2014年10月23日星期四

Complication of Kidney Disease, Hyperuricemia

Urea Acid is the final product of purine metabolism. Dysfunction of purine metabolism leads to the excessive secretion of urea acid. In addition, the decline of renal function will give rise to lower excretion of urea acid. These two above reasons can result in increase of urea acid content in blood, and then these urea acid accumulate in the blood and cause Hyperuricemia.
High urea acid content in blood easily leads to deposition of urate in joints, which is commonly called Gout. And when there is more and more deposition of urate in renal glomerulus and renal tubules, damages to the kidney will be caused or aggravated.
The two main causations of Hyperuricemia, namely, are more secretion of urea acid and less excretion of urea acid. Referring to the former causation, we can peruse a diet change to food low in purine. And according to data, people who take too much sea foods are more vulnerable to this disease. So, patients with this Hyperuricemia or kidney problems should pay much more attention to intake of sea food.
However, starvation causes the body to metabolize its own (purine-rich) tissues for energy. Thus, like a high purine diet, starvation increases the amount of purine converted to uric acid. Starvation also impairs the ability of the kidney to excrete uric acid, due to competition for transport between uric acid and ketenes.
In case that the excretion of urea acid is stocked, medicine should be adopted immediately to enhance the degradation of deposited urate. Xanthine oxidase inhibitors decrease the production of uric acid, by interfering with Xanthine oxidase Uricosurics increase the excretion of uric acid, by reducing the reabsorption of uric acid once the kidneys have filtered it out of the blood.

In addition to Gout, high content of urea acid can also give rise to vascular diseases like hypertension, arteriosclerosis and so on. So the taking under control of blood pressure is of great important.

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