The Clinical Aspects of Hyperuricemia and Gout

Abstract

Hyperuricemia is caused by a defect in renal transport in about 98% of all those affected. These patients have reduced uric acid clearance, which combined with purinrich food raises plasma uric acid levels to hyperuricemic values. Hyperuricemia is defined according to the limit of solubility of monosodium urate in extracellular fluid at pH 7.4 and 37°C to 6.5 mg/dl and more. In industrialized countries about 30% of the men and 3% of the women suffer from hyperuricemia [5, 6]. Depending on the duration and extent of the disease, patients develop gouty arthritis and nephrolithiasis (Table 1). In most patients with hyperuricemia caused by a defect in renal transport gouty arthritis occurs first. Nephrolithiasis is the first symptom in the majority of the patients who are overproducers because of an enzyme defect such as HGPRT deficiency. Some of the other diseases associated with hyperuricemia are hyperlipidemia, hypertension, obesity, atherosclerosis, hyperglycemia, diabetes mellitus, and ethanol consumption.