Urine specific gravity?

(from page 868-9, Mosby's Diagnostic and Laboratory Test Reference, 4th edition, by Kathleen Deska Pagana and Timothy James Pagana, 1999)

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"The specific gravity is a measure of the concentration of particles, including wastes and electrolytes, in the urine. A high specific gravity indicates a concentrated urine; a low specific gravity indicates dilute urine. Specific gravity refers to the weight of the urine compared to that of distilled water (which has a specific gravity of 1.000). It is the particles in the urine that give the urine it weight or specific gravity.

The specific gravity is used to evaluate the concentrating and excretory power of the kidney. Renal disease tends to diminish the concentrating capability of the kidney. As a result, chronic renal diseases are associated with a low specific gravity. The specific gravity must be interpreted in light of the presence or absence of glycosuria and proteinuria. The specific gravity is also a measurement of the hydration status of the patient. An overhydrated patient will have a more dilute urine with a lower specific gravity. The specific gravity of the urine in a dehydrated patient can be expected to be abnormally high. The measurement of urine specific gravity is easier and more convenient than the measurement of osmolality. The specific gravity correlates roughly with osmolality. Knowledge of the specific gravity is needed for interpreting the results of most parts of the urinalysis. Specific gravity is usually evaluated by the use of a refractometer or a dipstick.

Specific gravity is increased in dehydration, pituitary tumor or trauma that causes siadh, decrease in renal blood flow (as in heart failure, renal artery stenosis, or hypotension), glycosuria and proteinuria, water restriction, fever, excessive sweating, vomiting, diarrhea, and x-ray contrast dye.

Specific gravity is decreased in overhydration, diabetes insipidus, renal failure, diuresis, hypothermia, glomerulonephritis and pyelonephritis."

(from page 23-26, Fluid & Electrolyte Balance: Nursing Considerations, 4th edition, by Norma M. Metheny)

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"Urine specific gravity measures the ability of the kidneys to concentrate urine. In this test, the concentration of urine is compared with the 1.000 specific gravity of distilled water. Because urine contains electrolytes and other substances, its specific gravity is greater than 1.000. The range of specific gravity in urine is from 1.003 to 1.035; most random specimens are between 1.012 and 1.025. Typical urine osmolality (another measure of urine concentration) ranges from 500 to 800 mosm/kg; extreme ranges are from 50 to 1,400 mosm/kg.

Urinary specific gravity is elevated when there is a fluid volume deficit, as the healthy kidney seeks to retain needed fluid, thus excreting solutes in a small concentrated urine volume. However, one should be aware that heavy molecules not normally present in large quantities in urine can falsely affect specific gravity readings. For example, glucose, albumin, or radiocontrast dyes will elevate urinary specific gravity out of proportion to the actual concentration. Therefore, it is more accurate to measure urine osmolality in patients with glycosuria, proteinuria, or recent use of radiopaque dyes.

Specific gravity can be measured with a refractometer, a dipstick that has a reagent area for specific gravity, or with a urinometer. Freshly voided urine specimens at room temperature are desirable for testing specific gravity. Refrigerated samples may have falsely elevated readings, as may specimens exposed to excessive heat and dryness (a result of evaporation). Ideally, urinary specific gravity should be measured immediately after the specimen is collected; however, in some situations this is not possible."

"Diabetes insipidus (di) and syndrome of inappropriate antidiuretic hormone (adh) secretion (siadh) are disorders of water balance caused by adh disturbances at opposite ends of a continuum. In siadh, excessive adh secretion causes water retention. The opposite happens in di, which is characterized by large urine volumes due to inadequate amounts of adh." (metheny, page 10)

Clinical Manifestations of Diabetes Insipidus

Excessive urinary output regardless of fluid intake:

• Urinary output usually ranges between 3 to 20 liters/24 hours (depending on the severity of the pathologic process)
• Urinary output often exceeds 200 ml/hour
• In complete di, urinary specific gravity is less than 1.010, urine osmolality less than 300 mosml/liter
• In partial di, urinary specific gravity and urinary osmolality are somewhat higher (such as 1.010 - 1.023 and 300-800 mosm/liter, respectively)
• Inability of kidneys to concentrate urine by fluid restriction (a common test for this disorder)
• Intense thirst in the alert patient, resulting in an intake that corresponds to the urinary volume
• Serum osmolality and sodium levels greater than normal if water intake does not match urinary losses (severe hypovolemia may occur with inadequate fluid intake)

(page 78, Metheny)

Assessment for Diabetes Insipidus (di)

Be aware of patients at risk for di

• Central di
  • head trauma (particularly with fractures at the base of the skull or surgical procedures near the pituitary)
  • cerebral infections
  • brain tumors
• Nephrogenic di
  • hypokalemia
  • hypercalcemia
  • certain drugs (such as lithium and demeclocycline)
• Maintain an accurate I & O record for at-risk patients
  • Look for a significantly greater output than intake (a danger signal of impending hypernatremia). Fortunately, many patients keep themselves "in balance" by drinking about as much as they urinate. It is helpful to calculate and record cumulative amounts for several days to obtain a more accurate account of the patient's fluid balance status, particularly if onset of polyuria was insidious.
• Be alert for polyuria in at-risk patients.
  • It is frequently necessary to measure hourly urine volumes in such individuals to foster early detection. For example, a frequent directive in the care of postoperative neurosurgical patients is to report a urine volume greater than 200 ml in each of 2 consecutive hours or greater than 500 ml in a 2-hour period.
• Monitor urinary specific gravity in at-risk patients.
  • A persistently dilute urine is a hallmark of di. (the specific gravity may be as low as 1.005.)
• Monitor serum sodium levels at least once a day (more often as indicated) in at-risk patients.
  • Look for hypernatremia (serum sodium greater than 145 meq/liter). Once vasopressin therapy has been initiated, look for hyponatremia (a possible rebound effect).
• Monitor body weights
  • Look for weight loss paralleling polyuria. Maintaining a weight chart helps detect excessive fluid loss, particularly when i & o records are in doubt (as may occur in incontinent patients)." (page 81, metheny)

(from page 497, Pathophysiology: A 2-in-1 Reference for Nurses by Springhouse, Springhouse Publishing Company Staff)

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"Diabetes insipidus is related to an insufficiency of adh, leading to polyuria and polydipsia. The three forms of diabetes insipidus are neurogenic, nephrogenic, and psychogenic.

Neurogenic, or central, diabetes insipidus is an inadequate response of adh to plasma osmolarity, which occurs when an organic lesion of the hypothalamus, infundibular stem, or posterior pituitary partially or completely blocks adh synthesis, transport, or release. The many organic lesions that can cause diabetes insipidus include brain tumors, hypophysectomy, aneurysms, thrombosis, skull fractures, infections, and immunologic disorders. Neurogenic diabetes insipidus has an acute onset. A three-phase syndrome can occur, which involves progressive loss of nerve tissue and increased diuresis, normal diuresis, and polyuria and polydipsia, the manifestation of permanent loss of the ability to secrete adequate adh.

Nephrogenic diabetes insipidus is caused by an inadequate renal response to adh. The collecting duct permeability to water doesn't increase in response to adh. Nephrogenic diabetes insipidus is generally related to disorders and drugs that damage the renal tubules or inhibit the generation of cyclic adenosine monophosphate in the tubules, preventing activation of the second messenger. Causative disorders include pyelonephritis, amyloidosis, destructive uropathies, polycystic disease, and intrinsic renal disease. Drugs include lithium (eskalith), general anesthetics such as methoxyflurane, and demeclocycline (declomycin). In addition, hypokalemia or hypercalcemia impairs the renal response to adh. A rare genetic form of nephrogenic diabetes insipidus is a x-linked recessive trait.

Psychogenic diabetes insipidus is caused by an extremely large fluid intake, which may be idiopathic or related to psychosis or sarcoidosis. The polydipsia and resultant polyuria wash out adh more quickly than it can be replace. Chronic polyuria may overwhelm the renal medullary concentration gradient, rendering patients partially or totally unable to concentrate urine.

Regardless of the cause, insufficient adh causes the immediate excretion of large volumes of dilute urine and consequent plasma hyperosmolality. In conscious individuals, the thirst mechanism is stimulated, usually for cold liquids. With severe adh deficiency, urine output may be greater than 12 liters/day, with a low specific gravity. Dehydration develops rapidly if fluids aren't replaced."

Links on specific gravity of urine:

• What Is Urinalysis?