Effect of Uric Acid Control on Serum Creatinine

Yamamoto, Ted; Xie, John; Li, Zhongze; Field, Carey; Block, Clay A.; Taylor, Thomas H.

doi:10.1097/rhu.0000000000000850

Cited by 7 publications

(9 citation statements)

References 22 publications

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“…Certain foods, status, or medicines could induce hyperuricemia. Under renal dis-function or cell damage, SUA could be suddenly increased by changing renal function to cause hyperuricemia [76]. Drugs such as diuretics (thiazide), anticonvulsants (valproate and phenobarbital), cyclosporine, theophylline, and pyrazinamide have been reported to increase SUA levels [77] in addition to favipiravir (an antiviral drug) [78].…”

Section: The Causes Of Hyperuricemia Irrelevant To Goutmentioning

confidence: 99%

Why Does Hyperuricemia Not Necessarily Induce Gout?

Zhang

2021

Biomolecules

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Hyperuricemia is a risk factor for gout. It has been well observed that a large proportion of individuals with hyperuricemia have never had a gout flare(s), while some patients with gout can have a normuricemia. This raises a puzzle of the real role of serum uric acid (SUA) in the occurrence of gout flares. As the molecule of uric acid has its dual effects in vivo with antioxidant properties as well as being an inflammatory promoter, it has been placed in a delicate position in balancing metabolisms. Gout seems to be a multifactorial metabolic disease and its pathogenesis should not rely solely on hyperuricemia or monosodium urate (MSU) crystals. This critical review aims to unfold the mechanisms of the SUA role participating in gout development. It also discusses some key elements which are prerequisites for the formation of gout in association with the current therapeutic regime. The compilation should be helpful in precisely fighting for a cure of gout clinically and pharmaceutically.

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Section: The Causes Of Hyperuricemia Irrelevant To Goutmentioning

confidence: 99%

Why Does Hyperuricemia Not Necessarily Induce Gout?

Zhang

2021

Biomolecules

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“…The country-based estimation of hyperuricemia prevalence was extended to countries which have reported only one study. A study conducted in the United Kingdom (only study conducted among pediatric patients) had a prevalence of 69.8% (60.9-77.5%) [36], The United States [21] had a prevalence of 76.7% (72.0-80.9%), Italy [35], Brazil [33] and Cameroon [42] had a prevalence of 72.0% (44.6-89.1%), 54.1% (26.3-61.5%) and 67.0% (57.4-75.4%), while India [39] and South Korea [28] had reported a prevalence of 38.4% (15.7-67.5%) and 23.8% (8.8-50.5%) respectively.…”

Section: Geography Specific Prevalencementioning

confidence: 99%

Hyperuricemia—a serious complication among patients with chronic kidney disease: a systematic review and meta-analysis

Rashid

Katravath

Tiwari

et al. 2022

Exploration of Medicine

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Aim: Hyperuricemia as a putative risk factor for chronic kidney disease (CKD) progression remains controversial and debatable. This systematic review aims to explore the prevalence of hyperuricemia among CKD patients worldwide. Methods: This study was conducted in accordance with the Meta-analysis Of Observational Studies in Epidemiology (MOOSE) guidelines by using the existing literature from online databases such as MEDLINE/PubMed, ScienceDirect, Google Scholar, Cochrane library and grey literature. The effect size with corresponding 95% confidence interval (CI) was calculated to assess the pooled prevalence of hyperuricemia in chronic kidney patients. The subgroup analysis based on gender and geography was also carried out by utilizing comprehensive meta-analysis, version 2.0. Results: Twenty-three studies containing 212,740 participants were eligible for quantitative synthesis. The pooled prevalence of 43.6% (35.2–52.4%) hyperuricemia was reported in patients with CKD globally. In India, 38.4% of prevalence was observed. The gender specific prevalence (9 studies) was reported as 67.4% (60.9–73.3%) in case of male patients and 32.6% (26.7–39.1%) in female patients with 95% CI. Conclusions: The prevalence of hyperuricemia was reported to be reasonably high among CKD patients worldwide. During the management of CKD, this high prevalence demands more prudent attention for this clinical complication which possibly can lead to positive renal outcomes.

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“…Certain foods, status, or medicines could induce hyperuricemia. Under renal dis-function or cell damages, SUA could be suddenly increased by changing renal function to cause hyperuricemia [76]. Drugs such as diuretics (thiazide), anticonvulsants (valproate and phenobarbital), cyclosporine, theophylline, and pyrazinamide have been reported to increase SUA levels [77] in addition to favipiravir (an antiviral drug) [78].…”

Section: The Causes Of Hyperuricemia Irrelevant To Goutmentioning

confidence: 99%

Why Hyperuricemia Does Not Necessarily Induce Gout?

Zhang¹

2020

Preprint

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Hyperuricemia is a risk factor for gout. It has been well observed that a large proportion of hyperuricemia individuals have never had a gout attack(s), while some patients with gout can have a normuricemia. This raises a puzzle of the real role of serum uric acid (SUA) in the occurrence of gout attacks. As the molecule of uric acid has its dual effects in vivo with antioxidant property as well as being an inflammatory promoter, it has been placed in a delicate position in balancing metabolisms. Gout seems to be a multifactorial metabolic disease and its pathogenesis should not rely solely on hyperuricemia or MSU crystal. This critical review aims to unfold the mechanisms of the SUA role participating in gout development. It also discusses some key elements which are prerequisite for the formation of gout in association with the current therapeutic regime. The compilation should be helpful in precisely fighting for a cure of gout clinically and pharmaceutically.

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Effect of Uric Acid Control on Serum Creatinine

Abstract: Given that most serial measures were within the first few years of follow-up, and change in renal function occurs slowly over time, the between group difference of sUa of 0.18 mg/dL is close to a clinically significant creatinine difference of 0.2 mg/dL.

Cited by 7 publications

References 22 publications

Why Does Hyperuricemia Not Necessarily Induce Gout?

Why Does Hyperuricemia Not Necessarily Induce Gout?

Hyperuricemia—a serious complication among patients with chronic kidney disease: a systematic review and meta-analysis

Why Hyperuricemia Does Not Necessarily Induce Gout?

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