scholarly journals Sex-Specific Association of Uric Acid and Kidney Function Decline in Taiwan

2021 ◽  
Vol 11 (5) ◽  
pp. 415
Author(s):  
Po-Ya Chang ◽  
Yu-Wei Chang ◽  
Yuh-Feng Lin ◽  
Hueng-Chuen Fan

An elevated serum urate concentration is associated with kidney damage. Men’s uric acid levels are usually higher than women’s. However, postmenopausal women have a higher risk of gout than men, and comorbidities are also higher than in men. This study examined the sex differences in the relationship between hyperuricemia and renal progression in early chronic kidney disease (CKD) and non-CKD, and further examined the incidence of CKD in non-CKD populations among patients over 50 years of age. We analyzed 1856 women and 1852 men participating in the epidemiology and risk factors surveillance of the CKD database. Women showed a significantly higher risk of renal progression and CKD than men within the hyperuricemia group. After adjusting covariates, women, but not men resulted in an hazard ratio (HR) for developing renal progression (HR = 1.12; 95% CI 1.01–1.24 in women and HR = 1.03; 95% CI 0.93–1.13 in men) and CKD (HR = 1.11; 95% CI 1.01–1.22 in women and HR = 0.95; 95% CI 0.85–1.05 in men) for each 1 mg/dL increase in serum urate levels. The association between serum urate levels and renal progression was stronger in women. Given the prevalence and impact of kidney disease, factors that impede optimal renal function management in women and men must be identified to provide tailored treatment recommendations.

Author(s):  
Menglin Jiang ◽  
Dandan Gong ◽  
Yu Fan

AbstractElevated serum uric acid (SUA) levels may increase the risk of prehypertension. However, the findings from these studies remain conflicting. The objective of this study was to determine the relationship between SUA levels and risk of prehypertension by conducting a meta-analysis. We conducted a comprehensive literature search of PubMed, Embase, China National Knowledge Infrastructure, VIP, and the Wangfang database without language restrictions through May 2015. Observational studies assessing the relationship between SUA levels and prevalence of prehypertension were included. Pooled adjust odds ratio (OR) and corresponding 95% confidence intervals (CI) of prehypertension were calculated for the highest vs. lowest SUA levels. Prehypertension was defined as systolic blood pressure (BP) ranging from 120 to 139 mmHg or diastolic BP ranging from 80 to 89 mmHg. Eight cross-sectional studies with a total of 21,832 prehypertensive individuals were included. Meta-analysis showed that elevated SUA levels were associated with increased risk of prehypertension (OR: 1.84; 95% CI: 1.42–2.38) comparing the highest vs. lowest level of SUA levels. Subgroup analyses showed that elevated SUA levels significantly increased the risk of prehypertension among men (OR: 1.60; 95% CI: 1.12–2.21) and women (OR: 1.59; 95% CI: 1.17–2.16). Elevated SUA levels are positively associated with the risk of prehypertension in the general population. However, more well-designed longitudinal studies are needed before a definitive conclusion can be drawn due to the cross-sectional studies included are susceptible to bias.


2010 ◽  
Vol 25 (11) ◽  
pp. 3593-3599 ◽  
Author(s):  
L. Cain ◽  
A. Shankar ◽  
A. M. Ducatman ◽  
K. Steenland

2009 ◽  
Vol 36 (6) ◽  
pp. 1287-1289 ◽  
Author(s):  
NAOMI SCHLESINGER ◽  
JOSEPHINE M. NORQUIST ◽  
DOUGLAS J. WATSON

Objective.To study the frequency of normal serum urate (SU) levels during acute gout in the largest studies of acute gout treatment to date.Methods.Data collected from 2 randomized controlled clinical trials assessing the efficacy of etoricoxib or indomethacin for 7 days in acute gout were used to assess SU levels during acute gouty attacks. Efficacy was similar with both agents, so both groups were combined for analysis.Results.A total of 339 patients were enrolled in the 2 studies; 94% were male; mean age was 50.5 years. At baseline, 14% of patients had a “true” normal SU (≤ 6 mg/dl) and 32% had SU ≤ 8 mg/dl during acute gout. Baseline mean SU was 7.1 versus 8.5 mg/dl (p < 0.001) in those taking allopurinol versus nonusers. Patients taking chronic allopurinol were more likely to have lower SU at baseline compared to those not taking chronic allopurinol (p < 0.001) during the acute attack.Conclusion.A normal SU level at presentation does not exclude an acute gouty attack. In the largest studies of acute gout to date, attacks still occurred despite SU levels being below 6.8 mg/dl, the saturation level for urate. This may be attributed to persistence of tophi and an increased body uric acid pool. Additional studies are needed to determine the correlation between SU and the body uric acid pool as well as the relationship to timing of changes during acute gout.


2011 ◽  
Vol 342 (6) ◽  
pp. 461-466 ◽  
Author(s):  
Tamaki Yamada ◽  
Mitsuru Fukatsu ◽  
Tsuneya Wada ◽  
Sadao Suzuki ◽  
Takashi Joh

2021 ◽  
Vol 9 (F) ◽  
pp. 428-435
Author(s):  
Gede Wira Mahadita ◽  
Ketut Suwitra

In humans, the end product of purine metabolism is uric acid. Over 70% of uric acid is excreted through the kidneys. When renal function is impaired, uric acid secretion is also impaired. This directly correlates the prevalence of hyperuricemia with the severity of chronic kidney disease (CKD). It has been reported that the prevalence of hyperuricemia in patients with Stage I-III CKD is 40–60% and up to 70% in patients with Stage IV-V CKD. Some studies found a link between serum uric acid levels and decreased glomerular filtration rate (GFR), an independent risk factor for CKD development. Because CKD and serum uric acid levels are related, the relationship between the two frequently generates controversy. As such, this review of the literature discusses the role of uric acid in the pathogenesis and progression of CKD.


Author(s):  
Olga Kompaniets

The article is devoted to a review of the literature on the impact of hyperuricemia on the development and progression of chronic kidney disease (CKD). The tendency of changes of views on the role of uric acid in the pathogenesis of CKD is demonstrated. An analysis of experimental, epidemiological and clinical studies on the effects of uric acid on the physiology of the nephron and endothelial tissues, the relationship of hyperuricemia with metabolic and cardiorenal syndromes.


2020 ◽  
Vol 27 (30) ◽  
pp. 5056-5066 ◽  
Author(s):  
Pan Jing ◽  
Min Shi ◽  
Liang Ma ◽  
Ping Fu

Hyperuricemia, defined as the presence of elevated serum uric acid (sUA), could lead to urate deposit in joints, tendons, kidney and other tissues. Hyperuricemia as an independent risk factor was common in patients during the causation and progression of kidney disease. Uric acid is a soluble final product of endogenous and dietary purine metabolism, which is freely filtered in kidney glomeruli where approximately 90% of filtered uric acid is reabsorbed. Considerable studies have demonstrated that soluble uric acid was involved in the pathophysiology of renal arteriolopathy, tubule injury, tubulointerstitial fibrosis, as well as glomerular hypertrophy and glomerulosclerosis. In the review, we summarized the mechanistic insights of soluble uric acid related renal diseases.


2017 ◽  
Vol 46 (4) ◽  
pp. 315-322 ◽  
Author(s):  
Hernan Rincon-Choles ◽  
Stacey E. Jolly ◽  
Susana Arrigain ◽  
Victoria Konig ◽  
Jesse D. Schold ◽  
...  

Background: Hyperuricemia is associated with the progression of chronic kidney disease (CKD), but it is not known whether the relationship is causal. We examined the association of hyperuricemia and uric acid lowering therapy (UALT) with progression of CKD in patients with CKD 3 and 4 in the Cleveland Clinic CKD registry. Methods: We included 1,676 patients with CKD stages 3 and 4 from Ohio, who had measured their uric acid (UA) levels a year prior to the recording of the second eGFR <60 mL/min/1.73 m2, and follow-up eGFR, between 2005 and 2009. Our primary composite outcome included a 50% drop in eGFR or progression to ESRD. Secondary outcomes included the rate of decline in eGFR, all-cause mortality, progression to ESRD, and a composite measure of progression to ESRD or death. We assessed the association between UA, UALT, and outcomes using Cox models and competing risks regression models. Results: In multivariable models, higher UA was associated with the composite endpoint, but it reached statistical significance only in the 4th quartile (≥8.9 mg/dL). Receipt of UALT was significantly associated with increased risk of the composite outcome. Neither UA nor UALT (considered a time-dependent covariate) was significantly associated with mortality. The inference was similar for UA as high vs. low, quartiles, or continuous. Similarly, neither high UA nor UALT were significantly associated with ESRD, the composite of ESRD and mortality, or eGFR decline. Conclusions: Hyperuricemia is associated with increased risk of progression to ESRD in patients with CKD stages 3 and 4, but UALT does not ameliorate the risk, suggesting that the relationship is not causal.


Vascular ◽  
2020 ◽  
Vol 28 (4) ◽  
pp. 494-501 ◽  
Author(s):  
Ye Jiang ◽  
Ji-Yong Ge ◽  
Yu-Yan Zhang ◽  
Fang-Fang Wang ◽  
Yuan Ji ◽  
...  

Objective This study aims to investigate the relationship between serum uric acid and arterial stiffness in a healthy population. Methods Among the 979 participants, baPWV was non-invasively measured, the circulating levels of uric acid were tested, and the uric acid polymorphisms (rs2231142 and rs11722228) were genotyped. Then, the Mendelian randomization method was employed to test the relationship between serum uric acid and arterial stiffness in a healthy population. Results After adjusting for age, gender, antihypertensive medication, body mass index, waist-to-hip ratio, urea nitrogen, creatinine and diabetic mellitus, there was a significant allelic difference in uric acid levels for each genotype ( P <  0.0001 for rs2231142; P =  0.007 for rs11722228). However, there were no differences on the potential confounders between the genotypes of rs2231142 and rs11722228 ( P >  0.05). The baPWV was significantly associated with circulating levels of uric acid after adjusting for cardiovascular risk factors and other potential confounders ( P =  0.002). However, neither the single polymorphism, nor the accumulation of culprit alleles was associated with baPWV ( P =  0.92 for rs2231142; P =  0.60 for rs11722228; P for trend = 0.77 for the combined analysis of culprit alleles). Conclusion These results do not support the causal role of circulating levels of uric acid in the development of arterial stiffness.


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