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The difficulty that nonnephrologists sometimes have with the differential diagnosis of hyponatremic patients often results from misinterpreting the significance of measured and calculated serum osmolalities, effective serum osmolalities (tonicities), and the influence of various normal (eg, serum urea nitrogen) and abnormal (eg, ethanol) solutes. Among the more commonly held misconceptions are that high serum urea or alcohol levels will, by analogy with glucose, cause hyponatremia, and that a normal (or elevated) measured serum osmolality in a hyponatremic patient excludes the possibility of hypotonicity. This article describes typical and deliberately comparative data of the serum levels of sodium, glucose, urea nitrogen, and mannitol and/or ethanol (if present); calculated and measured osmolality; effective osmolality; and the potential risk of hypotonicity-induced cerebral edema for each of 6 prototypical hyponatremic states. This provides a helpful educational tool for untangling these interrelationships and for clarifying the differences among various hyponatremic conditions.

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We evaluated renal handling and plasma potassium (K) and aldosterone (PA) responses to acute oral K loading in 11 patients with tubulointerstitial renal disease (creatinine clearance 32 +/- 5 ml/min [SE] ) and 13 control subjects (creatinine clearance 123 +/- 5). After 4 days of a 10 mEq Na, 50 mEq K diet, the subjects received 0.5 mEq KCl/kg body weight. Prior to KCl there were no differences between the groups in plasma K or urinary K excretion (UKV). In the 4 hr following KCl, less of the load (13 +/- 4%) was excreted by patients than control subjects (54 +/- 5%; P less than 0.001). Plasma K at 3 hr post KCl, and the amount of retained potassium translocated into the intracellular compartment (patients 14 +/- 3; control subjects 7 +/- 2 mEq; P less than 0.05) were significantly higher in the patients than in control subjects. After KCl, PA levels increased in both groups, and the increments in the patients tended to exceed those of controls; patients with hypoaldosteronism, however, transferred less K into cells and had an even greater impairment of renal K excretion than those with normal baseline PA. The results indicate that the impaired response to an acute oral potassium load in chronic renal failure is related primarily to defective renal rather than extrarenal mechanisms.