Variations in the urine osmolality (Uosm) play a central role in the regulation of the plasma osmolality (Posm) and Na+ concentration. This response is mediated by osmoreceptors in the hypothalamus that influence both thirst and the secretion of ADH. (See "Chapter 6B: Antidiuretic hormone and water balance".) After a water load, for example, there is a transient reduction in the Posm, leading to suppression of ADH release. This diminishes water reabsorption in the collecting tubules, resulting in the excretion of the excess water in a dilute urine. Water restriction, on the other hand, sequentially raises the Posm, ADH secretion, and renal water reabsorption, resulting in water retention and the excretion of a concentrated urine.
These relationships allow the Uosm to be helpful in the differential diagnosis of both hyponatremia and hypernatremia (see Chap. 23 and 24). Hyponatremia with hypoosmolality should virtually abolish ADH release. As a result, a maximally dilute urine should be excreted, with the Uosm falling below 100 mosmol/kg. If this is found, then the hyponatremia is probably due to excess water intake at a rate that exceeds normal excretory capacity (a rare disorder called primary polydipsia). Much more commonly, the Uosm is inappropriately high and the hyponatremia results from an inability of the kidneys to excrete water normally. Lack of suppression of ADH release, due to volume depletion or the syndrome of inappropriate ADH secretion, is the most common cause of this problem. (See "Evaluation of adults with hyponatremia".)
In contrast, hypernatremia should stimulate ADH secretion, and the Uosm should exceed 600 to 800 mosmol/kg. If a concentrated urine is found, then extrarenal water loss (from the respiratory tract or skin) or the administration of Na+ in excess of water is responsible for the elevation in the plasma Na+ concentration. On the other hand, a Uosm below that of the plasma indicates primary renal water loss due to ADH lack or resistance. (See "Etiology and evaluation of hypernatremia".)
The Uosm (in addition to the FENa) also may be helpful in distinguishing volume depletion from postischemic acute tubular necrosis as the cause of acute renal failure. ADH levels tend to be elevated in both disorders, because hypovolemia is a potent stimulus to the release of ADH (see page 000). However, tubular dysfunction in acute tubular necrosis impairs the response to ADH, leading to the excretion of urine with an osmolality that is generally less than 400 mosmol/kg [1,2]. In comparison, the Uosm may exceed 500 mosmol/kg with hypovolemia alone if there is no underlying renal disease. Thus, a high Uosm essentially excludes the diagnosis of acute tubular necrosis. The finding of an isosmotic urine, however, is less useful diagnostically. It is consistent with acute tubular necrosis but does not rule out volume depletion, since there may be a concomitant impairment in concentrating ability, a common finding in the elderly or in patients with severe reductions in glomerular filtration rate * [3,4]*. (See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury (acute renal failure)".)
Urine specific gravity — The solute concentration of the urine (or other solution) also can be estimated by measuring its specific gravity, which is defined as the weight of the solution compared with that of an equal volume of distilled water. Plasma is approximately 0.8 to 1.0 percent heavier than water and therefore has a specific gravity of 1.008 to 1.010. Specific gravity is proportional to the weight, as well as the number, of particles in the solution, whereas osmolality is proportional only to the number of particles in solution. Thus, the relationship of specific gravity to osmolality is dependent upon the molecular weights of the solutes.