Prolonged hypernatremia associated with azotemia and hyponatriuria

Leehey, David J.; Daugirdas, John T.; Manahan, Ferdinand J.; Kellner, Kenneth; Ing, Todd S.

doi:10.1016/0002-9343(89)90358-6

Cited by 5 publications

(3 citation statements)

References 5 publications

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“…Clinical reports addressing various aspects of hyponatremia, including specific categories (34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49), general reviews (50-57), and treatment (58)(59)(60)(61), focus their analyses on combinations of losses or gains of TBNa, TBK, and TBW that decrease the fraction (TBNa + TBK)/TBW. Similarly, reports analyzing the pathogenesis and treatment of hypernatremia focus on combinations of losses or gains that increase the fraction (TBNa + TBK)/TBW (62)(63)(64)(65)(66)(67)(68)(69)(70)(71)(72).…”

Section: Clinical Reportsmentioning

confidence: 99%

Edelman Revisited: Concepts, Achievements, and Challenges

et al. 2022

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The key message from the 1958 Edelman study states that combinations of external gains or losses of sodium, potassium and water leading to an increase of the fraction (total body sodium plus total body potassium) over total body water will raise the serum sodium concentration ([Na]S), while external gains or losses leading to a decrease in this fraction will lower [Na]S. A variety of studies have supported this concept and current quantitative methods for correcting dysnatremias, including formulas calculating the volume of saline needed for a change in [Na]S are based on it. Not accounting for external losses of sodium, potassium and water during treatment and faulty values for body water inserted in the formulas predicting the change in [Na]S affect the accuracy of these formulas. Newly described factors potentially affecting the change in [Na]S during treatment of dysnatremias include the following: (a) exchanges during development or correction of dysnatremias between osmotically inactive sodium stored in tissues and osmotically active sodium in solution in body fluids; (b) chemical binding of part of body water to macromolecules which would decrease the amount of body water available for osmotic exchanges; and (c) genetic influences on the determination of sodium concentration in body fluids. The effects of these newer developments on the methods of treatment of dysnatremias are not well-established and will need extensive studying. Currently, monitoring of serum sodium concentration remains a critical step during treatment of dysnatremias.

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Section: Clinical Reportsmentioning

confidence: 99%

Edelman Revisited: Concepts, Achievements, and Challenges

et al. 2022

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“…Osmotic diuresis leads to increased losses of both water and monovalent cations. The tendency to develop hypernatremia in this setting is due to the lower cation concentration (sodium plus potassium) in the urine than in plasma which leads to water loss in excess of the cation loss[33,34]. …”

Section: Hypernatremiamentioning

confidence: 99%

Hypertonicity: Clinical entities, manifestations and treatment

Rondon‐Berrios

Argyropoulos

Ing

et al. 2017

WJN

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Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level.

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“…The sum is less than in osmotic diuresis [39]. Therefore, water loss is relatively greater than electrolyte loss [39] and osmotic diuresis inadequately compensated for water loss leads to hypernatremia and hypertonicity [44][45][46].…”

Section: Figure 4: Percent Of Hypertonicitymentioning

confidence: 99%