Viazzi Francesca, Bonino Barbara, Ratto Elena, Desideri Giovambattista, Pontremoli Roberto
G Ital Nefrol. 2015;32 Suppl 62.
Hyperuricemia is frequently found in association with several condition predisposing to cardiovascular events such as arterial hypertension and diabetes mellitus. This has led researchers to investigate possible pathogenetic mechanisms underlying this association. Several experimental studies and some indirect clinical evidence support a causal link between mild hyperuricemia and the developement of hypertension as well as new onset diabetes. At the tissue level, chronic exposure to increased uric acid has been shown to promote vascular changes leading to renal ischemia as well as stimulation of the renin angiotensin system. Furthermore, uric acid has been shown to promote the development of insulin resistance, hypertrglyceridemia and haepatic steatosis through pro-oxidative mechanisms. These experimental pathophysiological changes may be partly preventable by hypouricemic treatments. Whether clinical implications of these findings are confirmed by solid clinical intervention trials, mild hyperuricemia may soon change its status from risk predictor to treatment target for patients at high cardiovascular and renal risk.
高尿酸血症常与多种易引发心血管事件的疾病相关，如动脉高血压和糖尿病。这促使研究人员探究这种关联背后可能的致病机制。多项实验研究和一些间接临床证据支持轻度高尿酸血症与高血压以及新发糖尿病的发生之间存在因果联系。在组织水平上，长期暴露于升高的尿酸已被证明会促进血管变化，导致肾缺血以及刺激肾素 - 血管紧张素系统。此外，尿酸已被证明通过促氧化机制促进胰岛素抵抗、高甘油三酯血症和肝脂肪变性的发展。这些实验性病理生理变化可能通过降尿酸治疗部分预防。无论这些发现的临床意义是否得到可靠的临床干预试验证实，轻度高尿酸血症可能很快会从风险预测指标转变为心血管和肾脏高风险患者的治疗靶点。
