The role of afferent renal denervation in renovascular hypertension—another brick in the wall

Kiuchi, Márcio Galindo; Chen, Shaojie; Carnagarin, Revathy; Schlaich, Markus P.

doi:10.1007/s00424-020-02354-9

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2021

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“…Other than triggering RAAS, UA has been shown to induce hypertension through a crystal and pressure-independent kidney afferent arteriolopathy [ 27 , 28 , 29 ]. Afferent arteriolopathy can indeed lead to impaired renal blood flow, ischemia, and consequent renovascular hypertension [ 75 , 76 ]. However, the exact mechanism whereby UA can induce arteriolopathy remains partially unsolved.…”

Section: Discussionmentioning

confidence: 99%

Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

Piani

Cicero

Borghi

2021

JCM

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The relationship between serum uric acid (SUA) and hypertension has been a subject of increasing interest since the 1870 discovery by Frederick Akbar Mahomed. Several epidemiological studies have shown a strong association between high SUA levels and the presence or the development of hypertension. Genetic analyses have found that xanthine oxidoreductase (XOR) genetic polymorphisms are associated with hypertension. However, genetic studies on urate transporters and Mendelian randomization studies failed to demonstrate a causal relationship between SUA and hypertension. Results from clinical trials on the role of urate-lowering therapy in the management of patients with hypertension are not uniform. Our study sought to analyze the prognostic and therapeutic role of SUA in the hypertensive disease, from uric acid (UA) biology to clinical trials on urate-lowering therapies.

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