Excessive Sodium Loss Research Articles

Growth failure and metabolic acidosis due to total body sodium depletion in an infant with an ileostomy.

Sodium is an essential nutrient and inadequate sodium intake and/or excessive sodium losses can result in suboptimal growth. Infants with ileostomies are at significant risk of developing growth failure as a result of excessive sodium loss in their ileostomy effluent. Chronic sodium depletion can also limit the kidney's ability to excrete hydrogen and potassium ions, mimicking electrolyte abnormalities found in type 4 renal tubular acidosis. This report describes an infant with an ileostomy with severe growth failure, hyperkalaemia and metabolic acidosis-all of which promptly resolved with sodium supplementation.

Care Right Where You Are: Treating in Place to Avoid an Emergency Department Visit or Hospitalization

Care Right Where You Are: Treating in Place to Avoid an Emergency Department Visit or Hospitalization

Pharmacotherapy of sodium disorders in neurocritical care.

To describe the pathophysiology and pharmacotherapy of dysnatremia in neurocritical care patients. Sodium disorders may affect approximately half of the neurocritical care patients and are associated with worse neurological outcome and increased risk of death. Pharmacotherapy of sodium disorders in neurocritical care patients may be challenging and is guided by a careful investigation of water and sodium balance. In case of hyponatremia, because of excessive loss of sodium, fluid challenge with isotonic solution, associated with salt intake is the first-line therapy, completed with mineralocorticoids if needed. In case of hyponatremia because of SIADH, fluid restriction is the first-line therapy followed by urea if necessary. Hypernatremia should always be treated with hypotonic solutions according to the free water deficit, associated in case of DI with desmopressin. The correction speed should take into consideration the symptoms associated with dysnatremia and the rapidity of the onset.

Aminophylline-associated hyponatremia in a premature infant

Hyponatremia is common in preterm infants. The causes are usually related to the inability of the premature kidneys to excrete a given water load, excessive sodium losses, or inadequate sodium intake. Here, we present a case of severe hyponatremia in an extreme preterm infant, associated with the use of aminophylline. Aminophylline was administered intravenously on day 1 for the treatment of apnea of prematurity. On day 3, the patient developed hyponatremia which was not responsive to sodium replacement and fluid restriction. Due to concerns of aminophylline-induced hyponatremia, aminophylline was discontinued on day 6, and within 48 h of discontinuation, serum sodium normalized without the need for sodium supplementation. The purpose of the case report is to present a rare complication associated with aminophylline use and to shed light on potential deleterious effects associated with drug shortages.

Does Replacing Sodium Excreted in Sweat Attenuate the Health Benefits of Physical Activity?

International guidelines suggest limiting sodium intake to 86-100 mmol/day, but average intake exceeds 150 mmol/day. Participants in physical activities are, however, advised to increase sodium intake before, during and after exercise to ensure euhydration, replace sodium lost in sweat, speed rehydration and maintain performance. A similar range of health benefits is attributable to exercise and to reduction in sodium intake, including reductions in blood pressure (BP) and the increase of BP with age, reduced risk of stroke and other cardiovascular diseases, and reduced risk of osteoporosis and dementia. Sweat typically contains 40-60 mmol/L of sodium, leading to approximately 20-90 mmol of sodium lost in one exercise session with sweat rates of 0.5-1.5 L/h. Reductions in sodium intake of 20-90 mmol/day have been associated with substantial health benefits. Homeostatic systems reduce sweat sodium as low as 3-10 mmol/L to prevent excessive sodium loss. "Salty sweaters" may be individuals with high sodium intake who perpetuate their "salty sweat" condition by continual replacement of sodium excreted in sweat. Studies of prolonged high intensity exercise in hot environments suggest that sodium supplementation is not necessary to prevent hyponatremia during exercise lasting up to 6 hr. We examine the novel hypothesis that sodium excreted in sweat during physical activity offsets a significant fraction of excess dietary sodium, and hence may contribute part of the health benefits of exercise. Replacing sodium lost in sweat during exercise may improve physical performance, but may attenuate the long-term health benefits of exercise.

Zespół utraty soli z zasadowicą metaboliczną – konfiguracja typowa dla syndromu Barttera i mukowiscydozy

Salt-wasting syndrome accompanied with metabolic alkalosis results from excessive loss of sodium and/or chloride via gastrointestinal tract (chloride diarrhea), skin (cystic fibrosis) or kidney (Bartter syndrome). Most typical symptoms of salt-wasting syndrome in children are dehydration and failure to thrive. A history of a patient and thorough physical examination accompanied with targeted laboratory tests usually allow to establish accurate diagnosis. But in certain cases it may be misleading. Case report presented below points to difficulties in differentiation between Bartter syndrome and pseudo-Bartter syndrome in course of cystic fibrosis.

Indices of salt and water metabolism in tubenose goby Proterorhinus marmoratus pallas, introduced into Rybinsk Reservoir, and in indigenous carp Cyprinus carpio L. Depending on environmental salinity

Only a freshwater type of osmotic and ionic regulation was observed in indigenous carp and tubenose goby settled in the Rybinsk Reservoir within the range of endurable salinity. Carp tolerates direct transfer from freshwater into distilled water. The alien species tubenose goby does not survive 8-fold gradual dilution of the freshwater of Rybinsk Reservoir with distilled water and dies because of excessive loss of sodium by the organism. This indicates a higher water mineralization in the geographical range of inhabitance of the original parent population of tubenose goby. Within such an environment, fish cannot evolve adaptive abilities to survive in water of low mineralization. Within the tolerant salinity range, the water content in carp and tubenose goby is supported at the stable level, giving evidence of standard physiological functioning of the osmotic regulation. Hypohydremia is observed when the organism is exposed to water of critical salinity, indicating problems with osmotic regulation. Therefore, the tolerant range of salinity in carp and tubenose goby varies from 8 to 12 g/L NaCl, and the critical ranges are 8–12 g/L and 12–16 g/L NaCl. Tubenose goby tolerates higher salinity, within the ranges of both tolerant and critical salinity exceeding by 4 g/L those usual for carp. Such abilities of tubenose goby could have evolved only at high water salinity, indicating the Caspian Sea as the area of origin of the parent population of this species.

Transient pseudohypoaldosteronism in an infant with vesicoureteral reflux and urinary tract infection

This chapter discusses the effects, actions, and mechanism of action of aldosterone. Aldosterone, from phyletic evidence, appears to be the most recently evolved adrenocortical hormone. It is present in all groups of tetrapods starting with Amphibia but is found in only a few of the fish where it appears to be only systematically present in the lungfish. Adrenalectomy is shown to have comparable effects, including anorexia, muscular weakness, hypoglycaemia, hypotension, decreased blood volume, and disturbances in blood electrolyte levels. The most prominent of the latter are hyponatraemia and hyperkalaemia, which in mammals, principally reflects an excessive loss of sodium in the urine, accompanied by a failure to excrete sufficient potassium. Many of the systemic effects of adrenocortical insufficiency are related to these disturbances in electrolyte metabolism, and indeed the survival of many mammals can be substantially prolonged by providing additional sodium in the drinking water. Glucocorticoids are the only essential hormones for maintaining adrenalectomized mammals. In mammals, adrenocortical insufficiency, such as that occurring in Addison's disease or following adrenalectomy, apart from altering intermediary metabolism produces disturbances in renal electrolyte and water metabolism. The difficulties in excreting excess water are related to a deficiency of glucocorticoid hormones, while the excessive loss of sodium and retention of potassium primarily reflect the absence of aldosterone.

A New Drug Delivery System Targeting Ileal Epithelial Cells Induced Electrogenic Sodium Absorption: Possible Promotion of Intestinal Adaptation

We previously demonstrated the induction of the epithelial sodium channel, prostasin, and 11β-hydroxysteroid dehydrogenase type 2 and activation of sodium transport mediated by those molecules in the remnant ileum after total proctocolectomy. The aims of the present study were to develop a new drug delivery system that targets ileal epithelial cells and to enhance local mineralocorticoid action without systemic effects. Orally administered d-aldosterone-containing d,l-lactide/glycolide acid copolymer microspheres are absorbed in the rat terminal ileum and released aldosterone. Blood and terminal ileal tissues were collected 2 weeks after the administration of the microspheres, and the aldosterone concentrations, mRNA, and protein expressions of the above molecules and sodium transport were evaluated. Significantly high levels of tissue aldosterone in the absence of elevated plasma levels were detected in the microspheres-treated rats. Epithelial mRNA and protein expression of the above molecules increased significantly in the microspheres-treated animals. Electrogenic sodium transport in the ileum was enhanced in the microspheres-treated rats. Aldosterone-containing microspheres successfully induced the expression of the above molecules and activated sodium transport in the ileal mucosa, both of which are essential for intestinal adaptation. Pre- and/or postoperative treatment with this drug may compensate for the excessive loss of sodium and water following proctocolectomy.

Drospirenone and its antialdosterone properties

Drospirenone is a unique progestogen derived from 17α-spirolactone, with a pharmacologic profile very similar to that of endogenous progesterone. In contrast with other available progestins, drospirenone is a progestogen with aldosterone receptor antagonism (PARA) through its affinity for the mineralocorticoid receptor. It is thus able to act on the renin–angiotensin–aldosterone system (RAAS), which prevents excessive sodium loss and regulates blood pressure. Estrogen acts on the RAAS to stimulate the synthesis of angiotensinogen, which increases aldosterone levels and promotes sodium and water retention. When these effects are unopposed, for example during estrogen replacement therapy, they can lead to increases in weight and blood pressure. The antialdosterone properties exhibited by drospirenone promote sodium excretion and prevent water retention, conferring potential blood pressure benefits. In addition to its effects on the kidney, aldosterone has effects on the vasculature, myocardium and central nervous system, which may elicit a variety of pathophysiologic processes associated with cardiovascular disease. The antialdosterone properties of drospirenone may therefore confer additional cardiovascular benefits beyond the RAAS system. The combined actions of drospirenone on sodium and water retention and cardiovascular parameters make it a more attractive therapeutic option as a component of hormone replacement therapy than other synthetic progestins.

Episodic Hyponatremia in Mitochondrial Encephalomyopathy, Lactic Acidosis, and Strokelike Episodes (MELAS)

Various organ involvements and endocrinologic abnormalities associated with electrolyte imbalance, including hyponatremia, are seen in patients with mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS); however, the clinical significance of hyponatremia in these patients is rarely reported. We analyzed the serum sodium concentration profiles and clinical and laboratory data of seven patients with MELAS. We found that hyponatremia occurred episodically in four of the seven patients from an early stage of the disease. We identified excessive sodium loss in urine to be associated with the hyponatremic episodes and the causes of hyponatremia in two patients as relative adrenal insufficiency, acute renal failure, and serious paralytic ileus. However, even extensive examinations failed to reveal the cause in other patients. Because severe hyponatremia can cause serious complications, clinicians should pay attention to serum sodium levels and maintain them properly in patients with MELAS.

A Case of Cerebral Salt Wasting Syndrome Associated with Tuberculous Meningitis

Hyponatremia which is due to excessive sodium loss in the urine and decrease in extracellular fluid volume following an acute or chronic central nervous system injury, has been conjunctively described as cerebral salt wasting syndrome (CSWS). This syndrome is often confused with dilutional hyponatremia due to inappropriate secretion of antidiuretic hormone. Accurate diagnosis and management are mandatory for improvement of the course of the disease. This report describes a case of a 31-year- old male patient with CSWS associated with tuberculous meningitis. The patient exhibited hyponatremia, polyuria, excessive natriuresis, volume depletion, and hypotension. He was diagnosed to manifest CSWS and was treated by administration of fluids, salt, and fludrocortisone. After the respective treatments, symptoms of polyuria and hypotension were gradually resolved and hyponatremia was corrected. (Tuberc Respir Dis 2005; 59: 306-310)

Metabolic Adverse Reactions to Diuretics Clinical Relevance to Elderly Patients

There is a wide variety of diuretic-induced metabolic abnormalities of unequal severity. Renal failure can be caused by excessive sodium loss, or by certain drug combinations comprising, for instance, a nonsteroidal anti-inflammatory drug (NSAID) or an ACE inhibitor. Hyponatraemia is uncommon. It is encountered with thiazides, especially among women. A sodium level less than 120 mmol/L may result in neurological complications. Hypokalaemia is frequent and might increase the risk of cardiac arrhythmia. Hyperkalaemia induced by potassium-sparing diuretics is often combined with another contributive cause. Glucidic, lipidic and uric acid abnormalities are common, but their clinical effects are slight. They do not seem to worsen cardiovascular risks among elderly patients. Nevertheless, prescribing diuretics for elderly patients requires special precautions. Reducing the diuretic dose, as is now recommended for treating hypertension, seems to lessen adverse effects, and despite all the adverse reactions just mentioned, it has been proven that diuretics are beneficial in many diseases.

Hyponatremia and dehydration in an 11-month-old infant from cerebrospinal fluid loss from an inapparent traumatic dural laceration

The most common causes of hyponatremia in infants and young children are 1) water intoxication, 2) the syndrome of inappropriate antidiuretic hormone (SIADH), and 3) excessive sodium losses via the gastrointestinal tract, the kidneys, or the skin. In children with externalized ventriculostomy catheters, the loss of large volumes of cerebrospinal fluid (CSF) may also result in hyponatremia if there is inadequate sodium replacement.1 We describe a case of severe hyponatremia and dehydration in an 11-month-old child with an undetected traumatic dural laceration that permitted leakage of CSF.

Glue-sniffing and distal renal tubular acidosis

An index case is presented to introduce the subject of the acid-base and electrolyte abnormalities resulting from toluene abuse. These include metabolic acidosis associated with a normal anion gap and excessive loss of sodium and potassium in the urine. The major question addressed is, what is the basis for the metabolic acidosis? Overproduction of hippuric acid resulting from the metabolism of toluene plays a more important role in the genesis of the metabolic acidosis than was previously believed. This conclusion is supported by the observation that the rate of excretion of ammonium was not low during metabolic acidosis in six of eight patients, suggesting that distal renal tubular acidosis was not an important acid-base abnormality in most cases where ammonium was measured. The excretion of hippurate in the urine unmatched by ammonium also mandates an enhanced rate of excretion of the cations, sodium and potassium. The loss of sodium causes extracellular fluid volume contraction and a fall in the glomerular filtration rate, which may transform the normal anion gap type of metabolic acidosis into one with a high anion gap (accumulation of hippurate and other anions). Continuing loss of potassium in the urine leads to hypokalemia. An understanding of the metabolism of toluene provides the basis for the unusual biochemical abnormalities seen with abuse of this solvent.

Effect of Chronic Dietary Treatment with Nicotinic Acid on the Development and Maintenance of Deoxycorticosterone-Acetate-Salt-Induced Hypertension

Chronic dietary administration of either l-tryptophan (5.0%) or nicotinic acid (5.0%) reduced the elevated blood pressure of rats with established, deoxycorticosterone-acetate (DOCA)-salt-induced hypertension without affecting either body weight or cardiac hypertrophy. In a second study, chronic dietary administration of nicotinic acid (2.5 and 5.0%) provided significant protection against the development of an elevated blood pressure in rats treated with DOCA salt. A modest (approximately 10%) reduction in cardiac hypertrophy was also observed in the two nicotinic-acid-treated groups. Treatment with either dose of nicotinic acid did not, however, prevent either the renal hypertrophy characteristic of DOCA-salt-induced hypertension in rats or their reduced renal concentrating ability during a 24-hour dehydration; nor did treatment with nicotinic acid reduce the excessive ingestion of saline characteristic of chronic treatment with DOCA. In contrast, treatment with the higher dose of nicotinic acid prevented the excessive loss of sodium into urine characteristic of DOCA-salt-induced hypertension when the rats were loaded (3% of body weight, i.p.) with a hypotonic (0.075 M) saline solution. These results suggest that increased production of nicotinic acid resulting from dietary administration of tryptophan may play a role in the protective effect of tryptophan against the development of DOCA-salt-induced hypertension. These studies do not, however, provide a mechanism by which nicotinic acid may manifest its beneficial effects.

Extracellular fluid volume changes in very low birth weight infants during first 2 postnatal months

Serial extracellular volume (ECV) changes were measured in 18 infants of less than 32 weeks gestation. Results were compared with changes in body weight, fluid and sodium intake, urine output, and serum sodium concentration. Mean +/- SD ECV decreased from 550 +/- 116 mL/kg on day 1 to 359 +/- 66 mL/kg on day 14. Thereafter, mean ECV/kg remained between 336 +/- 42 and 349 +/- 54 mL/kg. Clinical hydration and serum sodium concentration usually remained normal during this reduction of stabilization of ECV/kg. Six episodes of hyponatremia occurred at 11 to 31 days of age. Mean ECV/kg was significantly lower in infants with hyponatremia compared with infants of similar age with normal serum sodium concentration (303 +/- 36 mL/kg vs 368 +/- 56 mL/kg, P less than 0.01). Sodium intake in the two groups was similar. We conclude that ECV in the VLBW infant decreases postnatally and is regulated within a range similar to that in older infants, and that postnatal natriuresis in the first 2 weeks of life represents physiologic reduction of the expanded ECV of the fetus. Late hyponatremia may indicate excessive sodium loss and ECV depletion.

EXTRACELLULAR FLUID VOLUME (ECV) CHANGES IN VERY LOW BIRTH WEIGHT (VLBW) INFANTS DURING THE FIRST TWO POSTNATAL MONTHS

Postnatal natriuresis among VLBW infants may represent physiologic reduction of the ECV or pathologic renal salt wasting. We assessed Na homeostasis between birth and hospital discharge by serial measurements of ECV in 18 preterm infants(mean GA 28 wk, SD 1.8). ECV was estimated as corrected bromide space on postnatal days 1, 7, 14, 21, 42 and 63. Results were compared to changes in body weight, Na intake and serum Na concentration.Mean body weight decreased from 1027 gm (SD 272) on day 1 to 937 gm (SD 217) on day 7, then returned to birth weight by day 14. Mean ECV was 550 ml/kg (SD 116) on day 1 and decreased to 359 ml/kg (SD 66) on day 14. Thereafter body weight and ECV increased proportionally so that mean ECV/kg remained between 336 ml/kg (SD 42) and 349 ml/kg (SD 54). ECV reduction and stabilization was usually isotonic.Six infants developed hyponatremia(serum Na < 135 mEq/l) between 11 and 31 days of age. Mean ECV/kg was significantly lower in these infants compared with infants in the same age range with serum Na > 135 mEq/l (303 ml/kg, SD 36, vs. 368 ml/kg, SD 56, p <.01). Sodium intake was not different in the 2 groups, however total fluid intake was greater in infants with hyponatremia and decreased ECV.In conclusion, the ECV of the VLBW infant decreases postnatally and is regulated within a range similar to older infants. These findings suggest that the initial postnatal natriuresis in the first 2 wks of life represents physiologic reduction of the expanded ECV of the fetus. Late hyrronatremia may indicate excessive sodium loss and ECV depletion.

Hyponatremia and Ultramarathons

To the Editor.— Marathon running is gaining increasing popularity. An understanding of the pathophysiology of exertion is important so that runners can be advised on how to minimize the medical hazards of their sport. We therefore read with great interest the report by Frizzell et al 1 describing severe acute hyponatremia in marathon runners. The authors attribute the hyponatremia detected in their patients to an excessive loss of sodium in sweat and to drinking hypotonic fluids. Undoubtedly these are important etiologic factors. The recent discovery of a putative natriuretic hormone, 2 atrial natriuretic peptide (ANP), is causing a major revision in the understanding of salt and water homeostasis. Increasing the circulating concentration of ANP has been shown to cause a salt-losing state in man. 3 There are to date no published data on the effects of exertion on circulating concentrations of ANP. We have therefore performed a pilot study to

Pseudohypoaldosteronism due to Sweat Gland Dysfunction

Pseudohypoaldosteronism is an uncommon disorder characterized by urinary sodium wasting and is attributed to a defect in distal renal tubular sodium handling with failure to respond to endogenous aldosterone. Sweat electrolyte values in other reported patients, when measured, have been normal. A 3.5-year-old girl developed repeated episodes of dehydration, hyponatremia, and hyperkalemia during the first 19 months of life. Serum sodium was as low as 113 mEq/liter and potassium as high as 11.1 mEq/liter. Her plasma and urinary aldosterone levels were persistently elevated (Figs. 1-4). Unlike patients with classic pseudohypoaldosteronism she demonstrated no urinary sodium wasting (Figs. 2 and 3). During episodes of hyponatremia and reduced sodium intake her urinary sodium was less than 5 mEq/liter. In addition, her sweat sodium concentration was consistently above 125 mEq/liter and salivary sodium concentration above 58 mEq/liter. Her chest x-ray, 72-hr fecal fat excretion, serum and urinary pancreatic amylase (amy-2) were normal, providing no evidence for cystic fibrosis. It is proposed that this patient represents a new variant of pseudohypoaldosteronism with excessive loss of sodium from the sweat and salivary glands instead of the kidneys.