Interrelations Between Serum Sodium Concentration, Serum Osmolarity and Total Exchangeable Sodium, Total Exchangeable Potassium and Total Body Water1

Edelman, Isidore S.; Leibman, J.; O'Meara, Maurice P.; Birkenfeld, L. W.

doi:10.1172/jci103712

Cited by 491 publications

(331 citation statements)

References 28 publications

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“…An intriguing possibility discussed by Noakes et al (34) is that some athletes are able to mobilize sodium from internal stores that otherwise are osmotically inactive. This exchangeable sodium store has been described by Edelman and colleagues, Titze and colleagues, and Heer and colleagues (81)(82)(83)(84)(85)(86). For example, in the study by Heer et al (86) participants were fed a diet of varying sodium amounts with a fixed amount of water ingestion.…”

Section: Pathophysiologymentioning

confidence: 83%

“…Despite these conditions, serum sodium levels remained constant without a concomitant increase in TBW. These studies indicated that up to one fourth of the total body sodium may exist in bone and cartilage stores that are not osmotically active (i.e., in an insoluble crystal compound) but potentially recruitable into an osmotically active form (81)(82)(83). In rats, this nonosmotically active sodium may reside bound to skin proteoglycans (87,88).…”

Section: Pathophysiologymentioning

confidence: 99%

“…Therefore, athletes who gain TBW and maintain a normal serum sodium concentration are able to mobilize this store of exchangeable sodium, whereas athletes who develop EAH either cannot mobilize the exchangeable pool or sodium or may osmotically inactivate sodium (34). The factors that govern the exchange of sodium between these compartments is unknown but may involve hormonal factors such as angiotensin II or aldosterone (81)(82)(83)(84)(85)(86). The magnitude of this effect in athletes is large with up to 700 mmol of sodium being mobilized from the osmotically inactive pool in the calculations by Noakes et al (34).…”

Section: Pathophysiologymentioning

confidence: 99%

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Exercise-Associated Hyponatremia

Rosner

Kirven

2007

Clinical Journal of the American Society of Nephrology

170

165

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Exercise-associated hyponatremia has been described after sustained physical exertion during marathons, triathlons, and other endurance athletic events. As these events have become more popular, the incidence of serious hyponatremia has increased and associated fatalities have occurred. The pathogenesis of this condition remains incompletely understood but largely depends on excessive water intake. Furthermore, hormonal (especially abnormalities in arginine vasopressin secretion) and renal abnormalities in water handling that predispose individuals to the development of severe, life-threatening hyponatremia may be present. This review focuses on the epidemiology, pathogenesis, and therapy of exercise-associated hyponatremia.

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Section: Pathophysiologymentioning

confidence: 83%

Section: Pathophysiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

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Exercise-Associated Hyponatremia

Rosner

Kirven

2007

Clinical Journal of the American Society of Nephrology

170

165

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“…Although clinically popular formulas are reasonably accurate in predicting the increase in serum sodium concentration from hypertonic saline infusion, in our experience, the formula tended to underestimate the increase, and in overcorrectors, the actual increase in sodium concentration was up to five times the predicted rate. The predictive formula that we used omits both potassium and the intercept in Edelman's empirical relationship (6,15,16). Severe hypokalemia was infrequent and potassium replacement was modest in this series.…”

Section: Discussionmentioning

confidence: 96%

Hypertonic Saline for Hyponatremia

Mohmand

Issa

Ahmad

et al. 2007

Clinical Journal of the American Society of Nephrology

159

112

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Background and objectives: Data regarding dosage-response relationships for using hypertonic saline in treatment of hyponatremia are extremely limited. Objectives of this study were to assess adherence to previously published guidelines (limiting correction to <12 mEq/L per d and <18 mEq/L per 48 h) in treating hyponatremia with hypertonic saline and to determine the predictive accuracy of the Adrogué-Madias formula.Design, setting, participants & measurements: A retrospective review was conducted of all 62 adult, hyponatremic patients who were treated with hypertonic saline during 5 yr at a 528-bed, acute care, teaching hospital.Results: Median infusion rate was 0.38 ml/kg per h, increasing serum sodium concentration by 0.47 ؎ 0.05 mEq/L per h, 7.1 ؎ 0.6 mEq/L per 24 h, and 11.3 ؎ 0.7 mEq/L per 48 h. In 11.3% of cases, the increase was >12 mEq/L per 24 h and in 9.7% was >18 mEq/L per 48 h. No patient's rate was corrected by >25 mEq/L per 48 h. Among patients with serum sodium <120 mEq/L, the observed increase in sodium exceeded the rise predicted by the Adrogué-Madias formula in 74.2%; the average correction in overcorrectors was 2.4 times the predicted. Inadvertent overcorrection was due to documented water diuresis in 40% of cases.Conclusions: The Adrogué-Madias formula underestimates increase in sodium concentration after hypertonic saline therapy. Unrecognized hypovolemia and other reversible causes of water retention pose a risk for inadvertent overcorrection. Hypertonic saline should be infused at rates lower than those predicted by formulas with close monitoring of serum sodium and urine output.

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“…3 However, in chronic illness with hypotonicity or hypertonicity (that is, hyponatremia or hypernatremia) the relationship between body water and total exchangeable cation must presumably be different from the findings in normotonic states, and in a population of patients with a wide variation of serum cation concentrations, the correlation coefficient of equation 1 must be expected to be decreased. For this situation the following relationship between the sodium concentration of serum water (Na ) s and the total exchangeable cation concentration (Nae + K(/TBW) has been defined4: (Na)s=b NaNe+ Ke +a (2) (N~)sb.TBW The significance of this relationship has been improved through the addition of the potassium concentration to the sodium concentration of serum water as shown in equation 35: (Na)s + (k)s bNae BKe+ a (3) This formula, which relates the cation concentration of serum water to the total exchangeable cation concentration, may be rewritten as follows5: Nae + Ke (Na)s+ (k)s b. TBW+a (4) With the assumption that the cation concentrations of the extracellular and intracellular water are equal, the term ((N e + K ) (N's+ (k)s represents the cation space, or the volume of dilution of cations, the variations of which should reflect the variations in total body water to the extent that the amount of exchangeable, osmotically inactive cation is unchanged. Since the variables of equation 4 cover a wider range than the variables of equations 2 and 3, the relationship expressed in equation 4 should be most suitable to include hypertonic, normotonic, and hypotonic disease states in a highly significant correlation.…”

mentioning

confidence: 99%

Interrelations Between Total Exchangeable Sodium, Potassium, Body Water, and Serum Sodium and Potassium Concentrations in Hyponatremic and Normonatremic Heart Disease

Olesen

1967

Circulation

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SUMMARYInterrelations between total body water, total exchangeable cation (sodium + potassium), and cation (sodium + potassium) concentration of serum water were examined in 20 normonatremic and 11 hyponatremic edematous cardiac patients. The total exchangeable cation and total body water were highly significantly correlated in the normonatremic and hyponatremic groups. However, for the combined groups the correlation coefficient was lower than that found in the individual populations, and in covariance analysis the cation content in relation to total body water was significantly lower in the hyponatremic than in the normonatremic group. When it is assumed that the total exchangeable cation differs little from the total osmotically active cation, and that the cation concentrations of the extracellular and intracellular water are approximately equal, the ratio: total exchangeable cation . cation concentration in serum water, that is, the cation space, should reflect the total body water. The cation space and total body water were highly significantly correlated in the normonatremic and hyponatremic groups, and the correlation coefficient remained at the same high level for the combined groups. The relationship between cation space and body water was very close to unity, and in covariance analysis no significant difference was found in cation space in relation to total body water. These results were confirmed in 10 sequential studies. It is concluded that the cation space in hyponatremic and normonatremic cardiac patients has proved to reflect the total body water very closely, and the implications of this finding are discussed.Additional Indexing Words: Alteration in body composition Cation space Cardiac edema A CCORDING TO current knowledge sodium is the predominant cation of the extracellular phase, and potassium is the preponderant cation of the cell mass, while small amounts of potassium are present in the extracellular compartment, and minor quantities of sodium are found in the cells. In actual

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Interrelations Between Serum Sodium Concentration, Serum Osmolarity and Total Exchangeable Sodium, Total Exchangeable Potassium and Total Body Water1

Cited by 491 publications

References 28 publications

Exercise-Associated Hyponatremia

Exercise-Associated Hyponatremia

Hypertonic Saline for Hyponatremia

Interrelations Between Total Exchangeable Sodium, Potassium, Body Water, and Serum Sodium and Potassium Concentrations in Hyponatremic and Normonatremic Heart Disease

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