Gout is a form of inflammatory arthritis resulting from the deposit of monosodium urate (MSU) crystals within joints and soft tissues. These crystals form when the concentration of uric acid in the blood becomes too high, a condition known as hyperuricemia. Laboratory tests are fundamental to diagnosing gout, helping to confirm the presence of crystals, monitor uric acid levels, assess organ function, and guide long-term treatment. The diagnostic process relies on a combination of tests, each providing specific information necessary for proper management.
The Definitive Diagnostic Test
The most conclusive test for diagnosing gout is the microscopic analysis of fluid drawn directly from an affected joint, a procedure known as arthrocentesis or joint aspiration. A physician uses a needle to withdraw a sample of synovial fluid from the inflamed joint, which is then promptly analyzed to identify the causative crystals.
The aspirated fluid is examined under a polarized light microscope for monosodium urate (MSU) crystals. These crystals are distinctly needle-shaped and exhibit “negative birefringence,” appearing bright yellow when aligned parallel to the filter and blue when aligned perpendicularly. The presence of MSU crystals in the joint fluid is considered the gold standard for a gout diagnosis.
This test is crucial for differentiating gout from other conditions causing similar symptoms, such as septic arthritis or pseudogout. Pseudogout involves calcium pyrophosphate (CPP) crystals, which are shorter and exhibit “positive birefringence.” The microscopic examination also checks for signs of infection, such as high white blood cell counts, which must be addressed immediately, especially since gout and joint infection can occur simultaneously.
Standard Blood Monitoring
While MSU crystals confirm the diagnosis, the Serum Uric Acid (SUA) test is the primary laboratory tool for long-term management and monitoring. This test measures the concentration of uric acid circulating in the bloodstream. Hyperuricemia, defined as a concentration above 6.8 mg/dL, is the underlying cause of gout, as this level exceeds the saturation point for MSU crystal formation.
A high SUA level alone is not sufficient for a gout diagnosis, as many people have hyperuricemia without developing symptoms. Conversely, up to 15% of patients experiencing an acute gout flare may have normal SUA levels during the attack. This temporary drop occurs because the body shifts uric acid into the joint space as crystals.
The SUA test becomes crucial once gout is confirmed, as it guides the effectiveness of urate-lowering therapy. The therapeutic goal is to maintain the SUA level below 6.0 mg/dL to prevent new crystal formation and allow existing crystals to dissolve. For patients with severe manifestations, such as visible deposits called tophi, a more stringent target of under 5.0 mg/dL is recommended until clinical remission is achieved.
Assessing Organ Function and Inflammation
Beyond the uric acid level, other blood tests assess overall health, inflammation, and kidney function, which is closely tied to uric acid regulation. Tests for kidney function, including Creatinine and Blood Urea Nitrogen (BUN), are necessary because the kidneys excrete the majority of uric acid. High levels of creatinine and BUN indicate reduced kidney function, which may explain high uric acid levels and influence the choice and dosing of gout medications.
Inflammatory markers are also measured to confirm the presence and severity of inflammation during an acute episode. C-Reactive Protein (CRP) and Erythrocyte Sedimentation Rate (ESR) are non-specific markers that elevate significantly during a gout flare. CRP levels rise rapidly within hours, while ESR elevations are typically more moderate and slower to peak.
These tests do not diagnose gout, but they confirm the patient is experiencing a significant inflammatory event. Monitoring the reduction of CRP and ESR values provides an objective measure of how well acute anti-inflammatory treatment is working. High inflammatory markers can also help rule out conditions like cellulitis or warn if a joint infection is suspected alongside gout.
Determining the Origin of High Uric Acid
For patients with complex or difficult-to-manage cases, determining the underlying metabolic cause of hyperuricemia is necessary. Uric acid is either produced excessively (overproduction) or inadequately removed by the kidneys (underexcretion). Understanding this mechanism is important for tailoring the long-term medication strategy.
The 24-hour urine collection test is used for this purpose, requiring the patient to collect all urine produced over a day. The total amount of uric acid excreted is measured and compared to the serum uric acid level. If the patient excretes a significantly high amount of uric acid, they are classified as an “overproducer.”
Conversely, if the patient has high serum uric acid but excretes a low amount in the urine, they are classified as an “underexcreter.” This distinction helps the physician decide between different classes of urate-lowering drugs. These include allopurinol, which reduces uric acid production, or uricosuric agents, which help the kidneys excrete more uric acid. This targeted approach ensures the most effective treatment is selected to maintain the serum uric acid target and prevent future attacks.