NLRP3 and endothelial dysfunction: Estrogen’s uricosuric effects in premenopausal women likely reduce SUA retention, mitigating its vascular toxicity.[19] Conversely, testosterone in men may amplify SUA-induced oxidative stress and endothelial dysfunction, exacerbating renal sodium retention and blood pressure elevation.[20,21] Furthermore, visceral adiposity, which is more common in men,[22] may interact with SUA to trigger inflammatory pathways (such as the NLRP3 inflammasome) and reduce nitric oxide bioavailability, thereby increasing the risk of HTN.[23–25]