Otto Busato, M.D. Internal Medicine and Nephrology Specialist by the Brazilian Medical Association. MA/PH.D., Rio Grande do Sul State University (UFRGS). Associate Professor at the Rio Grande do Sul State University School of Medicine (UFRGS).

Uric acid (UA) is a weak acid and its ionized form, monosodium urate, is the form found in the human plasma, in the extracellular fluid and in the synovia. Synovia is the viscid fluid that fills up the articular cavities.

Foods contain several substances comprised of molecules, they are:

hexoses (sugars).
fatty acids (fats) and
amino-acids (proteins).

The amino-acids break in the organism into other components such as:

nucleic acids and nucleotides and
purine bases.

Purines degrade into hypoxanthine and this converts into xanthine. Xanthine, under the action of the xanthine oxidase enzyme, converts into uric acid, and this into urates. Most urates are produced in the liver from endogenous and exogenous proteins (diet).

Urate concentration in the human plasma depends on the balance between:

on one hand, absorption and production, and
on the other hand, destruction and excretion.

Urate is easily eliminated by the kidneys in normal amounts of 600-700 mg/day on normal diets. As it is easily soluble in water, it's normally excreted in urine. In a normal individual, 1/3 of uric acid undergoes degradation and is excreted by the intestine, and 2/3 by the kidney. Urate salts are highly soluble at a 37º C temperature, but they can easily be deposited on peripheral joints, knees, ankles, heels and foot joints, where body temperature is lower.

When uric acid is above 8 mg% in the blood plasma, it can be deposited on any tissue of our organism, depending a great deal on the local conditions. There's presence of hyperuricemia when uric acid is increased in the plasma, and hypouricemia when it's decreased. Next, further details on these two conditions.


It's a poorly known asymptomatic clinical syndrome, from diverse causes, that must be investigated by physicians. It's defined as hypouricemia when the plasma level of uric acid is less than 2.5 mg%.

Some types of hypouricemia result from the increased loss of UA by the kidney, and may be accompanied by renal calculi due to excess UA in the urine.

Hypouricemia can be primary (permanent) or acquired (intermittent). Primary hypouricemia occurs in hereditary cases or when there is great loss of xanthine through the urine (hyperxanthinuria). Such loss highly decreases the material needed for the enzymatic conversion of xanthine into uric acid; consequently, there's a decreased amount of the acid in the plasma. In acquired hypouricemia, uric acid is too low because is eliminated in great amounts through the urine. This may happen due to the use of uricosuric substances that increase the loss of UA through the urine, such as high doses of aspirin, benziodarone, citrates, probenecid, ascorbic acid, estrogens, etc. Another type of acquired hypouricemia is the indiscriminate and uncontrolled use of allopurinol, a substance that inhibits the action of the xanthine oxidase enzyme, which turns xanthine into uric acid.


The treatment for hypouricemia consists of avoiding the causes that lead to a decrease in plasma uric acid.


Hyperuricemia is the term applied to the blood condition in which uric acid found in the plasma (serum) is above 6 mg% in women and 7mg% in men, occurring in 10-15% of the over-forty population. Usually asymptomatic, it's related to other diseases, as diabetes mellitus, hyperthyroidism, diuretics abuse and alcohol ingestion. Hyperuricemia can occur from overproduction or decrease in the renal and intestinal excretion of uric acid. Hyperuricemia commonly takes place with higher frequency in men from puberty onwards, with a higher incidence at 30-40 years, and, in women, during menoupause.

Hyperuricemia can be divided into 2 categories:

Primary, when uric acid is high in the blood, regardless of coexisting disorders or drugs that change urate production and excretion.
Secondary, when the rise results from existing disorders, drugs and diets that change UA production and excretion.

In 75% of the patients, hyperuricemia is asymptomatic. In 25%, there may be symptoms such as:

lithiasis (renal calculi),
renal diseases (nephritis), and
build-up of uric acid depositions in the bones (tophi).

Asymtomatic hyperuricemia occurs frequently with alcohol abuse, obesity and chronic use of drugs that inhibit the excretion of uric acid, as anti-inflammatory agents, acetylsalicylic acid (aspirin) and diuretics. The presence of hyperuricemia is associated to risk factors such as arterial hypertension, hyperlipidemia, diabetes and coronary vascular alterations.

(Read more about hyperuricemia in the chapter "Kidney and Gout".)


Since hyperuricemia is a risk factor for heart diseases, the plasma uric acid level must be maintained normal. For this, the doctor has to look for the causes to the increase and indicate the adequate treatment.

In the treatment of hyperuricemia, it's necessary to:

prevent the acute onset of uric arthritis (gout);
use anti-inflammatory and anti-allergic agents in the fits of pain;
use inhibitors in the overproduction and uricosuric agents in patients with difficulty eliminating uric acid by the kidney;
undertake the prevention of recurrent arthritis, lithiasis, nephritis and gout;
decrease the predisposing factors such as alcohol, improper diet and medications that lower uric acid excretion by the kidney;
prevent and revert the deposition of urate crystals on joints, bones and tissues;
prolong the treatment for time enough so that the urates are displaced from tissues and bones and the plasma level of uric acid returns to normal.

Diet is an important item in uric acid treatment, but not the only one. The non-recommended foods for hyperuricemia patients are:

those rich in purines, as meat, giblets and viscera in general (liver, heart, tongue and kidneys),
small fishes, sardine, trout, anchovy,
seafood as mussel, shrimp and fish roe
Broth and stew must be avoided as uric acid is highly soluble in water, and when meat is cooked in water, the acid diffuses into the liquids.
Some grains such as black beans, chick-peas, peas, lentil and whole grains are rich in purine; therefore, they must be avoided as well.

Finally, we must say that every diet, no matter how well it is conducted, can only lower the plasma values of uric acid by around 25%.

Questions you can ask your doctor

What are the organs compromised by uric acid?

What are the complications from a high level of uric acid?

Do uric acid calculi depend on the high level of uric acid?

What diet must I stick to?

Are there medications that increase the level of uric acid?