2002
DOI: 10.1152/ajprenal.00283.2001
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Abstract: Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature. Rats fed 2% oxonic acid and a low-salt diet for 7 wk developed mild hyperuricemia (1.8 vs. 1.4 mg/dl, P < 0.05), hypertension [147 vs. 127 mmHg systoli… Show more

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Cited by 707 publications
(644 citation statements)
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“…33 These effects, possibly mediated via activation of the renin-angiotensin system and downregulation of nitric oxide synthase, 34 might cause arterial stiffness.…”
Section: Discussionmentioning
confidence: 99%
“…33 These effects, possibly mediated via activation of the renin-angiotensin system and downregulation of nitric oxide synthase, 34 might cause arterial stiffness.…”
Section: Discussionmentioning
confidence: 99%
“…However, about 70% of uric acid, which is a final metabolite of purine bases, is excreted from the kidney; therefore, the deterioration of renal function causes hyperuricemia. Recent reports show that hyperuricemia plays a role in the initiation and progression of renal diseases in rodent models (1)(2)(3)(4) and that hyperuricemia indicates a poor renal prognosis in patients with IgA nephropathy (5). These findings suggest that hyperuricemia can directly cause both gouty kidney and other renal diseases.…”
Section: Introductionmentioning
confidence: 94%
“…2) In the late 1990s, our group discovered that administration of an uricase inhibitor (2% oxonic acid) in diet can mildly increase uric acid (1.5-3.0 mg/dl) in rats at a level that does not cause urate crystal deposition in the kidney [35]. Surprisingly, hyperuricemic rats developed systemic hypertension, glomerular hypertrophy, glomerular hypertension, afferent arteriolar disease, tubulointerstitial damage, and macrophage infiltration [36][37][38][39]. In a model of progressive renal disease (remnant kidney model), hyperuricemia accelerated renal injury, resulting in more glomerulosclerosis, tubulointerstitial fibrosis, and severe vascular injury [39,40].…”
Section: Insulin As An Endogenous Regulator Of Uric Acid In the Kidneymentioning
confidence: 99%