Abstract:
Introduction.
High blood pressure (HBP) is commonly associated with hyperuricemia. The
frequency of this association is determined by a decrease in renal perfusion
(characteristic of hypertensive patients) which would favor the reabsorption of uric
acid coupled with sodium and the development of arteriolopathy that induces tissue
ischemia with increased activity of xanthine oxidase, an enzyme involved in uric
acid formation.
Purpose.
Study of the clinical features and
evolution of hyperuricemia in patients
with nephrogenic hypertension.
Material and methods.
Retrospective and prospective study on a group of 100 patients with nephrogenic
hypertension hospitalized in the IMSP Nephrology Department of the Republican
Clinical Hospital "Timofei Moşneaga", in the period 2020-2021. All
patients were investigated clinically and paraclinically.
Conclusions.
1. Hyperuricemia causes Hypertension through a common action on the kidneys (by stimulating the renin-angiotensin system, renal vasoconstriction, NO reduction);
2. Hyperuricemia causes Arterial Hypertension a action on muscle vascular cells (by releasing inflammatory mediators, stimulating macrophages with IL-6 and TNF-synthesis;
3. Hyperuricemia causes Hypertension by activity of on arteries (through its ugly endothelial receptor, stimulates smooth muscle proliferation and inhibits endothelial function).
4. Diuretics and beta-bloquants for antihypertensive treatment promote the net reabsorption of urate and contribute to increased uric acid levels.
5. Hypertensive patients with hyperuricemia should be considered a population at high risk for cardiovascular events and gout.
