Laboratory Result Interpretations

psychogenic polydipsia

serum sodium is reduced below 135 mEq/L

Because the consumed water is excreted by the kidneys, the urine is also dilute in this ion.

In fact, the osmolality of urine will be low—that is, less than 300 mOsm/kg.

Often accompanying hyponatremia are low values of the hematocrit and low values of BUN

Urinalysis in the fluid-restricted patient will reveal urinary sodium of less than 25 mEq/L and low osmolalities.

The potassium may also be low, although it often remains within the reference range.

Because mainly water is excreted in urine in this condition, the total 24-hour sodium excre- tion will be low

block the chloride pump in the loop of Henle, thereby blocking the formation of the ion gra- dients via the countercurrent multiplier, necessary for water conservation. Thus, water is lost.

Also, because sodium is no longer retained because it follows chloride in the loop, it also is depleted from serum.

Thus, unlike in overhydration, the total 24-hour sodium excretion is high

pattern resembles overhydration (dilute serum and urine), except that loop diuretics cause severe potassium deple- tion unless the diuretic is combined with a potassium-sparing diuretic such as triamterene.

Combined hyponatremia and hypokalemia with a high uri- nary sodium and potassium 24-hour excretion point to diuretic use.

In this condition, secondary to head trauma, seizures, other CNS diseases, and neoplastic conditions, espe- cially lung, breast, and ovarian cancers that secrete ADH-like hormones, the serum sodium is depressed due to the excess retention of water in the collecting ducts.

This results in depletion of water in the renal tubules, thereby concentrating the urine.

Therefore, while the serum is dilute in sodium (hypotonic), the urine is concentrated to levels of over 40 mEq/L and the urine osmolality exceeds 300 mOsm/kg, while the serum osmolal- ity is less than 280 mOsm/kg.

This condition is second- ary to Addison disease and AIDS-related hypoadrenalism.

Without aldo- sterone, the Na+–K+ and Na+–H+ exchange in the distal convoluted tubules and collecting ducts does not occur.

Therefore, serum sodium concentra- tion is reduced, while serum potassium concentration increases, and there is a mild metabolic acidosis.

Urinary sodium increases but not to the high levels seen in SIADH, and the osmolality of urine is also not so elevated as in SIADH.

This rare condition resem- bles diuretic use except that the hyponatremia is not corrected with fluid restriction.

This syndrome is actually a complex of diseases, each of which is caused by mutations of genes that encode ion transporter proteins in the thick portion of the ascending loop of Henle.

caused by absence or mutations of the Na-K-2Cl symporter protein (SLC12A2 or NKCC2 gene) or the ROMK/KCNJ1- encoded potassium channel protein.

the CLCNKB gene–encoded chloride channel protein is defective.