26580 Supersaturation Profile, 24 Hour, Urine (SUP24)

​​​​​​​​​​Brushite Crystal, Calcium Oxalate Crystal, Hydroxyapatite Crystal, Kidney Stone Disease, Kidney Stone Profile, SAT24, Stone Risk Profile, Uric Acid Crystals

​​Calcium Oxalate Crystal, Brushite Crystal, Hydroxyapatite Crystal, Uric Acid Crystal,  Sodium, Potassium, Calcium, Magnesium, Chloride, Phosphorus, Sulfate, Citrate Excretion, Oxalate, pH, Uric Acid, Creatinine, Osmolality, Ammonium, Urea Nitrogen, Protein Catabolic Rate, Collection Duration, Volume

Diagnosis and management of patients with renal lithiasis:

    -Predicting the likely composition of the stone, in patients who have a radiopaque stone, for whom stone analysis is not available.  

     -May help in designing a treatment program.

Aiding in identification of specific risk factors for stones using a 24-hour urine collection

Monitoring the effectiveness of therapy by confirming that the crystallization potential has indeed decreased

Evaluating kidney excretion of acid and urine pH

Estimating a patient's protein intake

 Urine is often supersaturated with respect to the common crystalline constituents of stones, even in non-stone 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.

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 present in the 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 the urinary supersaturations identified. Treatment strategies include alterations in diet and fluid intake as well as drug therapy; all designed to decrease the urine supersaturation.

 SUPERSATURATION REFERENCE MEANS (Delta G: DG)

MEN:
Calcium oxalate: 1.89 DG
Brushite: 0.46 DG
Hydroxyapatite: 4.19 DG
Uric acid: 1.18 DG

​WOMEN:
Calcium oxalate: 1.59 DG
Brushite: 0.11 DG
Hydroxyapatite: 3.62 DG
Uric acid: 0.89 DG

INDIVIDUAL URINE ANALYTES

OSMOLALITY, 24 HOUR, URINE
0-11 months: 50-750 mOsm/kg
> or =12 months: 150-1,150 mOsm/kg
 
pH, 24 HOUR, URINE
4.5-8.0
 
SODIUM, 24 HOUR, URINE
> or =18 years: 22-328 mmol/24 hours
 
POTASSIUM, 24 HOUR, URINE
> or =18 years: 16-105 mmol/24 hours
 
CALCIUM, 24 HOUR, URINE
Males: <250 mg/24 hours
Females: <200 mg/24 hours
 
MAGNESIUM, 24 HOUR, URINE
51-269 mg/24 hours
 
CHLORIDE, 24 HOUR, URINE
> or =18 years: 34-286 mmol/24 hours
 
PHOSPHORUS, 24 HOUR, URINE
> or =18 years: 226-1,797 mg/24hours

SULFATE, 24 HOUR, URINE
7-47 mmol/24 hours

CITRATE EXCRETION, 24 HOUR, URINE
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, 24 HOUR, URINE
0.11-0.46 mmol/24 hours
9.7-40.5 mg/24 hours
Reference values have not been established for patients who are younger than 16 years of age.

URIC ACID, 24 HOUR, URINE
Males: > or =18 years: 200-1,000 mg/24 hours
Females: > or =18 years: 250-750 mg/24 hours

CREATININE, 24 HOUR, URINE
Males: > or =18 years: 930-2,955 mg/24 hours
Females: > or =18 years: 603-1,783 mg/24 hours

AMMONIUM, 24 HOUR, URINE
15-56 mmol/24 hour
Reference values have not been established for patients who are older than 77 years of age.

UREA NITROGEN, 24 HOUR, URINE
> or = 18 years: 7-42 g/24h

PROTEIN CATABOLIC RATE, 24 HOUR, URINE
56-125 g/24 hours

​ 

​ 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 non-stone formers, on average, the DG is more positive in those individuals who do form kidney stones. The reference values were 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 suggest ongoing gastrointestinal losses. Such patients are at risk of uric acid and calcium oxalate stones.
Low urine ammonium and high urine pH suggest 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 concentration 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 on the response. A fall in urine ammonium levels 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), which 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 of calcium phosphate. Of note, a urine pH below 6 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 above 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.