Test Catalog

Test ID: SAT24    
Supersaturation Profile, 24 Hour, Urine

Useful For Suggests clinical disorders or settings where the test may be helpful

Diagnosis and management of patients with renal lithiasis:

-In patients who have a radiopaque stone, for whom stone analysis is not available, the supersaturation data can be used to predict the likely composition of the stone. This may help in designing a treatment program

-Individual components of the supersaturation profile can identify specific risk factors for stones

-During follow-up, changes in the urine supersaturation can be used to monitor the effectiveness of therapy by confirming that the crystallization potential has indeed decreased

-Urine ammonium can be used to evaluate renal excretion of acid and urine pH

-The protein catabolic rate, calculated from the urine urea nitrogen, can be used to estimate a patient's protein intake

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Urine is often supersaturated, which favors precipitation of several crystalline phases such as calcium oxalate, calcium phosphate, and uric acid. However, crystals do not always form in supersaturated urine because supersaturation is balanced by crystallization inhibitors that are also present in urine. Urinary inhibitors include ions (eg, citrate) and macromolecules but remain poorly understood.

 

Urine supersaturation is calculated by measuring the concentration of all the ions that can interact (potassium, calcium, phosphorus, oxalate, uric acid, citrate, magnesium, sodium, chloride, sulfate, and pH). Once the concentrations of all the relevant urinary ions are known, a computer program can calculate the theoretical supersaturation with respect to the important crystalline phases (eg, calcium oxalate).(1)

 

Since the supersaturation of urine has been shown to correlate with stone type,(2) therapy is often targeted towards decreasing those urinary supersaturations that are identified. Treatment strategies include alterations in diet and fluid intake as well as drug therapy, all designed to decrease the urine supersaturation.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.

SUPERSATURATION REFERENCE MEANS (Delta G: DG)

Calcium oxalate: 1.77 DG

Brushite: 0.21 DG

Hydroxyapatite: 3.96 DG

Uric acid: 1.04 DG

Sodium urate: 1.76 DG

 

INDIVIDUAL URINE ANALYTES

OSMOLALITY

0-11 months: 50-750 mOsm/kg

> or =12 months: 150-1,150 mOsm/kg

 

pH

4.5-8.0

 

ALL REFERENCE RANGES BELOW ARE BASED ON 24-HOUR COLLECTIONS.

 

SODIUM

41-227 mmol/24 hours

Reference values have not been established for patients <16 years of age.

 

POTASSIUM

17-77 mmol/24 hours

Reference values have not been established for patients <16 years of age.

 

CALCIUM

Males: <250 mg/24 hours

Females: <200 mg/24 hours

Reference values have not been established for patients <18 years and >83 years of age

 

MAGNESIUM

51-269 mg/24 hours

Reference values have not been established for patients <18 years and >83 years of age

 

CHLORIDE

40-224 mmol/24 hours

Reference values have not been established for patients <16 years of age.

 

PHOSPHORUS

<1,100 mg/24 hours

 

SULFATE

7-47 mmol/24 hours

 

CITRATE EXCRETION

0-19 years: not established

20 years: 150-1,191 mg/24 hours

21 years: 157-1,191 mg/24 hours

22 years: 164-1,191 mg/24 hours

23 years: 171-1,191 mg/24 hours

24 years: 178-1,191 mg/24 hours

25 years: 186-1,191 mg/24 hours

26 years: 193-1,191 mg/24 hours

27 years: 200-1,191 mg/24 hours

28 years: 207-1,191 mg/24 hours

29 years: 214-1,191 mg/24 hours

30 years: 221-1,191 mg/24 hours

31 years: 228-1,191 mg/24 hours

32 years: 235-1,191 mg/24 hours

33 years: 242-1,191 mg/24 hours

34 years: 250-1,191 mg/24 hours

35 years: 257-1,191 mg/24 hours

36 years: 264-1,191 mg/24 hours

37 years: 271-1,191 mg/24 hours

38 years: 278-1,191 mg/24 hours

39 years: 285-1,191 mg/24 hours

40 years: 292-1,191 mg/24 hours

41 years: 299-1,191 mg/24 hours

42 years: 306-1,191 mg/24 hours

43 years: 314-1,191 mg/24 hours

44 years: 321-1,191 mg/24 hours

45 years: 328-1,191 mg/24 hours

46 years: 335-1,191 mg/24 hours

47 years: 342-1,191 mg/24 hours

48 years: 349-1,191 mg/24 hours

49 years: 356-1,191 mg/24 hours

50 years: 363-1,191 mg/24 hours

51 years: 370-1,191 mg/24 hours

52 years: 378-1,191 mg/24 hours

53 years: 385-1,191 mg/24 hours

54 years: 392-1,191 mg/24 hours

55 years: 399-1,191 mg/24 hours

56 years: 406-1,191 mg/24 hours

57 years: 413-1,191 mg/24 hours

58 years: 420-1,191 mg/24 hours

59 years: 427-1,191 mg/24 hours

60 years: 434-1,191 mg/24 hours

>60 years: not established

 

OXALATE

0.11-0.46 mmol/24 hours

 

URIC ACID

Diet-dependent: <750 mg/24 hours

 

CREATININE

Normal values mg per 24 hours:

Males: 955-2936 mg/24 hours

Females: 601-1689 mg/24 hours

Reference ranges for male and female patients <18 and >83 years of age have not been established.

 

The expected urine creatinine excretion per 24 hours:

Males: 13-29 mg/kg of body weight/24 hours

Females: 9-26 mg/kg of body weight/24 hours

 

Reference ranges for male and female patients <18 and >83 years of age have not been established.

Note: To convert to mg/kg of body weight/24 hours, divide the mg/24 hours result by body weight in kg.

 

AMMONIUM

15-56 mmol/24 hour

Reference values have not been established for patients <18 years and >77 years of age.

 

UREA NITROGEN

5.0-16.0 g/24 hours

 

PROTEIN CATABOLIC RATE

56-125 g/24 hours

Interpretation Provides information to assist in interpretation of the test results

Delta G (DG), the Gibbs free energy of transfer from a supersaturated to a saturated solution is negative for undersaturated solutions and positive for supersaturated solutions. In most cases the supersaturation levels are slightly positive even in normal individuals but are balanced by an inhibitor activity.

 

While the DG of urine is often positive, even in the urine of nonstone formers, on average, the DG is even more positive in those individuals who do form kidney stones. The "normal" values were simply derived by comparing urinary DG values for the important stone-forming crystalline phases between a population of stone formers and a population of non-stone formers. Those DG values that are outside the expected range in a population of non-stone formers are marked "abnormal."

 

If the urine citrate is low, secondary causes should be excluded including hypokalemia, renal tubular acidosis, gastrointestinal bicarbonate losses (eg, diarrhea or malabsorption), or an exogenous acid load (eg, excessive consumption of meat protein).

 

A normal or increased citrate value suggests that potassium citrate may be a less effective choice for treatment of a patient with calcium oxalate or calcium phosphate stones.

 

An increased urinary oxalate value may prompt a search for genetic abnormalities of oxalate production (ie, primary hyperoxaluria). Secondary hyperoxaluria can result from diverse gastrointestinal disorders that result in malabsorption. Milder hyperoxaluria could result from excess dietary oxalate consumption, or reduced calcium (dairy) intake, perhaps even in the absence of gastrointestinal disease. High urine ammonium and low urinary pH suggests ongoing gastrointestinal losses. Such patients are at risk of uric acid and calcium oxalate stones.

 

Low urine ammonium and high urine pH suggests renal tubular acidosis. Such patients are at risk of calcium phosphate stones.

 

Patients with calcium oxalate and calcium phosphate stones are often treated with citrate to raise the urine citrate (a natural inhibitor of calcium oxalate and calcium phosphate crystal growth). However, since citrate is metabolized to bicarbonate (a base) this drug can also increase the urine pH. If the urine pH gets too high with citrate treatment, one may unintentionally increase the risk of calcium phosphate stones. Monitoring the urine ammonium is one way to titrate the citrate dose and avoid this problem. A good starting citrate dose is about one-half of the urine ammonium excretion (in mEq of each). One can monitor the effect of this dose on urine ammonium, citrate, and pH values, and adjust the citrate dose based upon the response. A fall in urine ammonium should indicate whether the current citrate is enough to partially (but not completely) counteract the daily acid load of that given patient.

 

The protein catabolic rate is calculated from urine urea. Under routine conditions, the required protein intake is often estimated as 0.8 g/ kg body weight.

 

The results can be used to determine the likely effect of a therapeutic intervention on stone-forming risk. For example, taking oral potassium citrate will raise the urinary citrate excretion, which should reduce calcium phosphate supersaturation (by reducing free ionic calcium), but citrate administration also increases urinary pH (because it represents an alkali load) and a higher urine pH promotes calcium phosphate crystallization. The net result of this or any therapeutic manipulation could be assessed by collecting a 24-hour urine and comparing the supersaturation calculation for calcium phosphate before and after therapy.

 

Important stone-specific factors:

-Calcium oxalate stones: urine volume, calcium, oxalate, citrate, and uric acid excretion are all risk factors that are possible targets for therapeutic intervention.

-Calcium phosphate stones (apatite or brushite): urinary volume, calcium, pH, and citrate significantly influence the supersaturation for calcium phosphate. Of note, a urine pH of less than6 may help reduce the tendency for these stones to form.

-Uric acid stones: urine pH, volume, and uric acid excretion levels influence the supersaturation. Urine pH is especially critical, in that uric acid is unlikely to crystallize if the pH is greater than 6.

-Sodium urate stones: alkaline pH and high uric acid excretion promote stone formation.

 

A low urine volume is a universal risk factor for all types of kidney stones.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

The urine is often supersaturated with respect to the common crystalline constituents of stones, even in nonstone formers.

 

Individual interpretation of the supersaturation values in light of the clinical situation is critical. In particular, treatment may reduce the supersaturation with respect to one crystal type, but increase the supersaturation with respect to another. Therefore, the specific goals of treatment must be considered when interpreting the test results.

Clinical Reference Recommendations for in-depth reading of a clinical nature

1. Werness PG, Brown CM, Smith LH, Finlayson B: EQUIL2: a BASIC computer program for the calculation of urinary saturation. J Urol 1985;134:1242-1244

2. Parks JH, Coward M, Coe FL: Correspondence between stone composition and urine supersaturation in nephrolithiasis. Kidney Int 1997;51:894-900

3. Finlayson B: Calcium stones: Some physical and clinical aspects. In Calcium Metabolism in Renal Failure and Nephrolithiasis. Edited by DS David. New York, John Wiley and Sons, 1977, pp 337-382

Special Instructions Library of PDFs including pertinent information and forms related to the test