Uric Acid Nephrolithiasis in Gout

YÜ, TS'AI-FAN

doi:10.7326/0003-4819-67-6-1133

Cited by 200 publications

(22 citation statements)

References 32 publications

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“…In 1967, Yü and Gutman (29) investigated 1,258 patients with primary gout and reported a 22% prevalence of urolithiasis, based on history of urolithiasis during the course of gout. Shimizu et al (30) reported the prevalence of urolithiasis calculated from stone history was 16.2%.…”

Section: Discussionmentioning

confidence: 99%

Prevention of Comorbidity and Acute Attack of Gout by Uric Acid Lowering Therapy

et al. 2014

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The object of this study was to evaluate the effect of uric acid lowering therapy in reducing the new development of comorbidities and the frequency of acute attacks in gout patients. We retrospectively reviewed patients who were diagnosed to have gout with at least 3 yr of follow up. They were divided into 2 groups; 53 patients with mean serum uric acid level (sUA)<6 mg/dL and 147 patients with mean sUA≥6 mg/dL. Comorbidities of gout such as hypertension (HTN), type II diabetes mellitus (DM), chronic kidney disease, cardiovascular disease (CVD) and urolithiasis were compared in each group at baseline and at last follow-up visit. Frequency of acute gout attacks were also compared between the groups. During the mean follow up period of 7.6 yr, the yearly rate of acute attack and the new development of HTN, DM, CVD and urolithiasis was lower in the adequately treated group compared to the inadequately treated group. Tight control of uric acid decreases the incidence of acute gout attacks and comorbidities of gout such as HTN, DM, CVD and urolithiasis.Graphical Abstract

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Section: Discussionmentioning

confidence: 99%

Prevention of Comorbidity and Acute Attack of Gout by Uric Acid Lowering Therapy

et al. 2014

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“…Hyperuricosuria is most commonly associated with a high purine-containing (animal protein and beer) diet, uricosuric drugs, increased protein catabolism, and, more recently, the metabolic syndrome. Ten percent of patients with gout have associated hyperuricosuria, and the risk of uric acid stones is proportional to uric acid excretion: only 11% of patients with uric acid excretion <1.8 mmol/day have uric acid stones [33], whereas 23% of those excreting >3.6 mmol/day, and 50% of those excreting >6 mmol/day, have stones [34]. …”

Section: Investigation Of Renal Stonesmentioning

confidence: 99%

An Update and Practical Guide to Renal Stone Management

et al. 2010

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Renal stone disease covers kidney and lower urinary tract stones caused by a variety of conditions, including metabolic and inherited disorders, and anatomical defects with or without chronic urinary infection. Most cases are idiopathic, in which there is undoubtedly a genetic predisposition, but where environmental and lifestyle factors play an important role. Indeed, it is becoming apparent that renal stone disease is often part of a larger ‘metabolic picture’ commonly associated with type 2 diabetes, obesity, dyslipidaemia, and hypertension. Renal stone disease is a growing problem in the UK (and other developed and developing populations) with a cross-sectional prevalence of ∼1.2%. This means that there are currently ∼720,000 individuals with a history of kidney stones in the UK. Almost 40% of first-time stone formers will form a second stone within 3 years of the first episode if no prophylactic measures are instituted to prevent stone recurrence, since removal or disintegration of the first stone does not treat the underlying cause of stones in the majority of patients. The age of onset is getting younger and the sex ratio (until recently more men than women) is becoming almost even. Metabolic screening remains an important part of investigating renal stone disease, but to the disappointment and frustration of many doctors, medical treatment is still essentially pragmatic, except perhaps in cystinuria, and to a limited extent in primary hyperoxaluria (if pyridoxine-sensitive); although newer treatments may be emerging. This review summarizes current thinking and provides a practical basis for the management of renal stone disease.

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“…Uric acid calculi may be found in both gouty and nongouty subjects. In one large series, the incidence of uric acid nephro lithiasis was 22% in patients with primary gout and 42% in patients with secondary gout [28], In almost half of the cases with primary gout nephro lithiasis antedated the acute arthritis in some occasions by more than 20 years. Uric acid nephrolithiasis is frequently associated with hyperuricemia without any evidence of arthritis, although about one third of such patients give a family history of gout.…”

Section: Acute Hyperuricemic Nephropathy (Acute Tubular Blockade)mentioning

confidence: 99%

Hyperuricemic Nephropathy: Pathologic Features and Factors Influencing Urate Deposition

Klinenberg

Kippen

Bluestone

1975

Nephron

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The three general types of renal pathology associated with hyperuricemia are reviewed. Factors influencing urate solubility are discussed, as well as the effect of uricosuric drugs on renal urate handling, with particular emphasis upon their efficacy in competing with urate for protein binding sites. In addition, a new experimental model of hyperuricemic nephropathy is described which could yield valuable data concerning the complex relationships between hyperuricemia, urate deposition and renal function.

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Uric Acid Nephrolithiasis in Gout

Cited by 200 publications

References 32 publications

Prevention of Comorbidity and Acute Attack of Gout by Uric Acid Lowering Therapy

Prevention of Comorbidity and Acute Attack of Gout by Uric Acid Lowering Therapy

An Update and Practical Guide to Renal Stone Management

Hyperuricemic Nephropathy: Pathologic Features and Factors Influencing Urate Deposition

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