Serum uric acid: a mediator of cardio-reno-metabolic diseases

Author(s):  
Niki Katsiki ◽  
Vasilios Athyros
2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 848.2-849
Author(s):  
Z. Huang ◽  
T. LI

Background:Serum uric acid-to-creatinine ratio (SUA/Cr) is a useful index of renal function-normalized serum uric acid (SUA), which reflects endogenous SUA levels more precisely than SUA. SUA/Cr relates to disease activity and prognosis of several metabolic disorders, like metabolic syndrome, non-alcoholic fatty liver disease, and diabetes mellitus [1]. Besides, the urine uric acid-to-creatinine ratio is valuable for the assessment of gout [2]. However, no study focuses on the relationship between SUA/Cr and gout.Objectives:We aimed to investigate the relationship between SUA/Cr and the features of demography, manifestations, laboratory tests, and urate-lowering therapies (ULTs) in gout patients.Methods:This cross-sectional study was performed from December 2015 to February 2020. Medical records of gout patients who were regularly undergone follow-up were evaluated. Characteristics of gout patients, included age, gender, the duration of gout, body mass index (BMI), tophus, complications, the number of flares, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR), were recorded. Complications were defined as hypertension, coronary artery diseases, diabetes, strokes, and/or metabolic diseases. Information about ULT was obtained as well. The Spearman correlation analysis was used to assess the relationship between continuous variables. The Mann-Whiney U test or Kruskal-Wallis test was employed to compare the differences of SUA/Cr between genders, ULTs, and whether patients had tophus or complications. A P<0.05 was considered as statistically significant.Results:(1) Of 627 gout patients who were involved, 608 (96.97%) were male. Their median (range) of age and the duration of gout were 30.00 (51.00) years and 5.00 (30.00) years, respectively. (2) SUA/Cr negatively correlated with age (r=-0.71, P<0.05). SUA/Cr was similar between genders. (3) SUA/Cr positively correlated with BMI (r=0.14, P<0.05), while the coefficient correlation for the duration of gout and the number of flares did not reach statistically significant (P>0.05). SUA/Cr was significantly higher in patients with complications than the others [5.56 (9.26) vs. 4.16 (8.34), P<0.05], but whether patients with tophus or not shared similar SUA/Cr. (4) CRP and ESR did not associate with SUA/Cr (P>0.05). (5) Patients with combination therapy with xanthine oxidase inhibitor and uricosuric agent had a lower SUA/Cr compared with those who used ULTs monotherapy [3.44 (7.10) vs. 4.53 (7.91), P<0.05].Conclusion:SUA/Cr relates to some features of gout, so it may be a potential marker for its assessment.References:[1]Medicine (Baltimore) 2020;99(17):e19959.[2]J Korean Med Sci 2020;35(13):e95.Disclosure of Interests:None declared.


Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1115 ◽  
Author(s):  
Mariana O. C. Coelho ◽  
Alistair J. Monteyne ◽  
Ishara D. Kamalanathan ◽  
Vesna Najdanovic-Visak ◽  
Tim J. A. Finnigan ◽  
...  

Circulating uric acid concentrations have been linked to various metabolic diseases. Consumption of large boluses of nucleotides increases serum uric acid concentrations. We investigated the effect of a nucleotide-rich mixed meal on postprandial circulating uric acid, glucose, and insulin responses. Ten healthy adults participated in a randomised, controlled, double-blind, crossover trial in which they consumed a mixed-meal containing either nucleotide-depleted mycoprotein (L-NU) or high-nucleotide mycoprotein (H-NU) on two separate visits. Blood samples were collected in the postabsorptive state and throughout a 24 h postprandial period, and were used to determine circulating uric acid, glucose, and insulin concentrations. Mixed meal ingestion had divergent effects on serum uric acid concentrations across conditions (time x condition interaction; P < 0.001), with L-NU decreasing transiently (from 45 to 240 min postprandially) by ~7% (from 279 ± 16 to 257 ± 14 µmol·L−1) and H-NU resulting in a ~12% increase (from 284 ± 13 to 319 ± 12 µmol·L−1 after 210 min), remaining elevated for 12 h and returning to baseline concentrations after 24 h. There were no differences between conditions in blood glucose or serum insulin responses, nor in indices of insulin sensitivity. The ingestion of a nucleotide-rich mixed-meal increases serum uric acid concentrations for ~12 h, but does not influence postprandial blood glucose or serum insulin concentrations.


2019 ◽  
Author(s):  
Shulei Fan ◽  
Yang Zou ◽  
Amanda Y Wang ◽  
Mingjie Xu ◽  
Guisen Li ◽  
...  

Abstract Background: With the change of living standard and dietary structure, the incidence of hyperuricemia is on the rise. Hyperuricemia has become one of the metabolic diseases threatening human health. There is paucity of literature on the association between serum uric acid levels and the progression of CKD. This study aimed at assessing the effect of serum baseline uric acid level on the progression of CKD. Methods: This retrospective study included 800 CKD patients in our center. The information on baseline and follow-up characteristics were collected from our Renal Treatment System (RTS) database. Cox regression analysis was used to evaluate the risk factors for CKD progression. The Kaplan–Meier analysis was used to test associations between serum uric acid levels and renal survival rates. Results: A total of 800 patients were included in the study, and the mean age at entry was 36.6±14.4 years. There was no significant difference in gender distribution. The mean eGFR, Cr, serum uric acid at baseline were 99.23±31.54 ml/min/1.73㎡, 82.08±41.40 μmol/L, 371.60±103.18 μmol/L, respectively. 306 (38.3%) patients had HUA and 494 (61.7%) had non-HUA. We established different adjusted models and found that HUA was a risk factor for CKD patients to reach the composite endpoint after adjustment in six models. All models show that HUA was a risk factor for the progression of CKD. Among them, model 4 (adjusted for Cr + Alb + age + BP + gender) was the best model with the largest HR value (HR:2.010, 95%CI:1.310-3.084, P<0.05). The cumulative survival rate of non-hyperuricemia group was higher than that of hyperuricemia group (P<0.001). Conclusions: Hyperuricemia was not only widespread in patients with CKD, but also a risk factor for the progression of CKD. Anti-hyperuricemia therapy may need to be considered in CKD patients to slow the disease progression, which needs to be tested further in clinical studies. Key words: hyperuricemia, chronic kidney disease, renal function, progression


Human Cell ◽  
2021 ◽  
Author(s):  
Masatsune Ogura ◽  
Yu Toyoda ◽  
Masayuki Sakiyama ◽  
Yusuke Kawamura ◽  
Akiyoshi Nakayama ◽  
...  

AbstractElevated serum uric acid (SUA)—hyperuricemia—is caused by overproduction of urate or by its decreased renal and/or intestinal excretion. This disease, which is increasing in prevalence worldwide, is associated with both gout and metabolic diseases. Several studies have reported relationships between apolipoprotein E (APOE) haplotypes and SUA levels in humans; however, their results remain inconsistent. This prompted us to investigate the relationship between APOE polymorphisms and SUA levels. Our subjects were 5,272 Japanese men, premenopausal women, and postmenopausal women. Multiple linear regression analyses revealed the ε2 haplotype of APOE to be independently associated with higher SUA in men (N = 1,726) and postmenopausal women (N = 1,753), but not in premenopausal women (N = 1,793). In contrast, the ε4 haplotype was little related to SUA levels in each group. Moreover, to examine the effect of Apoe deficiency on SUA levels, we conducted animal experiments using Apoe knockout mice, which mimics ε2/ε2 carriers. We found that SUA levels in Apoe knockout mice were significantly higher than those in wild-type mice, which is consistent with the SUA-raising effect of the ε2 haplotype observed in our clinico-genetic analyses. Further analyses suggested that renal rather than intestinal underexcretion of urate could be involved in Apoe deficiency-related SUA increase. In conclusion, we successfully demonstrated that the ε2 haplotype, but not the ε4 haplotype, increases SUA levels. These findings will improve our understanding of genetic factors affecting SUA levels.


JAMA ◽  
1966 ◽  
Vol 196 (4) ◽  
pp. 364-365 ◽  
Author(s):  
L. A. Healey
Keyword(s):  

1970 ◽  
Author(s):  
Robert T. Rubin ◽  
Richard H. Rahe ◽  
Brian R. Clark ◽  
Ransom J. Arthur

Author(s):  
Sushma Goad ◽  
Anita Verma ◽  
Subhash Chandra

Background: To Study Serum Uric Acid level elevation in Hypertensive Disorders of Pregnancy. Methods: 50 Patients diagnosed as having Pre-eclampsia with age between 18-37 years and 50 controls with similar age group. Results: The mean serum uric acid level in control group was 3.41 ± 0.62 and in patient 7.01 ± 0.58 which was statistically significant (p =0.001). Conclusion: Serum uric acid levels were significantly higher in preeclampsia could be a useful indicator of fetal complication in preeclampsia patients. Keywords: serum uric acid, preeclampsia, laboratory.


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