Sodium and its anion constitute the primary extracellular solutes determining tonicity. 1 Thus,sodiumisthemajordeterminantofextracellular fluid volume (ECFV). In normal humans, the kidney is primarily responsible for maintaining the homeostasis of total body sodium. With a sodium-restricted diet (40 to 50 mEq/d), urinary sodium concentration decreases to less than 10 mEq/L within three to five days. During this time period, a negative sodium balance approximating 1.5 L of saline occurs in individuals previously on normal sodium diets (150 to 200 mEq/d).Whereasthekidneysensestheresultant decrease in total body sodium during a sodium-restricted diet, and thereby conserves sodium, the most astute clinician would not be able to detect any change in sodium content on physical examination. The normal kidney, therefore, is much better at detecting modest changes in total body sodium and, thus, ECFV.In normal humans, this exquisite modulation of total body sodium by the kidney involves both acute and chronic mechanisms. 1 Sodium restriction is associated with stimulation of the renin-angiotensin-aldosterone system. Angiotensin II then stimulates the sympathetic nervous system. Both angiotensin and ␣-adrenergic stimulation increases tubular sodium reabsorption very rapidly. However, the sodium-retaining effect of aldosterone at the collecting duct takes longer because of the time necessary for new protein synthesis involving the epithelial sodium channel, the Na/KATPase, and the ROMK potassium channel. These effects of aldosterone are best determined by a decrease in urinary sodium concentration and an increase in urinary potassium concentration. While these urinary electrolytes in normal subjects provide a sensitive index of total body sodium, plasma sodium concentration does not. A low plasma sodium concentration can be associated with an increase in total body sodium (heart failure or cirrhosis; hypervolemic hyponatremia), a decrease in total body sodium (diuretic use, primary adrenal insufficiency, or gastrointestinal losses; hypovolemic hyponatremia), or a near-normal total body sodium (syndrome of antidiuretic hormone secretion [SIADH]; euvolemichyponatremia).However,assessment of urinary sodium concentration and, particularly, fractional excretion of sodium (FE Na ) in these hyponatremic disorders is of diagnostic value where there is oliguria. 2
CIRCUMSTANCES WHERE URINARY SODIUM CONCENTRATION DOES NOT REFLECT TOTAL BODY SODIUMThe presence of diuretics negates the value of urinary sodium concentration as an index of total body sodium. When the assessment of ECFV is pivotal for clinical care, the diuretics may be temporarily discontinued (for example, Lasix: last 6 h) and the urinary electrolytes reassessed after the duration of action of the diuretics is passed; 24 to 48 h is generally
ABSTRACTUp to 30% of hospitalized critically ill patients may have a rise in serum creatinine concentration. In addition to history and physical examination, there is diagnostic value in assessing urinary electrolytes, solute exc...