Japanese woman was admitted to our hospital for severe weakness owing to potassium deficiency caused by type 1 renal tubular acidosis (RTA1). Sicca complex, serological tests, and lip biopsy revealed that she had Sjögren's syndrome (SS). Acidosis was corrected by alkali supplement treatment. She also had an impaired renal function with proteinuria, and high absorbance on Ga scintigram was recognized in both kidneys. She was taking warfarin potassium after aortic valve substitution due to aortic regurgitation, therefore renal biopsy was not performed. Prednisone (20 mg/day) was administered for renal inflammation. One month later, she suffered severe chest wall pains with some local tender points over the costae of both sides, which was presumed to be due to pseudo-fractures based on osteomalacia. Hypokalemic paralysis and osteomalacia should be taken into consideration in the diagnosis of SS with RTA1.

Acidosis, Renal Tubular↗

PubMed1982

Effect of low potassium-diet on Na-K-ATPase in rat nephron segments.

Na-K-ATPase activity was determined in 10 segments of the rat nephron using a fluorometric microassay method [4]. The enzyme activity showed three peaks (greater than 200 pmol ADP min-1 mm-1) along the nephron of normal rats. These peaks were in the S1 portion of the proximal tubule, the medullary thick ascending limb from the inner stripe and the distal convoluted tubule. Feeding the rats a low potassium diet for 8 weeks produced a significant decrease in Na-K-ATPase activity in the cortical collecting duct, but no significant change in this enzyme in any other segment. The low potassium diet did not produce a significant change in Mg-ATPase in any nephron segments. We conclude that Na-K-ATPase activity along the rat nephron shows a pattern that is qualitatively similar to that seen in the rabbit nephron [4]. However, quantitatively the Na-K-ATPase activity in the rat nephron is greater than in the corresponding segments of the rabbit nephron. The results are consistent with the greater rate of glomerular filtration and Na+ reabsorption per rat nephron. Furthermore, our results suggest that the decrease in potassium excretion during potassium deficiency is modulated, at least in part, by the level of Na-K-ATPase activity in the cortical collecting duct.

Absorption↗

PubMedDate not supplied

[Seasonal fluctuations in the electrolyte content in diabetes mellitus].

Results of examination of 257 patients suffering from diabetes mellitus demonstrated a reduction of sodium, potassium and magnesium content in their plasma. Erythrocytes also displayed a reduction of potassium and magnesium, and some increase of sodium content. Reduction of electrolyte level in the plasma and erythrocytes was more pronounced in winter; the erythrocyte sodium content was less in summer than in winter. The 24-hour sodium potassium and magnesium excretion is increased, during winter in particular. The efficacy of treatment of diabetic patients with panangin and potassium chloride for the purpose of elimination of magnesium and potassium deficiency was demonstrated. A conclusion was drawn on the expediency of using these drugs in the complex treatment of diabetic patients, particularly in winter.

Adolescent↗

PubMed1980

Body composition in cachexia resulting from malignant and non-malignant diseases.

The body composition of 23 patients with cachexia resulting from malignant or benign inflammatory disease was studied. Skinfold thickness and radioisotope tracer measurements enabled us to estimate total body fat, lean body mass, the ratio of fat loss to lean body loss, erythrocyte and plasma volumes, total body water, extra-, and intracellular water volumes, total body potassium, and intracellular potassium concentration. The total body fat and lean body mass information suggests that the body composition in cancerous cachexia differs from that in cachexia caused by benign inflammatory disease, in that lean tissue appears to be better conserved in the former. The radioactive tracer studies showed that the cachectic patients were anemic, potassium-deficient, and overhydrated; however, fluid partitioning into extra- and intracellular compartments was normal.

Adolescent↗

PubMed1990

Rhabdomyolysis in the hyperosmolal state.

PURPOSE: We undertook this study to determine the occurrence of rhabdomyolysis in the hyperosmolal state. PATIENTS AND METHODS: We reviewed 130 hospital admissions due to diabetic ketoacidosis or hyperosmolal coma, or both. Thirty-one patients (12 men and 19 women) were found to be in the hyperosmolal state. Sixteen of 31 patients showed biochemical evidence of rhabdomyolysis. The clinical and biochemical features of the patients with rhabdomyolysis (Group I) and the patients without rhabdomyolysis (Group II) were compared. RESULTS: Patients in Group I showed a 100-fold increase (7,156 +/- 2,820 IU/L) in serum creatine phosphokinase (CPK) when compared to the patients in Group II (61 +/- 11 IU/L). The mean serum osmolality was much higher (p less than 0.001) in patients with rhabdomyolysis (381 +/- 12 mOsm/kg) than in those without rhabdomyolysis (324 +/- 4 mOsm/kg). The serum sodium level was elevated (p less than 0.001) in Group I patients (151 +/- 4 mEq/L) but not in Group II patients (133 +/- 2 mEq/L). There was a linear association between serum CPK versus serum sodium (r = 0.62, p less than 0.05) and serum CPK versus serum osmolality (r = 0.05, p less than 0.05). The mean serum potassium level was lower (p less than 0.01) in Group I than in Group II. Only two patients (12%) in Group I and almost half the patients (seven of 15) in Group II were hyperkalemic. The mean serum phosphorus level was lower in Group II than in Group I. Four patients in Group I and one patient in Group II developed acute renal failure. CONCLUSION: Subclinical rhabdomyolysis is a common finding in the hyperosmolal state. Absence of hyperkalemia in the presence of muscle injury, hyperosmolality, hyperglycemia, and acidosis suggested pre-existing total-body potassium deficiency in many of these patients. In addition to hypokalemia, the hyperosmolal state predisposes to the development of rhabdomyolysis.

Adult↗

PubMed1993

Sudden infant death syndrome (SIDS): oxygen utilization and energy production.

Reid found selenium (Se) deficient soils were a common factor in two populations with the highest incidence of SIDS world-wide (Indian population of King County Washington State, USA and the population of Canterbury, New Zealand). Reid compared a map of the selenium responsive livestock areas in New Zealand with areas of low soil iodine (I). She found that the 1989 report of areas of the highest SIDS incidence coincided with Se responsive livestock areas combined with low soil iodine. Foster found the 1983-84 incidence of SIDS in USA has the strongest positive correlation with the incidence of goitre in World War I troops (1916). Sodium and strontium were positively related. Emery found a hypernatraemic SIDS victim in a very cold environment. Robertson and Parker associated increased sodium (Na) (used in Scunthorpe, England, as a water softener) with increased incidence of SIDS. Godwin's study of White Muscle Disease in lambs describes Se protection. Skeletal muscle mitochondria from dystrophic animals showed lowered respiratory rates with palmitoyl-dl-carnitine and acetyl-dl-carnitine as substrate. Dystrophic organelles failed to respond to ADP. Rognun found elevated hypoxanthine and an enhanced immune response in most SIDS victims. A syndrome associated with potassium deficiency has been described as a killer of healthy, young Asian men, most often during sleep. This paper describes the interactions of sodium (Na), potassium (K), selenium (Se), and iodine (I) to some factors affecting the utilization of oxygen and the production of energy.

Adenosine Triphosphate↗

PubMed1998

ECG changes during furosemide-induced hypokalemia in the rat.

Electrolyte abnormalities have become an increasingly important cause of arrhythmias owing to the widespread use of high-potency diuretics. Hypokalemia is one of the common complications of diuretic use. Although some studies of hypokalemia induced by furosemide as well as of potassium-deficient diets in the rat have been reported, the electrocardiographic (ECG) changes during hypokalemia in the rat are poorly understood. This study was designed to examine such changes. For this purpose, hypokalemia was induced by furosemide administration, and the diagnostic criteria for ECG manifestations of hypokalemia were determined. During hypokalemia, conduction in most parts of the heart was suppressed to an extent depending on plasma potassium concentration. Prolongation of the QT interval was also observed, which agrees with findings in humans and dogs. Furthermore, prolonged durations of the P wave and QRS complex were observed during hypokalemia in the rat. The extent of alteration of the PR interval induced by hypokalemia was less significant than that of P wave and QRS complex durations. These results suggest that the excitabilities of the myocardium in the atria and ventricles may be affected by extracellular potassium level rather than by the atrioventricular conduction system in the rat. Wave amplitude, except that of the P wave, was decreased by severe hypokalemia. These changes were not dependent on the plasma potassium concentration. Typical T wave changes observed with hypokalemia in humans and dogs did not occur in the rat. The ECG manifestations of acute hypokalemia in the rat did not include the typical T wave changes seen in species with ST-segment type ECGs; however, other ECG parameter changes occurring with hypokalemia were qualitatively similar to those in other species. These results may be useful for testing the toxicity of potassium-depleting drugs in the rat.

Animals↗

PubMed1984

Endocrine physiology of electrolyte metabolism.

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.

Adrenal Cortex Hormones↗

PubMed1975

Experimentally induced intestinal obstruction in sheep: paradoxical aciduria in metabolic alkalosis.

Ewes with surgically prepared obstruction of the duodenum were used as a model in the study of ruminant metabolic alkalosis and paradoxical aciduria. Metabolic alkalosis occurred as a result of irreversible chloride loss, presumably into the abomasum and forestomachs. Analysis of data on serum and urinary electrolye concentrations provided limited support for the explanation of paradoxical aciduria in terms of chloride and potassium deficiencies. The accumulation undetermined anions in the serum indicated that the decreased urinary pH was due to the excretion of titratable acid.

Alkalosis↗

PubMed1976

The purine nucleotide cycle. A pathway for ammonia production in the rat kidney.

Particle-free extracts prepared from kidney cortex of rat catalyze the formation of ammonia via the purine nucleotide cycle. The cycle generates ammonia and fumarate from aspartate, using catalytic amounts of inosine monophosphate, adenylosuccinate, and adenosine monophosphate. The specific activities of the enzymes of the cycle are 1.27+/-0.27 nmol/mg protein per min (SE) for adenoylosuccinate synthetase, 1.38+/-0.16 for adenylosuccinase, and 44.0+/-3.3 for AMP deaminase. Compared with controls, extracts prepared from kidneys of rats fed ammonium chloride for 2 days show a 60% increase in adenylosuccinate synthetase and a threefold increase in adenylosuccinase activity, and a greater and more rapid synthesis of ammonia and adenine nucleotide from aspartate and inosine monophosphate. Extracts prepared from kidneys of rats fed a potassium-deficient diet show a twofold increase in adenylosuccinate synthetase and a threefold increase in adenylosuccinase activity. In such extracts the rate of synthesis of ammonia and adenine nucleotide from aspartate and inosine monophosphate is also increased. These results show that the reactions of the purine nucleotide cycle are present and can operate in extracts of kidney cortex. The operational capacity of the cycle is accelerated by ammonium chloride feeding and potassium depletion, conditions known to increase renal ammonia excretion. Extracts of kidney cortex convert inosine monophosphate to uric acid. This is prevented by addition of allopurinol of 1-pyrophosphoryl ribose 5-phosphate to the reaction mixture.

AMP Deaminase↗

PubMed1976

[Laxative abuse, plasma potassium levels and chronic interstitial nephritis due to phenacetin abuse (author's transl)].

In 154 patients with phenacetin nephropathy and in 26 patients with phenacetin abuse but without nephropathy a laxative abuse was observed in 3.2% and 15.4%, hypokalemia (3.5 maequ/l or less) in 9.1% and 3.9, respectively. The mean plasma potassium concentration was normal in both groups (4.45 and 4.22 maequ/l, respectively). These data do not support the recently proposed hypothesis that the simultaneous abuse of laxatives contributes to the development of analgesic nephropathy, and that the absence of laxative intake might explain the lack of renal damage in some phenacetin abusers. Although it cannot be excluded that long-standing potassium deficiency in consequence of an abuse of laxatives or diuretics exerts an additional nephrotoxic effect in some cases, this mechanism seems not to be involved in the majority of patients with phenacetin nephropathy.

Cathartics↗

PubMed2002

The KlTrk1 gene encodes a low affinity transporter of the K+ uptake system in the budding yeast Kluyveromyces lactis.

Potassium uptake in Saccharomyces cerevisiae is mediated by at least two proteins, known as Trk1p and Trk2p. Direct involvement in cation movements has been demonstrated for Trk1p, which is the high affinity transporter. S. cerevisiae cells also show low affinity potassium uptake, perhaps mediated by Trk2p. Mutants lacking Trk1p, lose high affinity system, but when grown with moderate potassium concentrations, Trk2p seems to replace it. Mutants lacking both proteins are viable but require at least 10 mM K(+) in the medium to sustain growth. Here we report the cloning and characterization of a gene from Kluyveromyces lactis encoding a homologue of these two proteins. KlTrkp is a 1070 amino acid peptide that shows, overall, higher homology with Trk2p than with Trk1p, and its disruption gives rise to cells with deficient potassium transport and with an increased K(+) requirement for normal growth. Determination of kinetic parameters in the K. lactis wild-type and Kltrk1Delta strains, as well as in Sctrk1Delta Sctrk2Delta S. cerevisiae cells expressing KlTrk1, indicated that this is a low affinity component of a major potassium uptake system in K. lactis.

Amino Acid Sequence↗

PubMed1984

A case of hypokalemic myopathy associated with transient hypothyroidism.

A case of transient hypothyroidism in the course of hypokalemic myopathy is reported. A 69-year-old woman had severe muscle weakness and marked potassium deficiency associated with alkalosis during treatment with thiazide diuretics. The cause of muscle weakness proved to be hypokalemic myopathy confirmed by clinical findings and muscle biopsy. After the episode of hypokalemic myopathy, serum levels of thyroid hormone were lowered (T4; 3.8 micrograms/dl, T3; 54 ng/dl) and that of TSH was elevated (25.1 microU/ml). Antithyroid microsomal antibody was positive (1:25600) and anti-thyroglobulin antibody was negative. About one month after potassium supplement, her thyroid functions returned to normal, along with normalization of serum potassium level. This is the first documented case report of hypokalemic myopathy accompanied by transient hypothyroidism in a patient with autoimmune thyroiditis. We suggest that this transient hypothyroidism might be induced by hypokalemia during the course of autoimmune thyroiditis.

Aged↗

PubMedDate not supplied

Renal artery stenosis with normal angiotensin II values. Relationship between angiotensin II and body sodium and potassium on correction of hypertension by captopril and subsequent surgery.

The case is reported of a young woman with severe hypertension, unilateral renal artery stenosis, variously normal or marginally high plasma concentrations of active renin, angiotensin II, aldosterone, sodium, and potassium; and normal total exchangeable and total body sodium and potassium. Arteriograms and ureter catheterization showed the stenosis to be severe, but the unstimulated renal vein renin and angiotensin II differential to be modest. Captopril caused an initial fall in angiotensin II and arterial pressure. During prolonged captopril treatment, plasma angiotensin II and aldosterone remained depressed; exchangeable and total body sodium and potassium were unaltered. Blood pressure fell further to normal levels during prolonged captopril treatment, while subsequent surgical correction of the renal artery stenosis was curative; absolute values of blood pressure and plasma angiotensin II were similar in both situations. The findings support, without proving, the concept that chronic modest elevation of angiotensin II may be responsible for sustained hypertension in unilateral renal artery stenosis. Patients of this type contrast sharply with those, also with severe renal artery stenosis or occlusion, who have gross elevation of renin, angiotensin II, and aldosterone, with sodium and potassium deficiency. Captopril or surgery are effective in both syndromes, but the manner of response to treatment differs markedly.

Adult↗