A patient is suspected to have diabetes insipidus, a disorder in which the body
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A patient is suspected to have diabetes insipidus, a disorder in which the body does not concentrate the urine sufficiently (possibly due to a lack of antidiuretic hormone, ADH). A urine specimen is sent to the lab for urinalysis, specifically a determination of the specific gravity of the urine. The urine must have a specific gravity less than 1.008 in order to validate the diagnosis of diabetes insipidus. Does the patient possibly have diabetes insipidus if 10.00mL of the urine has a mass of 9.9985g?Explanation / Answer
Diabetes insipidus (DI) is a disorder in which polyuria (urine output exceeding 3 liters per day in adults) due to decreased collecting tubule water re-absorption is induced by either decreased secretion of antidiuretic hormone (ADH) (central DI) or resistance to its renal effects (nephrogenic DI). In most patients, degree of polyuria is primarily determined by the degree of ADH deficiency or resistance. Hence, the urine output may range from 2 L/day with mild partial DI to over 10 to 15 L/day in patients with severe disease.
Normally, an increase in water intake sequentially lowers plasma osmolality, decreases ADH secretion and reduces collecting tubule permeability to water; as a result, the excess water is rapidly excreted in a dilute urine. However, changes in water intake do not result in appropriate changes in urine output in patients with DI because ADH release or effect is relatively fixed. Instead, urine output is relatively constant, regardless of water intake, unless dietary salt and/or protein intake change. Assume, for example, that a patient has moderately severe nephrogenic DI which, because of the ADH reisstance, will not respond to hormone replacement. The urine osmomolaility in this patient cannot be raised above 150 mosmol/kg (normal maximum urine osmolality is 900 to 1200 mosmol/kg). in this setting, excretion of solutes (primarily sodium and potassium salts and urea) is the major determinant of urine output. If solute excretion is in the usual range (e.g. 750 mosmol/kg), then daily urine output will be 5 L/day (750 / 150 =5). In this patient, urine output will rise if solute excretion is increased and will fall if solute excretion is reduced).
Therefore, one way to diminish polyuria in patients with DI is to restrict salt and protein intake, which in turn will reduce solute load and solute excretion. If, for example, solute excretion fell to 525 mosmol/day, the urine output would fall to 3.5 L/day. On the other hand, degree of poluria can be enhanced by increasing solute excretion. Each gram of protein catabolized produces about 170 mg of urea. So, a protein load of 70 g will generate approximately 11.2 g of urea nitrogen, which corresponds to approximately 400 mmol of urea. At a typical osmolality of 300 to 500 mosmol/kg in solute diureses, an increased urea excretion of this magnitude will require a urine output of 0.8 to 1.3 liters.
Signs of diabetes insipidus:
There may be signs of dehydration and the bladder can be grossly enlarged and palpable.
24-hour urinary collection will show urine volume >3 litres/24 hours.
If urine osmolality is <200 mOsmol/kg in presence of polyuria (>3 L/day), diabetes insipidus is suspected.
Standard method for diagnosing diabetes insipidus is a water deprivation test. Water deprivation lasts 4-18 hours, with hourly measurements of body weight and urine osmolality, until 2-3 consecutive samples vary by <30mOsm/kg (or <10%) or until patient loses 5% of body weight.
At this point, serum ADH level is measured and then 5 units of ADH is injected. Urine osmolality is then measured 30-60 minutes later.
If the patient is producing more than 10 L of urine per day, then water restriction is only done during the day under close supervision and is not done after midnight. Spot urine samples for measuring osmolality are collected hourly, beginning at 7:00 a.m., until 3 successive measurements are within 50 to 100 mmol/kg of each other. Blood is then drawn to measure serum osmolality and plasma vasopressin levels. Next, vasopressin is administered and urine is obtained for osmomolality every 30 minutes during the next three hours. This is done to account for a bladder with a large capacity and/or with time-lag required to reconstruct medullary gradient.
In patients with complete diabetes insipidus, water deprivation increases plasma osmolality but urine osmolality remains below 290 mmol/kg and does not increase. In those with complete central diabetes insipidus, urine osmolality will increase by approximately 200 mmol/kg in response to exogenous vasopressin. In contrast, vasopressin will not increase urine osmomolaity in patients with complete NDI. In Central Diabetes Insipidus, urine osmolality remains less than (<) plasma osmolality after dehydration. After ADH injection, urine osmolality increases by more than 50%.
In Nephrogenic Diabetes Insipidus, urine osmolality remains less than plasma osmolality. After ADH injection, urine osmolality increases by less than 50%.
In patients with partial diabetes insipidus, water deprivation will increase urine osmolality to 400 to 500 mmol/kg. administration of exogenous vasopressin will increase urine osmolality by approximately 200 mmol/kg in patients with partial central diabetes insipidus but not in patients with partial NDI. A water deprivation study will not distinguish between patients with partial NDI and those with primary polydipsia. Measuring urine volume during a water deprivation test is not useful.
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