Treatment
Children with Kawasaki disease should be hospitalized and cared for by a physician who has experience with this disease. In an academic medical center, care is often shared between pediatric cardiology, pediatric rheumatology, and pediatric infectious disease specialists (although no specific infectious agent has yet been identified). To prevent damage to coronary arteries, treatment should be started immediately following the diagnosis.Intravenous immunoglobulin  (IVIG) is the standard treatment for Kawasaki disease and is administered in high doses with marked improvement usually noted within 24 hours. If the fever does not respond, an additional dose may be considered. In rare cases, a third dose may be given. IVIG is most useful within the first seven days of fever onset, to prevent coronary artery aneurysm. IVIG given within the first 10 days of the disease reduces the risk of damage to the coronary arteries in children, without serious adverse effects.Salicylate therapy, particularly aspirin, remains an important part of the treatment (though questioned by some) but salicylates alone are not as effective as IVIG. There is limited evidence to indicate whether children should continue to receive salicylate as part of their treatment. Aspirin therapy is started at high doses until the fever subsides, and then is continued at a low dose when the patient returns home, usually for two months to prevent blood clots from forming. Except for Kawasaki disease and a few other indications, aspirin is otherwise normally not recommended for children due to its association with Reye syndrome.
While a vegetarian diet is typically seen as beneficial with respect to conditions such as gout, care should be taken to avoid associated health conditions.Transient hypouricemia sometimes is produced by total parenteral nutrition. Paradoxically, total parenteral nutrition may produce hypouricemia followed shortly by acute gout, a condition normally associated with hyperuricemia. The reasons for this are unclear. Genetics
Genetic mutations known to cause hypouricemia are of two kinds:  mutations causing xanthine oxidase deficiency, which reduces the production of uric acid;  and mutations causing abnormal kidney function that increases the excretion of uric acid. Collectively known as familial renal hypouricemia, these latter mutations are of two types, involving defects of presecretory and postsecretory reabsorption.A genetic mutation in Dalmatian dogs causes hypouricemia due to a kidney defect that interferes with reabsorption of uric acid. A similar mutation has been reported in a human brother and sister.In humans, loss-of-function mutations in the gene URAT1 are associated with presecretory reabsorption defects. Medical conditions
Medical conditions that can cause hypouricemia include:

Fanconi syndrome
Hyperthyroidism
Multiple sclerosis
Myeloma
Nephritis
Wilsons disease
Purine nucleoside phosphorylase (PNP) deficiency

Diagnosis
Uric acid clearance should also be performed, increase in clearance points to proximal tubular defects in the kidney, normal or reduced clearance points to a defect in xanthine oxidase. Treatment
Idiopathic hypouricemia usually requires no treatment. In some cases, hypouricemia is a medical sign of an underlying condition that does require treatment. For example, if hypouricemia reflects high excretion of uric acid into the urine (hyperuricosuria) with its risk of uric acid nephrolithiasis, the hyperuricosuria may require treatment.