Dietary purines are largely catabolized in the gut, rather than used by the body for the synthesis of nucleic acids. The end-product of purine catabolism in humans is uric acid. The diet account for less than half of the uric acid appearing in the bloodstream. Most of the plasma uric acid, or urate, originates from catabolism of the purines synthesized by the the body (endogenous purines). The major purine are adenine and guanine. They occur mainly as nucleotides, such as adenosine triphosphate (ATP) and guanosine triphosphate (GTP), and as part of nucleic acids. For example, the adenine in RNA occurs as adenosine monophosphate, and the adenine in DNA occurs as deoxyadenosine monophosphate.
Normal serum uric acid is 0.025 to 0.080 mg / ml in males and 0.015 to 0.060 mg / ml in females. A uric acid level greater than 0.070 gm / ml is associated with an increase risk for gout. Purine-restrict diet can result in plasma uric acid levels of 0.005 to 0.0015 mg / ml. About two-thirds of the uric acid in the body is excreted via the urine; the rest is excreted in the feces. Urine acid account for only about 5% of urinary nitrogen.
Gout is a metabolic disease characterized by the painful inflammation of joints.

Gout is a type of arthritis. Hyperuricemia is a risk factor for gout and for the development of uric acid stones in kidneys. Gout often presents as a violent attack of pain in the big toe. Less commonly, it involves the wrists, ankles, or knees. The pain spontaneously disappears after a few days, but recurs, with an increasing frequency. Eventually, crystalline deposits of uric acid accumulate in the joints and appear as bumps on the skin, each with a diameter of millimeter to a few centimeters. The deposits of urate lead to erosion of the bone and to destruction of the joint. Gout can be crippling.
The mechanism producing the pain and inflammation of the gouty attack involves the neutrophils. The neutrophil is a type of white blood cell that consumed foreign objects. Such as bacteria, and attack them with toxin forms of oxygen, such HOOH and HO*. Hight plasma uric acid results in the formation and deposit of uric acid crystals in joints. The urate crystals are taken up by the neutrophils. The neutrophil release toxin forms of oxygen, as well as hydrolytic enzymes. This reaction is part of the inflammatory response of gout and contributes to the pain and fever of the gouty attack. Uric acid stones account for about 10% of all kidney stones in the United States. Most kidney stones consist of calcium phosphate or calcium oxalate. The risk for developing urate stone increase with increased levels of plasma urate and with increased levels of urinary urate. Sometime the stones that form in the kidney are excreted in the urine, where they appear as a fine gravel. A large stone can obstruct the ureter, impairing the formation of the urine and leading to intense pain. Kidney stones are also called renal calculi.

Hyperuricemia and gout are treated with drugs, such as allopurinol. Allopurinol inhibits one of the enzymes of the purine catabolic pathway and decrease the formation of uric acid. Dietary intervention may be part of the treatment programe. Dietary intervention involves the elimination of foods containing high levels of purine. This reduces exogenous purines as a source of uric acid. These foods include glandular and organ meats, dried legumes, shrimp, sardines, and mackerel. Other sources of meats and fish are restricted but not eliminate. High dietary protein can stimulate the formation of uric acid. The mechanism of this effect is no clear. It is thought that high levels of dietary can interfere with the normal regulation of pathway of purine catabolism, resulting in an increase in its rate.

Source: Nutritional Biochemistry P479