The Kidney in Gout

Talbott, John H.; Terplan, Kornel

doi:10.1097/00005792-196012000-00001

Cited by 234 publications

(103 citation statements)

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“…Prior to the availability of treatments for hyperuricemia, 25% of gouty subjects developed proteinuria, 50% suffered from chronic renal insufficiency, and 10-25% developed end stage renal disease [8]. These patients commonly showed renal lesions such as arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis, which was historically described as "Gouty nephropathy".…”

Section: Clinical Evidence For Hyperuricemia In Renal Diseasementioning

confidence: 99%

The conundrum of hyperuricemia, metabolic syndrome, and renal disease

et al. 2008

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The level of serum uric acid in human has been increasing over the last decades, and correlates with an increase prevalence of renal disease and metabolic syndrome. Understanding the role of uric acid in these conditions may provide clues for preventing the current epidemic of renal disease. Controversy still remains if hyperuricemia is simply a consequence or a cause of renal disease although epidemiological studies have attempted to resolve this issue. In this review, we discuss the clinical and experimental evidence for a causal role of hyperuricemia in renal diseases and potential relationships of hyperuricemia with metabolic syndrome.

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Section: Clinical Evidence For Hyperuricemia In Renal Diseasementioning

confidence: 99%

The conundrum of hyperuricemia, metabolic syndrome, and renal disease

et al. 2008

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“…Approximately 20 to 60% of patients with gout have mild or moderate renal dysfunction (1); before the availability of uric acid lowering agents, as many as 10 to 25% of patients with gout developed end-stage renal disease (2). The histologic lesion termed "gouty nephropathy" consists of glomerulosclerosis, interstitial fibrosis, and renal arteriolosclerosis, often with focal interstitial urate crystal deposition (2,3). These histologic findings have been observed in autopsies of 79 to 99% of patients with gout (3).…”

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confidence: 99%

A Role for Uric Acid in the Progression of Renal Disease

Kang

Nakagawa²,

Li³

et al. 2002

Journal of the American Society of Nephrology

1,176

770

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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 were fed 2% OA for 6 wk after 5/6 remnant kidney (RK) surgery with or without the xanthine oxidase inhibitor, allopurinol, or the uricosuric agent, benziodarone. Renal function and histologic studies were performed at 6 wk. Given observations that uric acid induces vascular disease, the effect of uric acid on vascular smooth muscle cells in culture was also examined. RK rats developed transient hyperuricemia (2.7 mg/dl at week 2), but then levels returned to baseline by week 6 (1.4 mg/dl). In contrast, RKϩOA rats developed higher and more persistent hyperuricemia (6 wk, 3.2 mg/dl). Hyperuricemic rats demonstrated higher BP, greater proteinuria, and higher serum creatinine than RK rats. Hyperuricemic RK rats had more renal hypertrophy and greater glomerulosclerosis (24.2 Ϯ 2.5 versus 17.5 Ϯ 3.4%; P Ͻ 0.05) and interstitial fibrosis (1.89 Ϯ 0.45 versus 1.52 Ϯ 0.47; P Ͻ 0.05). Hyperuricemic rats developed vascular disease consisting of thickening of the preglomerular arteries with smooth muscle cell proliferation; these changes were significantly more severe than a historical RK group with similar BP. Allopurinol significantly reduced uric acid levels and blocked the renal functional and histologic changes. Benziodarone reduced uric acid levels less effectively and only partially improved BP and renal function, with minimal effect on the vascular changes. To better understand the mechanism for the vascular disease, the expression of COX-2 and renin were examined. Hyperuricemic rats showed increased renal renin and COX-2 expression, the latter especially in preglomerular arterial vessels. In in vitro studies, cultured vascular smooth muscle cells incubated with uric acid also generated COX-2 with time-dependent proliferation, which was prevented by either a COX-2 or TXA-2 receptor inhihbitor. Hyperuricemia accelerates renal progression in the RK model via a mechanism linked to high systemic BP and COX-2-mediated, thromboxane-induced vascular disease. These studies provide direct evidence that uric acid may be a true mediator of renal disease and progression.

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“…Human histopathologic data shows interstitial inflammation and fibrosis coexisting with crystalline uric acid deposits, which are interpreted by some as "smoking guns." 6 A scatter of physiology studies also showed abnormal indices of renal and endothelial function in the backdrop of asymptomatic hyperuricemia. None of these provide proof and most of them are challenged by studies showing contrary results.…”

mentioning

confidence: 99%

Posing the Question Again

Moe¹

2010

Journal of the American Society of Nephrology

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The Kidney in Gout

Cited by 234 publications

References 1 publication

The conundrum of hyperuricemia, metabolic syndrome, and renal disease

The conundrum of hyperuricemia, metabolic syndrome, and renal disease

A Role for Uric Acid in the Progression of Renal Disease

Posing the Question Again

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