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For in vitro diagnostic use only.
It is suggested to perform an internal quality control. For The components of the kit are stable until expiration date this purpose the following human based control sera are QN 0050 CH
with normal or close to normal control values SUMMARY OF TEST
Reagent A
4 x 90 ml (liquid) blue cap
QP 0050 CH
In humans, uric acid is the major product of the catabolism of the purine nucleosides, adenosine and guanosine. The daily synthe- Reagent B
4 x 10 ml (liquid) red cap
If required, a multiparametric, human based calibrator is sis rate of uric acid is approximately 400 mg; dietary sources con- Composition in the test: phosphate buffer pH 7.0 50 mM, tribute another 300 mg. In men consuming a purine-free diet, the TOOS 0.34 mM, 4-aminoantypyrine 0.3 mM, uricase 450 U/l, AT 0030 CH
total body pool of exchangeable urate is estimated at 1200 mg; this same value is estimated to be 600 mg in women. Hyperuri- Please contact Customer Care for further information.
cemia is most commonly defi ned by serum or plasma uric acid Standard:
uric acid 5 mg/dl - 5 ml
concentrations greater than 7.0 mg/dl (0.42 mmol/l) in men or Linearity
greater than 6.0 mg/dl (0.36 mmol/l) in women. Asymptomatic hyperuricemia is frequently detected through biochemical scree- MATERIALS REQUIRED BUT NOT SUPPLIED
If the value is exceeded, it is suggested to dilute sample ning; long-term follow-up of asymptomatic hyperuricemic patients 1+9 with saline and to repeat the test, multiplying the result is undertaken because many are at risk for renal disease that may Current laboratory instrumentation. Spectrophotometer develop as a result of hyperuricemia and hyperuricosuria; few of UV/VIS with thermostatic cuvette holder. Automatic micro- these patients ever develop the clinical syndrome of gout. Gout pipettes. Glass or high quality polystyrene cuvettes. Saline Sensitivity/limit of detection (LOD)
occurs when monosodium urate precipitates from supersaturated the limit of detection is 0.16 mg/dl.
body fl uids; the deposits of urate are responsible for the clinical REAGENT PREPARATION
signs and symptoms. Renal disease associated with hyperurice-mia may take one or more of several forms: (1) gouty nephropathy Add one vial of reagent B to a bottle of reagent A. Mix by Interferences
with urate deposition in renal parenchyma, (2) acute intratubular no interference was observed by the presence of: deposition of urate crystals, and (3) urate nephrolithiasis. Renal If reagents are mixed in reduced quantities, mix 9 parts of retention of uric acid may occur in acute or chronic renal disease of any type or as a consequence of administration of drugs; diuretics, Stability of working reagent: ≥ 90 days at 2-8°C, away from in particular, are implicated in the latter instance. Organic acidemia due to increased acetoacetic acid in diabetic ketoacidosis or to Stability of unmixed reagents: up to expiration date on Precision
lactic acidosis may interfere with tubular secretion of urate. Increa- sed nucleic acid turnover and consequent increase in catabolism Stability since fi rst opening of vials of unmixed reagents: of purines may be encountered in rapid proliferation of tumor cells as well as in massive destruction of tumor cells on therapy with certain chemotherapeutic agents. Hyperuricemia is also attributa- PRECAUTIONS
ble to primary defects of enzymes in the pathways of purine meta- Reagent may contain some non-reactive and preservative bolism. The Lesch-Nyhan syndrome is characterized by complete components. It is suggested to handle carefully it, avoiding defi ciency of HGPRT, the major enzyme of the purine salvage Methods comparison
pathways. This sex-linked genetic disorder is manifested clinically Perform the test according to the general “Good Labora- a comparison between Chema and a commercially availa- by mental retardation, abnormal muscle movements, and beha- vioral problems; and biochemically by hyperuricemia, hyperuricaci-duria, and markedly decreased levels of HGPRT in erythrocytes, SPECIMEN
fi broblasts, and other cells. Less severe defi ciency of HGPRT displays a clinical spectrum of mild to moderate neurological Serum, plasma heparinate. Oxalate, citrate and fl uoride defects. Quantitation of urinary uric acid excretion is an aid in could yeld a small decrease of uric acid. Urine.
selecting appropriate treatment for asymptomatic hyperuricemia. Uric acid is stable 5 days at 4-25°C.
About one in fi ve patients with clinical gout also has urinary tract Dilute urine sample 1:10 with deionized water.
uric acid stones. Although formation of urinary tract stones is a complex process, about 50% of patients with uric acid stones have TEST PROCEDURE
either hyperuricosuria or excretion of a persistently acid urine or This product is made to be used in professional laborato- both. Undissociated uric acid is relatively insoluble, whereas urate ries. Please consult local regulations for a correct waste at pH 7.0 is more than 10 times more soluble. Thus, in patients with urinary pH persistently less than 6.0, relatively small amounts S56: dispose of this material and its container at hazar- of uric acid in urine may produce supersaturation. Measurement dous or special waste collection point.
of both urine pH and uric acid excretion is important in the investi- S57: use appropriate container to avoid environmental gation of uric acid urolithiasis. In any patient with urolithiasis, iden- tifi cation of crystals present in urine may provide a signifi cant clue S61: avoid release in environment. Refer to special to the nature of stones present. Hypouricemia, often defi ned as serum urate concentrations less than 2.0 mg/dl (0.12 mmol/l), is REFERENCES
much less common than hyperuricemia. It may be secondary to any one of a number of underlying conditions. Severe hepatocel- Barham D., Trinder P. - Analyst, 97 142 (1972) lular disease with reduced purine synthesis or xanthine oxidase Mix, incubate at 37°C for 5 minutes.
Fossati P., Prencipe L., Berti G. - Clin. Chem. 26 277 (1980).
activity is one possibility. Another is defective renal tubular reab- Read absorbances of standard (As) and samples (Ax) Tamaoku K., Murao Y., Akiura K., Ohkura Y. - Anal. Ch.Acta, 136 sorption of uric acid. Defective reabsorption may be congenital, Tietz Textbook of Clinical Chemistry, Second Edition, Burtis- as in generalized Fanconi’s syndrome, or acquired. The reabsorp- tion defect may be acquired acutely because of injection of radio- RESULTS CALCULATION
HU Bergmeyer - Methods of enzymatic analysis, (1987).
opaque contrast media or chronically because of exposure to toxic MANUFACTURER
agents. Overtreatment of hyperuricemia with allopurinol or urico-suric drugs, as well as cancer chemotherapy with 6-mercaptopu- uric acid mg/dl = Ax/As x 5 (standard value) rine or azathioprine, may also cause hypouricemia.
Methods in current use for measuring uric acid fall into two groups: phosphotungstic acid (PTA) methods and uricase methods. PTA methods are subject to many interferences, including endogenous compounds such as glucose and ascorbic acid in plasma or urine and glutathione, ergothionine, and cysteine spilled into plasma from hemolyzed erythrocytes; other compounds interfere too. Uri- 24 hours urine sample (uric acid mg/24h): case methods are inherently more specifi c because they have, either as a single step or as the initial step, urate oxidation cataly- uric acid mg/24h = Ax/As x 5 x 10 x diuresis (dl) zed by the enzyme uricase. Preliminary precipitation of protein is (standard value, dilution and diuresis in dl) not required. In a majority of uricase methods, only guanine, xan-thine, and a few other structural analogues of uric acid interfere, and then only at concentrations improbable in biological fl uids. Uri- EXPECTED VALUES
case methods have replaced PTA methods in most current instru- mentation. Most current enzymatic assays for uric acid in serum involve a peroxidase system coupled with one of a number of oxygen acceptors to produce a chromogen. PRINCIPLE OF THE METHOD
Uric acid in sample is oxidized to allantoin in presence of the enzyme uricase and H O is generated. The H O reacts Each laboratory should establish appropriate reference inter- with TOOS and 4-aminoantipyrine in the presence of pero- xidase to form a violet dye. The intensity of color formed is proportional to the uric acid concentration and can be measured photometrically between 510 and 560 nm.


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