2002
DOI: 10.1097/01.asn.0000034910.58454.fd
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Abstract: Abstract. Hyperuricemia is associated with renal disease, but it is usually considered a marker of renal dysfunction rather than a risk factor for progression. Recent studies have reported that mild hyperuricemia in normal rats induced by the uricase inhibitor, oxonic acid (OA), results in hypertension, intrarenal vascular disease, and renal injury. This led to the hypothesis that uric acid may contribute to progressive renal disease. To examine the effect of hyperuricemia on renal disease progression, rats we… Show more

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Cited by 1,137 publications
(813 citation statements)
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References 37 publications
(43 reference statements)
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“…Several recent studies have shown that the UA might contribute in the pathophysiology of PAH. For example, UA increases cyclo-oxygenase-2 and ET-1 expression in vascular smooth muscle cells (VSMC) [18,19]. UA also inhibits vasodilatation in the lung by reducing nitric oxide production by endothelial cells [20].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Several recent studies have shown that the UA might contribute in the pathophysiology of PAH. For example, UA increases cyclo-oxygenase-2 and ET-1 expression in vascular smooth muscle cells (VSMC) [18,19]. UA also inhibits vasodilatation in the lung by reducing nitric oxide production by endothelial cells [20].…”
Section: Discussionmentioning
confidence: 99%
“…UA also inhibits vasodilatation in the lung by reducing nitric oxide production by endothelial cells [20]. In rats, acute elevation of UA with uricase inhibitor allantoxanamide leads to increase in medial thickness of pulmonary arterioles [18].…”
Section: Discussionmentioning
confidence: 99%
“…The potential role of renal uric acid accumulation in the pathogenesis of UAKD is unknown. Uric acid crystals are not typically seen in tissue specimens [30]. A recent hypothesis linking uric acid to renal vascular damage and the development of chronic kidney disease (CKD) may provide a partial explanation [31].…”
Section: Pathophysiologymentioning
confidence: 99%
“…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%
“…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]. These lesions were significantly ameliorated by lowering uric acid with either allopurinol or benziodarone (a uricosuric agent), suggesting a role for uric acid in this process.…”
Section: Insulin As An Endogenous Regulator Of Uric Acid In the Kidneymentioning
confidence: 99%