2002
DOI: 10.1159/000066303
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Abstract: Background/Aims: Rats with mild hyperuricemia develop systemic hypertension, interstitial renal disease, afferent arteriolopathy, and increased renin expression [Mazzali et al.: Am J Physiol 2002;6:F991–F997]. We hypothesized that hyperuricemia might also induce glomerular changes. Methods: We reviewed renal biopsies of rats previously made hyperuricemic for 7 weeks with the uricase inhibitor, oxonic acid. Controls included normal rats and oxonic acid-treated rats administered allopurinol, benziodarone, hydroc… Show more

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Cited by 231 publications
(177 citation statements)
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“…Second, there is evidence that uric acid may have a causal role in hypertension, 7 the metabolic syndrome, 29,30 and renal disease. 31,32 Adjusting for blood pressure, the metabolic syndrome, and renal function may, therefore, remove mechanisms by which uric acid may cause hypertension, that is, overadjustment in our multivariable model. It is possible that our age-adjusted risk estimates more accurately reflect the risk for hypertension conferred by hyperuricemia than do our multivariable-adjusted risk estimates.…”
Section: Discussionmentioning
confidence: 99%
“…Second, there is evidence that uric acid may have a causal role in hypertension, 7 the metabolic syndrome, 29,30 and renal disease. 31,32 Adjusting for blood pressure, the metabolic syndrome, and renal function may, therefore, remove mechanisms by which uric acid may cause hypertension, that is, overadjustment in our multivariable model. It is possible that our age-adjusted risk estimates more accurately reflect the risk for hypertension conferred by hyperuricemia than do our multivariable-adjusted risk estimates.…”
Section: Discussionmentioning
confidence: 99%
“…In addition, an increase in renin expression is also observed in hyperuricemic rats [36]. A relationship between serum uric acid and plasma renin activity has been described in humans [48].…”
Section: Uric Acid Glomerular Hemodynamic and Arteriolar Diseasementioning
confidence: 92%
“…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%
“…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: 97%