Hyperuricemia is a condition characterized by elevated levels of serum uric acid (SUA) in the blood. It is a chronic metabolic disorder due to purine metabolism disorders that may be primary or induced by other pathogenetic disorders. It is an important risk factor for the development of cardiovascular (CHD) and chronic kidney disease (CKD). The meta-analysis of two studies with adjusted risk assessments indicates that hyperuricemia is independently associated with an increased risk of peripheral neuropathy in patients with type 2 diabetes.
The decrease in SUA values with xanthine oxidase inhibitors has been associated with a favorable response in regard to arterial blood pressure, arterial rigidity, vascular wall thickening, oxidative stress, left ventricular hypertrophy and renal function.
The development of hyperuricemia occurs by way of two main mechanisms:
1. Increased purine synthesis;
2. Decreased kidney elimination.
The subject of this work is the early and specific manifestations of hyperuricemia, mechanisms of kidney involvement and methods of treatment depending on the degree of glomerular filtration.
Together with hypertension, obesity, dyslipidemia and insulin resistance, hyperuricemia is an invariable part of the metabolic syndrome and increasing cardiovascular risk that impacts renal function. Any increase in SUA by 60 μmol/L significantly increases cardiovascular mortality and overall mortality, and this dependence remains significant after considering the impact of all potential factors. Timely and adequate treatment of hyperuricemia leads to improvement of endothelial function, decrease of elevated blood pressure, retardation of the progression of renal involvement and prevention of the worsening of glomerular filtration rate.
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