URICEMIA: CAUSES, SYMPTOMS, TREATMENTS - ANATOMY AND PHYSIOLOGY - 2025

The uricemia sos uric acid levels in the blood. This term is not associated with any pathology, since there is a certain normal amount of this element in the blood. However, in popular slang, high uric acid values ​​are understood as uricaemia, although that corresponds to the correct definition of hyperuricemia.

Uric acid is a normal product of purine catabolism. These, together with the pyrimidines, are the nitrogenous bases of DNA. The enzyme xanthine oxidase is responsible for the final catabolism of purines (adenine and guanine) in muscle, kidney, liver, intestinal and vascular tissue, obtaining uric acid as the final product.

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Despite the fears that uric acid generates, it is not always related to pathological events. Recent studies have demonstrated the role of this compound in the antioxidant capacities of plasma and in the integrity of endothelial cells. Likewise, its importance in type 2 immune responses has been proven.

However, uric acid is best known for its pathological role. This "villain" actively participates in the generation of inflammatory, cardiovascular, renal and metabolic joint diseases. Depending on the symptoms and severity of the clinical picture, the most appropriate treatment will be decided.

Causes

Unlike most mammals, humans and large primates lack the active enzyme uricase (urate oxidase). This enzyme can metabolize uric acid to a highly water-soluble element, which can be eliminated by the kidneys. Due to this deficiency, humans can suffer from hyperuricemia.

Despite the above, xanthine oxidase is able to maintain purine metabolism and uric acid production within normal limits in most people for a long time.

What happens then so that the uricemia rises? There are some theories that seek to explain this phenomenon.

Lifestyle

Diets high in purines and proteins (fish, organ meats, meat broths), the consumption of alcohol and excess carbohydrates contribute to the appearance of hyperuricemia.

A sedentary lifestyle worsens this condition, as does smoking. Obese patients tend to have higher levels of uric acid in the blood.

Medicines

Some drugs frequently used for the treatment of cardiovascular diseases can increase uric acid.

Thiazides and loop diuretics cause hyperuricemia. Low-dose aspirin decreases the renal excretion of uric acid and therefore increases its serum levels.

Renal insufficiency

As might be expected, patients with renal failure, either acute or chronic, may suffer from hyperuricemia. Low renal excretion in these patients also reduces the amount of uric acid in the urine, so hyperuricemia in this case is not due to an increase in production but rather a decrease in elimination.

Non-modifiable causes

Plasma uric acid levels are usually higher in men than in women. These concentrations increase with age.

Postmenopausal women have higher uric acid levels than women of childbearing age, which implies some hormonal control of uricaemia.

Symptoms

Depending on the organ or system affected by uric acid, we can observe different symptoms.

Gout

It is a form of chronic inflammatory arthritis. Although it is not uric acid that is deposited directly in the joints but monosodium urate crystals, these crystals are formed thanks to the immune action of the body on the remains of damaged or dead cells that expel nucleic acids (purines) from their inside.

Gout has 4 stages described in its natural history, but only 3 of them are of clinical importance:

Stage 1

Asymptomatic period. In this phase, urate crystals begin to deposit in the periarticular tissues. Organic damage may already occur, but there are no clinical signs of it.

Stage 2

Also known as an acute gout attack, it can appear spontaneously or after small local trauma. Although it can affect any joint in which there are crystal deposits, the most affected is the metatarsophalangeal of the big toe, an episode known as podagra.

It is characterized by the appearance of sudden pain in the affected area, often described as "explosive." Lasts 1 or 2 days, during which there is functional impotence.

There may be a local volume increase, although this is not always the case. The pain subsides after the third day. Later crises can affect more than one joint.

Stage 3

Intercritical period. As its name shows, it is about the time between one acute crisis and another. The duration of this phase can be weeks, months and even years.

Although there is no presence of pain, the crystals can continue to accumulate in the tissues, preparing the ground for future painful crises.

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Stage 4

Advanced drop. It usually occurs in patients without adequate treatment. It is characterized by the development of stiffness and chronic inflammation of the affected joint, accompanied by painless but deforming subcutaneous nodules known as cat-like tophi. This stage is not very common today thanks to the treatments.

Kidney disorders

Hyperuricemia increases the risk of acute renal failure, either by altering the activity of intraglomerular mesangial cells or by damaging the cells of the proximal tubular epithelium.

Likewise, high levels of uric acid in the blood have been classified as an independent risk factor for chronic kidney failure in type 2 diabetic patients.

On the other hand, the accumulation of uric acid in the kidney leads to the formation and deposit of stones. These stones are capable of causing kidney colic and are a major risk factor for urinary infections.

Metabolic syndrome and cardiovascular disease

Several studies have recently shown that uric acid is associated with metabolic syndrome and its particular components: obesity, dyslipidemia, high blood pressure, increased C-reactive protein, insulin resistance, and endothelial dysfunction.

Also the elevation of uric acid is related to a high risk of coronary heart disease and heart attacks. This relationship is accentuated in patients with a history of hypertension and diabetes.

Treatment

In addition to the change in lifestyle and diet, there are drug treatments that can help improve the patient, including:

- NSAIDs (ibuprofen, ketoprofen, diclofenac, ketorolac, meloxicam).

- Colchicine.

- Steroids.

- Hypouricemic agents (allopurinol). They inhibit xanthine oxidase and decrease uric acid production.

- Uricosuric (probenecid). Increases renal excretion of uric acid.

References

1. Grassi, Davide and collaborators (2013). Chronic Hyperuricemia, Uric Acid Deposit and Cardiovascular Risk. Current Pharmaceutical Design, 19 (13): 2432-2438.
2. El Ridi, Rashika and Tallima, Hatem (2017). Physiological functions and pathogenic potential of uric acid: A review. Journal of Advanced Research, 8 (5): 487-493.
3. Prado de Oliveira, Erick and Burini, Roberto Carlos (2012). High plasma uric acid concentration: causes and consequences. Diabetolgy & Metabolic Syndrome, 4:12.
4. Mayo Clinic Staff (2018). High Uric Acid Levels. Recovered from: mayoclinic.org
5. Goicochea, Marian and collaborators (2012). Hyperuricemia, gout and chronic kidney disease. Extraordinary Supplement Nephrology, 3: 8-15.
6. Wikipedia (2018). Gout. Recovered from: en.wikipedia.org