Gout (Hyperuricemia): Test and Diagnosis

Laboratory parameters of the 1st order – obligatory laboratory tests.

  • Uric acid*

Notice. * During an acute gout attack, uric acid levels may be normal or decreased, especially if preceded by uric acid-lowering therapy. The optimal time for uric acid determination is therefore two to three weeks after the attack. Sometimes it is the rapid drop in uric acid concentration that triggers a gout attack. Thus, a normal uric acid level does not exclude gout.

It is not uncommon for renal dysfunction to be diagnosed at the same time as hyperuricemia. In such cases, it is no longer possible to distinguish whether the gout is primarily caused by a renal excretory defect or is secondary to renal insufficiency (see: table below).

2nd order laboratory parameters – depending on the results of the history, physical examination, etc. – for differential diagnostic workup

  • Urine examination, if necessary 24h urine examination (especially for the determination of uric acid).
  • Renal parameters – urea, creatinine (creatinine clearance if necessary).
  • Inflammatory parameters – CRP (C-reactive protein) [normal] or ESR (erythrocyte sedimentation rate) [increased only in the attack].
  • Cholesterol
  • Triglycerides
  • Liver parameters – aspartate aminotransferase (AST, GOT), gamma-glutamyl transferase (γ-GT, gamma-GT; GGT), alanine aminotransferase (ALT, GPT) (elevated only in liver parenchyma damage); carbodeficient transferrin (CDT) ↑ (in chronic alcoholism)* * – with these parameters a good diagnostic statement about drinking behavior can be made.
  • TSH, ft3, fT4 – both hypothyroidism and hyperthyroidism are associated with an increased risk of hyperuricemia.
  • Synovial analysis (joint puncture) – in case of atypical manifestation and normal uric acid concentration, the affected joint should be punctured and the effusion should be examined (cell count and cell differentiation, bacteriology); microscopic examination of the joint puncture must be performed immediately after puncture, since uric acid crystals in the joint puncture are readily soluble in water [gold standard is polarization optical detection of phagocytized uric acid crystals in the joint puncture].
  • Gene variant of the fructose transporter gene SLC2A9 – this leads to the disturbance of the renal excretion of uric acid

* These parameters can be used to make a good diagnostic statement about drinking behavior in relation to alcohol (with abstinence, the values normalize within 10-14 days).

The following table provides assistance in the laboratory diagnosis of hyperuricemia of various causes:

Renal tubular excretory dysfunction for uric acid. Uric acid overproduction due to enzyme defect Excretion disorder due to renal insufficiency Uric acid overproduction due to increased cellular breakdown
Serum uric acid (up to 6.4 mg/dl or 381 µmol/l) + (between 8-14 mg/dl or 476-833 µmol/l) +++ (zw.12-22 mg/dl or 714-1,309 µmol/l) + to +++ (zw.8-22 mg/dl or 476-1.309 µmol/l) + to +++ (between 8-22 mg/dl or 476-1.309 µmol/l)
Renal uric acid excretion (800-1,200 mg/day). – – +++ – – + to +++
Uric acid clearance (5-12 ml/min) – Up to – Normal – To – – analogous to the reduction in creatinine clearance. Normal
Creatinine clearance (80-120 ml/min) Normal Normal – until – – Normal