The osmolality test is requested to help evaluate the body's water balance or its ability to produce and concentrate urine. It is used to help investigate low sodium levels (hyponatraemia), to detect the presence of toxins such as methanol and ethylene glycol, and to monitor osmotically active drug therapies such as mannitol. It is also requested to help monitor the effectiveness of treatment for any conditions found to be affecting a person's osmolality.
Serum and urine osmolality are often used together to help investigate causes of hyponatraemia. Hyponatraemia can occur either due to loss of sodium (e.g. in the urine) or increased fluid volume in the bloodstream. Increased fluid may be due to either increased intake of fluids (e.g. excessive drinking) or retention of fluid by the kidneys (observed as decreased urine output). People who chronically drink excessive amounts of water either by choice or due to a psychological condition may have chronic hyponatraemia.
Serum and urine osmolality are also often used together to help investigate causes of either a high or low urine output.
Decreased urine output may also be due to a variety of causes, including:
1) An appropriate response to dehydration
2) Decreased blood flow to the kidneys
3) Damage to tubular cells in the kidneys.
Urine sodium is often requested along with urine osmolality to help determine the cause of hyponatraemia.
Serum osmolality and calculation of the osmolar gap (the difference between measured and calculated osmolality) is used to help detect the presence of ingested toxins such as methanol. The two calculations required are as follows:
Osmolar gap = measured osmolality – calculated osmolality
An osmolal gap of greater than 10 is considered abnormal and represents the presence of an osmotically active substance (such as methanol) in the blood.
Stool osmolality may sometimes be requested to help evaluate chronicdiarrhoea, for which a cause cannot be found. People with watery chronic diarrhoea may have an osmotically active substance that is inhibiting the reabsorption of water by the intestines. Sometimes a stool osmotic gap is calculated.
Physiological mechanisms normally maintain plasma osmolality within a tight range.
A high plasma osmolality may be observed in the following conditions
1. Water depletion (dehydration). This would be accompanied by a reduced urine output.
2. An elevated glucose concentration in the blood (due to uncontrolled Diabetes Mellitus). Urine output also increases in this disorder.
3. Following ingestion of toxins, including alcohol, because they contribute to the number of particles of solute in the plasma.
4. Diabetes Insipidus (“water diabetes”), a condition in which the urine is always very dilute, leading to water loss from the body and possible dehydration. It results from too little ADH or failure of the kidneys to respond to it. Persons with Diabetes Insipidus can have a high plasma osmolality in the presence of inappropriately dilute urine. High concentrations of calcium or low concentrations of potassium in the blood can also impair the kidneys response to ADH, causing symptoms of Diabetes Insipidus.
A decreased plasma osmolality may be seen in water intoxication or any disorder that causes water retention by the kidneys. For example, in a disorder called “Syndrome of Inappropriate ADH Secretion” (SIADH) there is overproduction of anti-diuretic hormone (ADH) by the hypothalamus resulting in a dilute serum (low osmolality). This is normally detected by finding persistently low plasma sodium in the presence of inappropriately concentrated urine.
Calculation of "free water clearance" is sometimes used to help evaluate the ability of the kidney tubules to appropriately concentrate and dilute urine. When urine osmolality is about the same as plasma osmolality, then free water clearance is zero. When blood volume decreases and urine is concentrated, then free water clearance will be negative. When fluid levels are increased and urine is dilute, then free water clearance will be positive..
This article was last reviewed on 18 February 2014. | This article was last modified on 3 June 2016.
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