Contemporary Dietary Intake: Too Much Sodium, Not Enough Potassium, yet Sufficient Iodine: The SALMEX Cohort Results.

Initiatives to reduce sodium intake are encouraged globally, yet there is concern about compromised iodine intake supplied through salt. The aim of the present study was to determine baseline sodium, potassium, and iodine intake in a sample of workers from our Institution in Mexico City (SALMEX Cohort). Methods. From a cohort of 1009 workers, appropriate 24-h urine and three-day dietary recall was collected in a sample of 727 adult subjects for assessment of urinary sodium, potassium, and iodine concentrations. Median urinary iodine excretion (UIE) was compared across categories of sodium intake of <2, 2⁻3.6, and ≥3.6 g/day. Results. Average sodium intake was 3.49 ± 1.38 g/day; higher in men than women (4.14 vs. 3.11 g/day, p ≤0.001). Only 10.6% of the population had sodium intake within the recommended range (<2 g/day); 45.4% had high (2⁻3.6 g/day) and 44% had excessive intake (>3.6 g/day). Average urinary Na/K ratio was 3.15 ± 1.22 (ideal < 1), higher in men (3.42 vs. 3.0, p ≤ 0.001). The multivariate analysis showed that sodium intake was associated with age (p = 0.03), male sex (p < 0.001), caloric intake (p = 0.002), UKE (p < 0.001) and BMI (p < 0.001). Median iodine intake was 286.7 µg/day (IQR 215⁻370 µg/day). Less than 2% of subjects had iodine intake lower than recommended for adults (95 µg/day); 1.3% of subjects in the recommended range of salt intake had low iodine intake. There is a direct relationship between iodine and sodium urinary excretion (r = 0.57, p < 0.0001). Conclusions. In the studied population, there was an excessive sodium intake and an imbalance between sodium and potassium intake. Only 10.6% of the population had sodium intake within the recommended values, but iodine intake in this group appears to be adequate.

Associations between dietary salt, potassium and blood pressure in South African adults: WHO SAGE Wave 2 Salt & Tobacco.

BACKGROUND & AIMS: In June 2016, South Africa implemented legislation mandating maximum sodium levels in a range of processed foods with a goal of reducing population salt intake and disease burden from hypertension. Our aim was to explore the relationship between salt and blood pressure (BP) in a subsample of the World Health Organization Study on global AGEing and adult health (SAGE) Wave 2 before implementation of legislation in South Africa. METHODS & RESULTS: Blood pressure (BP) was measured in triplicate (n = 2722; median age 56 years; 33% male) and 24-h urine collected in a nested subsample (n = 526) for sodium, potassium and creatinine analysis. Hypertension prevalence was 55% in older adults (50-plus years) and 28% in younger adults (18-49 years). Median salt intake (6.8 g/day) was higher in younger than older adults (8.6 g vs 6.1 g/day; p < 0.001), and in urban compared to rural populations (7.0 g vs 6.0 g/day; p = 0.033). Overall, 69% of participants had salt intakes above 5 g/day. Potassium intakes were generally low (median 35 mmol/day) with significantly lower intakes in rural areas and older adults. Overall, 91% of adults failed to meet the daily potassium recommendation of 90 mmol/d. Salt intakes above 5 g/day, and to a greater extent, a dietary sodium-to-potassium (Na:K) ratio above 2 mmol/mmol, were associated with significantly steeper regression slopes of BP with age. CONCLUSION: These preliminary results indicate that high dietary Na:K ratio may lead to a greater increase in BP and hypertension risk with age. Interventions to increase potassium intakes alongside sodium reduction initiatives may be warranted.

Prolonged QT interval in bulimia nervosa.

A 39-year-old woman with an unremarkable history presented to the emergency department with three episodes of collapse. Each episode was witnessed by her son who described a loss of consciousness followed by rapid and complete recovery. The patient appeared well and examination was unremarkable. Her ECG showed a marked QTc prolongation of 642 ms (normal <470 ms) and low serum potassium at 1.8 mmol/l (3.5-5.3 mmol/l). The patient was moved to the coronary care unit and started on potassium replacement. On the ward a thorough history was taken and the patient confessed to being very conscious about his body shape and weight and admitted to episodes of binge eating and self induced vomiting. Her history suggested bulimia nervosa which is known to cause electrolyte disturbances and cardiac arrhythmia. Over the following 2 days the patient's potassium increased and the QTc interval normalised; the patient was discharged with an outpatient referral for a psychiatric opinion.

[Potassium magnesium homeostasis: physiology, pathophysiology, clinical consequences of deficiency and pharmacological correction].

The metabolism of K and Mg is closely linked. Mg deficiency may arise together with and contribute to the persistence of K deficiency. Isolated disturbances of K balance do not produce secondary abnormalities in Mg homeostasis. In contrast, primary disturbances in Mg balance, particularly Mg depletion, produce secondary K depletion. This appears to result from an inability of the cell to maintain the normally high intracellular concentration of K, perhaps as a result of an increase in membrane permeability to K and / or inhibition of Na+-K+-ATPase. Cases of Mg deficiency accompanying with Mg-dependent or -independent K deficiency are not uncommon among the general population. K and Mg deficiencies are found in patients with chronic alcoholism, cardiac diseases, diabetes mellitus (type II), genetic forms of renal potassium and magnesium wasting (Gitelman's and Bartter's syndromes), severe diarrhea and vomiting, malnutrition, during therapy with some kind of drugs. Various K-Mg salts allowing simultaneously eliminating deficiency of Mg and K are described in the literature. K-Mg aspartate is most distributed among K-Mg salts. It can be used as adjuvant therapy in ischaemic heart disease (in angina pectoris and conditions after myocardial infarction), prophylaxis and adjuvant therapy of cardiac arrhythmia (e.g. prevention of toxic symptoms during therapy with digoxin). Differences in metabolism and utilisation of D- and L-amino acids probably may effect on pharmacological properties of K-Mg L- and D-aspartates, and what is more pharmacological doses of Mg and K salts may induce toxicity which differs according to the nature of the anions. In our research it was established, that L-aspartate salts are better delivery forms for cations such as Mg and K than D-aspartate salts. K-Mg L-aspartate can be more beneficial in the treatment of several forms of primary Mg and K deficiency than K-Mg DL-aspartate and K-Mg D-aspartate.

ESPE/LWPES consensus statement on diabetic ketoacidosis in children and adolescents.

Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus (TIDM). Mortality is predominantly related to the occurrence of cerebral oedema; only a minority of deaths in DKA are attributed to other causes. Cerebral oedema occurs in about 0.3-1% of all episodes of DKA, and its aetiology, pathophysiology, and ideal method of treatment are poorly understood. There is debate as to whether physicians treating DKA can prevent or predict the occurrence of cerebral oedema, and the appropriate site(s) for children with DKA to be managed. There is agreement that prevention of DKA and reduction of its incidence should be a goal in managing children with diabetes.

[Therapy of cardiac arrhythmias. Clinical significance of potassium- and magnesium aspartate in arrhythmias]. / Therapie von Herzrhythmusstörungen. Die klinische Bedeutung von Kalium- und Magnesiumaspartat bei Arrhythmien.

UNLABELLED: Potassium and magnesium deficiencies usually coexist and represent a risk factor for cardiac arrhythmias. Serum levels--in particular of magnesium--are inconclusive for establishing a possible electrolyte deficiency. Basic treatment of arrhythmia should therefore include the administration of potassium and magnesium, since the benefit is great, and the possible side effects is negligible. A placebo-controlled study involving patients with cardiac arrhythmias revealed that appreciably fewer ventricular asystoles occurred after three weeks of treatment with potassium and magnesium aspartate, even when serum levels were within the normal range prior to initiating treatment. Patients older than 50, and those with previous coronary heart disease and/or myocardial infarction derived particular benefit from this form of treatment. CONCLUSION: These results underscore the key role played by potassium and magnesium in the treatment of cardiac arrhythmias.

Magnesium and potassium deficiency. Its diagnosis, occurrence and treatment in diuretic therapy and its consequences for growth, protein synthesis and growth factors.

Thiazides and loop diuretics facilitate the loss of K and Mg through the kidneys leading to deficiencies that may require treatment with supplements. These losses may be overlooked, however, because serum concentrations may remain normal even when the muscle concentrations are appreciably reduced. In 76 patients who had received diuretics for 1-17 years, the mean concentrations of K, Mg and Na,K-pumps in skeletal muscle biopsies were significantly lower than in those from an age- and sexmatched control group, and muscle Mg and K concentrations were significantly correlated. The serum concentrations, however, were only below the control range in a few patients. The fact that Mg,K deficiencies may often be overlooked emphasises the need for data on the contents of skeletal muscle. A recently developed simple biopsy needle procedure permitted the detection of disorders of electrolytes during long-term diuretic treatment despite normal serum concentrations. With the same technique it was possible to detect repletion of the muscle electrolytes after a Mg supplementation period. Oral Mg supplementation could reestablish normal Mg as well as K status in patients in long-term diuretic therapy, provided that the supplementation was maintained for 6 months. Moreover, the normalization of muscle Mg and K was accompanied by a restoration of the concentration of Na,K-pumps measured as the [3H]ouabain binding site capacity in skeletal muscle. Mg and K contents were closely correlated in human muscle biopsies from patients on diuretic treatment, but also in rat muscle which had been moderately Mg depleted in vivo or in vitro. In isolated soleus muscle, which had been moderately Mg-depleted in vitro, reduction in cellular K could not be ascribed to reduced Na,K-pump mediated K-influx. The reduced K content might rather be related to increased K efflux from the muscles. In rats, insufficient dietary supplies of K, Mg and Zn were characterized by inhibition of growth and protein synthesis. These effects could not readily be related to the loss of these elements from muscle tissue, but rather should be seen as a response to a general deficiency. The most marked evidence of deficiency was seen in the serum levels, which pointed to the serum concentration as a possible mediator for the regulation of tissue growth. IGF-I is a low molecular weight peptide possessing growth promoting properties in many tissues probably as an interplay of both autocrine/paracrine and endocrine actions. In both animals and man insufficient supplies of energy and protein are accompanied by growth retardation and a decrease in serum IGF-I.(ABSTRACT TRUNCATED AT 400 WORDS)

[Heart rate disorders in potassium and magnesium deficiency]. / Hjerterytmeforstyrrelser ved kalium- og magnesiummangel.

Potassium and magnesium deficiencies are common in patients with heart disease. These are often coexistent and pathophysiologically related. Potassium deficiency cannot be treated without correction of concomitant magnesium deficiency. Correlations between serum levels and body stores are very poor for both ions. Therefore diagnosis and treatment of these conditions based on serum levels alone are erroneous. There is some evidence that it is primarily the intracellular depletion of these ions which is arrhythmogenic. Magnesium infusion has been proved effective in treatment of torsade de pointes ventricular tachycardia and arrhythmias induced by digoxin-intoxication, and is recommended in these conditions. Whether it is effective in other forms of arrhythmia is not yet elucidated.

Localization of phosphorus metabolites and sodium ions in the rat kidney.

Relative amounts of phosphorus-containing metabolites and sodium ions present in different regions of the in vivo rat kidney were obtained using a surface-coil probe and recently developed NMR rotating-frame methods. During altered physiologic states, changes in distribution of metabolites and sodium ions within the kidney were identified in one-dimensional metabolite maps. This technique may have important applications to disorders commonly found in clinical medicine.

Current approaches to management of potassium deficiency.

Current issues related to oral potassium supplementation are reviewed, with emphasis on recommendations for the appropriate use of potassium supplementation for both replacement and preventive therapy. Dietary potassium intake, potassium-sparing diuretics, and the various forms of oral potassium supplements are reviewed in terms of indications for use, advantages, and limitations. Attention is given to controversial areas, i.e., gastrointestinal tolerance of controlled-release potassium oral dosage preparations and the need for potassium supplementation in hypertensive patients treated with diuretics.

Intracellular and exchangeable potassium in cirrhosis. Evidence against the occurrence of potassium depletion in cirrhosis with ascites.

The intracellular potassium content of leukocytes, the extracellular fluid volume (82Br space), and exchangeable potassium were determined in 28 patients with cirrhosis of the liver (18 with ascites) and in 15 hospitalized controls. No intracellular potassium depletion could be identified in these patients. Leukocyte potassium was similar in cirrhotic patients with and without ascites (355.9 +/- 25.3 and 348.1 +/- 31.9 mEq/kg of dry solids, respectively) and in hospitalized controls (359.7 +/- 27.4) (mean +/- SD). The extracellular fluid volume was similar in controls and cirrhotics without ascites, but markedly increased in cirrhotics with ascites. The exchangeable potassium (mEq/kg of body weight) was similar in nonascitic cirrhotics and in hospitalized controls, but significantly lower in patients with cirrhosis and ascites. However, when the estimated weight of the extracellular fluid volume was substrated from the total body weight, thus obviating the influence of the increased extracellular fluid volume of ascitic patients in the body weight, the exchangeable potassium (mEq/kg of "corrected" body weight) was similar in cirrhosis with ascites (52.9 +/- 6.7 mEq/kg), nonascitic cirrhotics (55.8 +/- 6.1 mEq/kg) and hospitalized controls (55.0 +/- 8.3 mEq/kg), and a significant correlation was obtained between the exchangeable potassium and the leukocyte potassium content. In five patients, the measurements were repeated after relieving ascites with diuretics. No change was observed in the leukocyte potassium, but exchangeable potassium (mEq/kg of body weight) increased, reaching values not significantly different from controls or nonascitic cirrhotics. The exchangeable potassium (mEq/kg of "correct" body weight) did not change. Our results strongly suggest that potassium depletion was not present in the series of cirrhotic patients studied.