Urine osmolality

Water-deprivation study results—weight, pulse, urine and plasma osmolality, urine specific gravity, and blood pressure are obtained, and then fluids are... 

Urine osmolality <100 mOsm/kg (anti-diuretic hormone [ADH] suppressed)... 

Beer potomania syndrome or tea and toast diet ° Urine osmolality >100 mOsm/kg (ADH present)... 

If urine osmolality is <300 mOsm/L, may use 0.9% saline if mild signs and symptoms (i.e., headache, nausea, vomiting, and weakness)... 

While some clinical and laboratory findings assist in the general diagnosis of ARF, others are used to differentiate between prerenal, intrinsic, and postrenal ARF. For example, patients with prerenal ARF typically demonstrate enhanced sodium reabsorption, which is reflected by a low urine sodium concentration and a low fractional excretion of sodium. Urine is typically more concentrated with prerenal ARF and there is a higher urine osmolality and urine plasma creatinine ratio compared to intrinsic and postrenal ARF. 

Urine osmolality Greater than Less than... 

Urine osmolality is generally fixed at 300 mOsm/L (300 mmol/L)... 

Fluid restriction is generally unnecessary as long as sodium intake is controlled. The thirst mechanism remains intact in CKD to maintain total body water and plasma osmolality near normal levels. Fluid intake should be maintained at the rate of urine output to replace urine losses, usually fixed at approximately 2 L/day as urine concentrating ability is lost. Significant increases in free water intake orally or intravenously can precipitate volume overload and hyponatremia. Patients with stage 5 CKD require renal replacement therapy to maintain normal volume status. Fluid intake is often limited in patients receiving hemodialysis to prevent fluid overload between dialysis sessions. 

TBW depletion (often referred to as dehydration ) is typically a more gradual, chronic problem compared to ECF depletion. Because TBW depletion represents a loss of hypotonic fluid (proportionally more water is lost than sodium) from all body compartments, a primary disturbance of osmolality is usually seen. The signs and symptoms of TBW depletion include CNS disturbances (mental status changes, seizures, and coma), excessive thirst, dry mucous membranes, decreased skin turgor, elevated serum sodium, increased plasma osmolality, concentrated urine, and acute weight loss. Common causes of TBW depletion include insufficient oral intake, excessive insensible losses, diabetes insipidus, excessive osmotic diuresis, and impaired renal concentrating mechanisms. Long-term care residents are frequently admitted to the acute care hospital with TBW depletion secondary to lack of adequate oral intake, often with concurrent excessive insensible losses. 

Serum creatinine, blood urea nitrogen, urinalysis, urine osmolality, specific gravity. 

Lithium reduces the kidney s ability to concentrate urine and may cause a nephrogenic diabetes insipidus with low urine specific gravity and low osmolality polyuria (urine volume greater than 3 L/day). This may be treated with loop diuretics, thiazide diuretics, or triamterene. If a thiazide diuretic is used, lithium doses should be decreased by 50% and lithium and potassium levels monitored. 

Common laboratory tests are used to classify the cause of ARF. Functional ARF, which is not included in this table, would have laboratory values similar to those seen in prerenal azotemia. However, the urine osmolality-to-plasma osmolality ratios may not exceed 1.5, depending on the circulating levels of antidiuretic hormone. The laboratory results listed under acute intrinsic renal failure are those seen in acute tubular necrosis, the most common cause of acute intrinsic renal failure. 

Patients with SIADH should be treated with 3% saline plus, if the urine osmolality exceeds 300 mOsm/kg, a loop diuretic (furosemide, 40 mg IV every 6 hours). 

FIGURE 78-1. Diagnostic algorithm for the evaluation of hyponatremia. (CHF, congestive heart failure EABV, effective arterial blood volume SIADH, syndrome of inappropriate antidiuretic hormone UNa, urine sodium concentration Uosm, urine osmolality.)... 

Statistical Methods. Means of treatment groups for plasma retention of BSP, plasma osmolality, total plasma protein concentration and urine flow rates were compared by students t test for independent sample means (17). Plasma enzyme activity data were converted to a quantal form and analyzed by the Fischer Exact Probability Test (18). Values greater than 2 standard deviations (P < 0.05) from the control value were chosen to indicate a positive response in treated fish. 

Concentrating ability of the kidney (measurement of urine osmolality assessed following withdrawal of food and water for 24 h free water clearance)... 

A second unusual action of this class of diuretics is their utility in treating nephrogenic diabetes insipidus. Patients who have an adequate supply of ADH but whose kidneys fail to respond to ADH excrete large volumes of very dilute urine, not unlike those who have an ADH deficiency. The thiazides reduce glomerular filtration modestly and decrease positive free water formation (Ch2o), that is, production of dilute urine. These actions combine to cause patients with nephrogenic diabetes insipidus to excrete a somewhat reduced urine volume with increased osmolality. 

The major characteristics of the renal response to mannitol diuresis include a fall in urine osmolality and a decrease in the osmolality of the interstitial fluid of the renal medulla. The quantity of urine formation and Na excretion is generally proportional to the amount of mannitol excreted. Although there is a significant inhibition of proximal water reabsorption, the effects of mannitol on proximal Na+ reabsorption are not marked. 

Fig. 1 Polyuria and impaired urinary concentrating function in aquaporin (AQP) null mice, a Location of AQPs in kidney tubules, b Daily urine output of mice of indicated genotype given free access to food and water, c Urine osmolality before and after a 36-h water deprivation in mice of indicated genotype. Data from Ma et al. (1997, 1998, 2000b)...

Diabetes insipidus Urine volume and osmolality, plasma osmolality... 

At one time, sustained-release preparations were thought to reduce renal toxicity, but more recent evidence has cast doubt on this assumption ( 313). A patient on long-term maintenance lithium should have renal function monitored periodically (i.e., every 12 months) with a urinalysis, BUN, and creatinine. If abnormal, a more intensive evaluation should include 24-hour urine osmolality and creatinine clearance. It is advisable to reduce maintenance lithium to optimal minimal dose-blood levels and, if possible, to avoid concomitant antipsychotics, which may enhance toxicity. Some data support the use of a once-a-day dose schedule to minimize peak lithium concentrations over a 24-hour period (314). 

Hyponatmemia is common with the thiazides and to a lesser extent with the loop diuretics. It occurs when the osmolality of the urine persistently exceeds that of the fluid intake and is associated with the inability of the kidney to produce a dilute urine. It is not usually severe. The origin is multifactorial and involves unrestricted fluid intake and increased ADH activity due to volume depletion. Co-administration of dipsogenic drugs, such as the tricyclic antidepressants, or those with ADH-like effects, such as chlorpropamide, can exacerbate the problem. There are rare occasions when hyponatraemia (Nan- concentration less than 100 mmol-L-l) can be of sufficient severity to be life threatening. 

Urea concentration in the medulla plays an important role maintaining the high osmolarity of the medulla and in the concentration of urine. ADH secretion is regulated by serum osmolality and by volume status. A new class of drugs, the vaptans (see under Agents That Alter Water Excretion), are ADH antagonists. 

An 87-year-old woman received intra-articular betamethasone (Diprophos) 7 mg on three occasions for painful knee joints over 6 months. Six weeks after the last injection she developed diffuse pain and contractures in the legs, fatigue, nausea, abdominal pain, and weight loss of 6 kg. Both knee joints were tender but there was no effusion. Her serum sodium concentration was 123 mmol/1, serum osmolality 254 mosmol/kg, urine sodium 136 mmol/1, and urinary osmolality 373 mosmol/kg. The syndrome of inappropriate antidiuretic hormone secretion was diagnosed, but despite treatment she remained drowsy and hyponatremic. About a week later, she developed hypotension and symptoms of an acute abdomen. Further investigations showed that her basal cortisol concentration was low (36 nmol/1) but it increased to 481 nmol/1 after a short tetracosactide test, consistent with acute adrenal crisis. She recovered rapidly after treatment with oral hydrocortisone, but still required glucocorticoid substitution several months later. 

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