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  • Measurement of electrolyte free water clearance is extremely useful in understanding the pathophysiology of hyponatremia and hypernatremia.
  • Treatment of hyponatremia should be guided by the degree of symptomatology, rather than the magnitude of the hyponatremia per se.
  • Hyperkalemia should be treated emergently if typical electrocardiographic (ECG) changes are present; hence ECG monitoring is indispensable in this setting.
  • Hypocalcemia need only be treated urgently if it is symptomatic.
  • Severe hypomagnesemia may have significant consequences itself, including cardiac arrhythmias and muscle weakness; lesser degrees of hypomagnesemia often accompany hypokalemia and hypocalcemia and correction of the magnesium deficit facilitates correction of the other electrolyte abnormalities.
  • Severe hyperphosphatemia is seen in the setting of renal failure and/or massive cell lysis.
  • Total body phosphate stores may be significantly reduced and produce organ dysfunction even in the face of normal or minimally decreased serum levels; if suspicion for a depleted state exists, treatment should be given.




Sodium is the chief extracellular cation and is critical to regulating extracellular and intravascular volume. Total body sodium determines clinical volume status, but sodium concentration does not correlate with volume status. Both hypernatremia and hyponatremia occur in the presence of hypo-, eu-, and hypervolemia. The sodium concentration itself is the single ion that best represents serum osmolality; essentially all of the clinically relevant symptoms of dysnatremia are secondary to alterations in osmolality. Hypernatremia is largely synonymous with hyperosmolality, while hyponatremia is generally indicative of hypoosmolality.


Osmolality and tonicity are related but separate concepts. Osmolality measures all of the solutes in solution, while tonicity only includes particles that are unable to cross from the intracellular to the extracellular compartment. It is these particles which are osmotically active, and by drawing water across compartments they may alter cell volume. Sodium and potassium are the primary determinants of tonicity.


Balancing water intake and excretion is the principal means by which the body regulates sodium concentration. Water balance is maintained by thirst and antidiuretic hormone (ADH). Following a water load, osmolality falls and osmoreceptors in the hypothalamus suppress thirst and ADH release. The latter signals the kidney to produce dilute urine to clear the water load. In states of water deprivation (or a solute load) osmoreceptors detect the rise in osmolality and increase thirst and ADH.


The kidney regulates osmolality and sodium concentration by diluting or concentrating urine. Producing dilute urine allows the kidney to clear a water load, raising plasma osmolality. In order to make dilute urine, multiple criteria must be met:


  1. Tubular fluid must be delivered to the diluting segment of the nephron. This can be assured in any patient with adequate effective arterial blood volume (EABV) and a normal or near normal glomerular filtration rate (GFR).

  2. There must be intact sodium resorption in the diluting segments of the kidney (i.e., the thick ascending limb of the loop of Henle [TALH]) and the distal convoluted tubule. Loop and ...

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