Changes In Serum Uric Acid Research Articles

In-Hospital Serum Uric Acid Change Predicts Adverse Outcome in Patients With Heart Failure

BackgroundElevated serum uric acid (UA) is associated with an increased risk of adverse outcome in patients with heart failure (HF), but it remains unknown whether the change of serum UA level during the treatment of acute decompensated HF (ADHF) predicts adverse events. Methods and ResultsWe retrospectively analyzed consecutive 1562 patients who were hospitalized for ADHF. Serum UA levels both at admission and discharge were available in 1246 patients (78 years of age, range 69–84 years, 40% female). UA values increased or unchanged (group I) in 766 patients and it decreased in the remaining patients (group D). Group I was characterized by older age, higher proportion of females, preserved left ventricular ejection fraction, and the features of less severity of HF such as lower plasma N-terminal pro B-type natriuretic peptide level and lower percentage of catecholamine use. Nevertheless, group I was associated with higher incidence of the primary end point defined as the composite of all-cause death and ADHF rehospitalization (P = .013, log-rank test). UA change, but not UA at discharge, was an independent predictor of the primary end point (hazard ratio 1.30, interquartile range 1.04–1.64, P = .022). Age, estimated glomerular filtration rate, left ventricular ejection fraction, dose of loop diuretics, and thiazide prescription at discharge were independently associated with the UA change. ConclusionsIn patients with HF, UA change through the treatment of ADHF might predict future adverse outcome.

Comparison of uric acid reduction and renal outcomes of febuxostat vs allopurinol in patients with chronic kidney disease

Whether the clinical trial treatment effect of urate-lowering therapy (ULT) in patient with chronic kidney disease (CKD) is generalizable to real-word settings is unclear. This study aimed to compare febuxostat with allopurinol for uric acid reduction and renal protection in patients with CKD. Adult CKD patients newly treated with ULT were identified using electronic health records from 2010 to 2015 from a large healthcare delivery system in Taiwan. Patients with renal replacement therapy or undergoing ULT for <3 months were excluded. Propensity score–matched cohort study design was conducted to compare outcomes between patients initiated with febuxostat or allopurinol therapy. Cox regression analyses were employed to compare the adjusted hazards ratio (aHR) of incident event of estimated glomerular filtration rate (eGFR) ≥ 30% decrease, and the difference in longitudinal changes in serum uric acid (SUA) and eGFR between groups was analyzed using linear mixed model. Overall, 1050 CKD patients who initiated febuxostat (n = 525) or allopurinol (n = 525) treatment were observed for 2.5 years. Compared with allopurinol, febuxostat use was associated with higher rate of patients maintaining SUA target <6 mg/dL in >80% of follow-up time with a reduction in mean SUA change. There were no significant differences in the mean eGFR changes over time between the febuxostat and allopurinol groups or in the risk of eGFR decline ≥30% of baseline. Febuxostat was associated with greater reduction in SUA level than allopurinol in patients with CKD. However, febuxostat and allopurinol showed no difference in renal function changes during study follow-up. These findings require further investigation with long-term follow up in CKD patients with hyperuricemia.

Sex-specific association of serum uric acid dynamics with the incidence of metabolic syndrome in a health check-up Chinese population: a prospective cohort study

ObjectiveMany studies have demonstrated that elevated serum uric acid (SUA) level is linked with metabolic syndrome (MetS). However, whether there is a sex difference in the association between SUA and...

Effect of sodium-glucose transport protein 2 inhibitors on serum uric acid: an outpatient based prospective interventional study

Background: Hyperuricemia is considered to be associated with increased risk of cardiovascular diseases. It has been found to be related to features of metabolic syndromes like hyperglycemia and dyslipidemia. Sodium-glucose transport protein 2 (SGLT2) inhibitors are known to have a decremental effect on serum uric acid level. We evaluated the effect of SGLT2 inhibitors on serum uric acid of diabetic population.Methods: In this prospective study we recruited 50 type 2 diabetes mellitus (T2DM) patients who were on metformin monotherapy and were having inadequate glycemic control. Patients were prescribed SGLT2 inhibitors as an add-on therapy. Serum uric acid of the subjects was measured at the baseline and after 3 months. The primary outcome was to observe changes in serum uric acid (SUA) levels from the baseline to the end of the study. Glycemic changes were determined by observing the changes in glycated haemoglobin (HbA1c) levels (if any).Results: The study population was predominantly male (82%). BMI wise most of the subjects (44%) were overweight. Mean HbA1c of total population was 7.65±0.5, whereas mean serum uric acid was 6.31±0.72 at the baseline. After 3 months HbA1C and serum uric acid levels were 7.45±0.50 and 6.06±0.64 respectively. Both the changes were statistically significant (p&lt;0.005).Conclusions: SGLT2 inhibitors could improve glycemic control and lower SUA levels in patients with uncontrolled T2DM. Randomized study with bigger sample size and longer study period are required to further demonstrate the effect of SGLT2 inhibitors on serum uric acid and explore the potential underlying mechanisms.

Clinical Predictors of the Hypoglycemic Effect of Sodium-Glucose Co-transporter-2 Inhibitors in Hyperuricemic Patients: A Retrospective Descriptive Observational Study.

Sodium-glucose co-transporter-2 (SGLT2) inhibitors decrease glycated hemoglobin (HbA1c) and prevent the progression of cardiovascular and kidney diseases. Because uric acid and electrolytes are physiologically similar to blood glucose in renal excretion, we assessed predictors for the hypoglycemic effect of SGLT2 inhibitor treatment by focusing on serum uric acid and serum electrolytes. We performed a retrospective descriptive observational study at the Tokyo Women's Medical University, Medical Center East, from June 2015 to July 2018. Patients who received treatment with any type of SGLT2 inhibitor were selected, which included a total of 165 patients. The response to SGLT2 inhibitors defined as changes in HbA1c after SGLT2 inhibitor treatment was the main outcome measure. Multiple linear regression analysis was used to assess predictors for the hypoglycemic effect by SGLT2 inhibitors. Among the 165 patients, SGLT2 inhibitor treatment decreased HbA1c from 8.2 to 7.6% after 12 weeks (p < 0.01). Multiple linear regression analysis revealed that predictors of early response to SGLT2 inhibitors were serum uric acid values (p = 0.014) and baseline HbA1c (p < 0.001). Furthermore, late response to SGLT2 inhibitors was associated with serum uric acid value (p = 0.047) and baseline HbA1c (p < 0.001). Serum uric acid did not vary during SGLT2 inhibitor treatment; specifically, the SGLT2 inhibitors did not reduce serum uric acid levels. There was no correlation between changes in serum uric acid and HbA1c (p = 0.13). Thus, this study showed that serum uric acid value is associated with the control of diabetes mellitus during SGLT2 inhibitor treatment. Further studies are required to validate these results.

Associations between changes in serum uric acid and the risk of myocardial infarction

BackgroundThe role of serum uric acid (SUA) in development of myocardial infarction (MI) is controversial. The current study aimed to investigate the association between both baseline SUA and changes in SUA and the risk of MI. MethodsThe current study included 71,449 Chinese participants (mean age, 50.9 years) free of MI during the time of follow-up. Participants were divided into 4 categories according to the SUA levels between baseline and the second follow-up: stable low, elevated, reduced and stable high. Multivariate Cox proportion models were used to calculated hazard ratios (HRs) and their 95% confidence intervals (CIs) for MI. ResultsDuring a median follow-up of 8.96 years, 837 MI cases were identified. After adjustment for potential confounders, MI risk was only associated with stable high SUA, the HR was 1.42 (95%CI: 1.02–1.92, p = 0.03), compared with those with stable low SUA. However, there was no association between hyperuricemia at baseline and MI, the HR was 1.14 (95%CI: 0.91–1.42, p = 0.19) compared with those with normal SUA. Subgroup analyses stratified by age, sex, hypertension, diabetes and estimated glomerular filtration rate were also confirmed no significant difference (p-interaction >0.05 for all). Furthermore, mediation analyses revealed 14.14% of association was mediated by hypertension. ConclusionsOnly stable high SUA was associated with increased higher risk of MI. Changes in SUA levels in any other direction or high SUA levels at baseline were not associated with risk of MI.

Febuxostat does not delay progression of carotid atherosclerosis in patients with asymptomatic hyperuricemia: A randomized, controlled trial.

BackgroundAn elevated level of serum uric acid (SUA) is associated with an increased risk of cardiovascular disease. Pharmacological intervention with urate-lowering agents, such as the conventional purine analogue xanthine oxidase (XO) inhibitor, allopurinol, has been used widely for a long period of time in clinical practice to reduce SUA levels. Febuxostat, a novel non-purine selective inhibitor of XO, has higher potency for inhibition of XO activity and greater urate-lowering efficacy than conventional allopurinol. However, clinical evidence regarding the effects of febuxostat on atherosclerosis is lacking. The purpose of the study was to test whether treatment with febuxostat delays carotid intima-media thickness (IMT) progression in patients with asymptomatic hyperuricemia.Methods and findingsThe study was a multicenter, prospective, randomized, open-label, blinded-endpoint clinical trial undertaken at 48 sites throughout Japan between May 2014 and August 2018. Adults with both asymptomatic hyperuricemia (SUA >7.0 mg/dL) and maximum IMT of the common carotid artery (CCA) ≥1.1 mm at screening were allocated equally using a central web system to receive either dose-titrated febuxostat (10–60 mg daily) or as a control-arm, non-pharmacological lifestyle modification for hyperuricemia, such as a healthy diet and exercise therapy. Of the 514 enrolled participants, 31 were excluded from the analysis, with the remaining 483 people (mean age 69.1 years [standard deviation 10.4 years], female 19.7%) included in the primary analysis (febuxostat group, 239; control group, 244), based on a modified intention-to-treat principal. The carotid IMT images were recorded by a single sonographer at each site and read in a treatment-blinded manner by a single analyzer at a central core laboratory. The primary endpoint was the percentage change from baseline to 24 months in mean IMT of the CCA, determined by analysis of covariance using the allocation adjustment factors (age, gender, history of type 2 diabetes, baseline SUA, and baseline maximum IMT of the CCA) as the covariates. Key secondary endpoints included changes in other carotid ultrasonographic parameters and SUA and the incidence of clinical events. The mean values (± standard deviation) of CCA-IMT were 0.825 mm ± 0.173 mm in the febuxostat group and 0.832 mm ± 0.175 mm in the control group (mean between-group difference [febuxostat − control], −0.007 mm [95% confidence interval (CI) −0.039 mm to 0.024 mm; P = 0.65]) at baseline; 0.832 mm ± 0.182 mm in the febuxostat group and 0.848 mm ± 0.176 mm in the control group (mean between-group difference, −0.016 mm [95% CI −0.051 mm to 0.019 mm; P = 0.37]) at 24 months. Compared with the control group, febuxostat had no significant effect on the primary endpoint (mean percentage change 1.2% [95% CI −0.6% to 3.0%] in the febuxostat group (n = 207) versus 1.4% [95% CI −0.5% to 3.3%] in the control group (n = 193); mean between-group difference, −0.2% [95% CI −2.3% to 1.9%; P = 0.83]). Febuxostat also had no effect on the other carotid ultrasonographic parameters. The mean baseline values of SUA were comparable between the two groups (febuxostat, 7.76 mg/dL ± 0.98 mg/dL versus control, 7.73 mg/dL ± 1.04 mg/dL; mean between-group difference, 0.03 mg/dL [95% CI −0.15 mg/dL to 0.21 mg/dL; P = 0.75]). The mean value of SUA at 24 months was significantly lower in the febuxostat group than in the control group (febuxostat, 4.66 mg/dL ± 1.27 mg/dL versus control, 7.28 mg/dL ± 1.27 mg/dL; mean between-group difference, −2.62 mg/dL [95% CI −2.86 mg/dL to −2.38 mg/dL; P < 0.001]). Episodes of gout arthritis occurred only in the control group (4 patients [1.6%]). There were three deaths in the febuxostat group and seven in the control group during follow-up. A limitation of the study was the study design, as it was not a placebo-controlled trial, had a relatively small sample size and a short intervention period, and only enrolled Japanese patients with asymptomatic hyperuricemia.ConclusionsIn Japanese patients with asymptomatic hyperuricemia, 24 months of febuxostat treatment did not delay carotid atherosclerosis progression, compared with non-pharmacological care. These findings do not support the use of febuxostat for delaying carotid atherosclerosis in this population.Trial registrationUniversity Hospital Medical Information Network Clinical Trial Registry UMIN000012911.

Impact of Uric Acid on Hypertension Occurrence and Target Organ Damage: Insights From the STANISLAS Cohort With a 20-Year Follow-up.

Recent studies have shown that hyperuricemia may be associated with incident hypertension (HTN). We examined whether serum uric acid (SUA) is a predictor of HTN and target organ damage (TOD) 20 years later in initially healthy middle-aged individuals. Participants from the Suivi Temporaire Annuel Non-Invasif de la Santé des Lorrains Assurés Sociaux (STANISLAS) a single-center familial longitudinal cohort study (961 initially healthy adults and 570 children) underwent clinical and laboratory measurements at baseline and after approximately 20 years. Blood pressure (BP: using ambulatory BP measurements), urine albumin-to-creatinine ratio, estimated glomerular filtration rate (eGFR), left ventricular hypertrophy (LVH), diastolic dysfunction, and carotid-femoral pulse wave velocity (PWV) were measured at the end of follow-up. In the parent population, higher baseline or last SUA levels and higher change in SUA (ΔUA) were significantly associated with an increased risk of HTN development, even after adjusting for known HTN risk factors (all P < 0.01). Higher baseline SUA was marginally associated with an increased risk of having high carotid-femoral PWV (P = 0.05). The association of SUA with BP increase was body mass index dependent (the increase in BP being greater in leaner subjects; interactionp < 0.05), and the association of SUA with eGFR decline was age dependent (the decline in eGFR being greater in older subjects; interactionp < 0.05). There was no significant association between SUA and diastolic dysfunction or LVH. In the whole population (i.e. including children), a significant association between SUA at baseline and the risk of HTN and higher carotid-femoral PWV was also found (both P < 0.02). Increased SUA is associated with the development of HTN and vascular/renal TOD in initially healthy midlife subjects.

Evaluation of high-sensitivity C-reactive protein and uric acid in vericiguat-treated patients with heart failure with reduced ejection fraction.

AimsThe effects of vericiguat vs. placebo on high‐sensitivity C‐reactive protein (hsCRP) and serum uric acid (SUA) were assessed in patients with heart failure with reduced ejection fraction (HFrEF) in the Phase 2 SOCRATES‐REDUCED study (NCT01951625).Methods and resultsChanges from baseline hsCRP and SUA values at 12 weeks with placebo and vericiguat (1.25 mg, 2.5 mg, 5.0 mg and 10.0 mg, respectively) were assessed. The probability of achieving an hsCRP value of ≤3.0 mg/L or SUA value of <7.0 mg/dL at week 12 was tested. Median baseline hsCRP and SUA levels were 3.68 mg/L [interquartile range (IQR) 1.41–8.41; n = 335] and 7.80 mg/dL (IQR 6.40–9.33; n = 348), respectively. Baseline‐adjusted mean percentage changes in hsCRP were 0.2%, −19.5%, −24.3%, −25.7% and −31.9% in the placebo and vericiguat 1.25 mg, 2.5 mg, 5.0 mg and 10.0 mg groups, respectively; significance vs. placebo was observed in the vericiguat 10.0 mg group (P = 0.035). Baseline‐adjusted mean percentage changes in SUA were 5.0%, −1.3%, −1.1%, −3.5% and −5.3% in the placebo, and vericiguat 1.25 mg, 2.5 mg, 5.0 mg and 10.0 mg groups, respectively; significance vs. placebo was observed in the 5.0 mg and 10.0 mg groups (P = 0.0202 and P = 0.004, respectively). Estimated probability for an end‐of‐treatment hsCRP value of ≤3.0 mg/L and SUA value of <7.0 mg/dL was higher with vericiguat compared with placebo. The effect was dose‐dependent, with the greatest effect observed in the 10.0 mg group.ConclusionsVericiguat treatment for 12 weeks was associated with reductions in hsCRP and SUA, and a higher likelihood of achieving an hsCRP value of ≤3.0 mg/L and SUA value of <7.0 mg/dL.

Interactive association of baseline and changes in serum uric acid on renal dysfunction among community-dwelling persons.

BackgroundChronic kidney disease (CKD) is a major public health concern. Baseline serum uric acid (SUA) levels were independently associated with incident renal dysfunction, but whether baseline and changes in SUA produce an interactive effect on renal dysfunction remains unclear.MethodsThe subjects comprised 460 men aged 68 ± 10 (mean ± standard deviation) years and 635 women aged 68 ± 9 years from a rural village. We have found participants who underwent a similar examination 3 years later, and analyzed the relationship between baseline SUA, changes in SUA, and a 3‐year follow‐up renal function evaluated by estimated glomerular filtration rate (eGFR).ResultsA total of 93 (20.2%) men and 76 (12.0%) women had hyperuricemia (men: SUA ≥ 7.0 mg/dL and women: SUA ≥ 6.0 mg/dL) at baseline. Multiple regression analysis using changes in eGFR as objective variable, adjusted for risk factors as explanatory variables, showed that the baseline SUA and changes in SUA were linearly associated with changes in eGFR (β = －0.115, P < .001 and β = －0.431, P < .001, respectively). In both normal SUA group and hyperuricemia group, changes in SUA significantly associated with changes in eGFR (β = －0.473, P < .001 and β = －0.197, P = .009, respectively). Participants with increased SUA from normal to hyperuricemia group had greater eGFR decline over the follow‐up period, and their multivariate‐adjusted 3‐year follow‐up eGFR was significantly lower than in other groups (P < .001).ConclusionOur data demonstrated that baseline and longitudinal changes in SUA were independently and interactively associated with the renal function decline among community‐dwelling persons.

Dietary Interventions for Gout and Effect on Cardiovascular Risk Factors: A Systematic Review.

Gout is one of the most prevalent inflammatory rheumatic disease. It is preceded by hyperuricemia and associated with an increased risk for cardiovascular disease, both related to unhealthy diets. The objective of this systematic review is to better define the most appropriate diet addressing both disease activity and traditional cardiovascular risk factors in hyperuricemic patients. We included clinical trials with patients diagnosed with hyperuricemia or gout, investigating the effect of dietary interventions on serum uric acid (SUA) levels, gout flares and—if available—cardiovascular risk factors. Eighteen articles were included, which were too heterogeneous to perform a meta-analysis. Overall, the risk of bias of the studies was moderate to high. We distinguished four groups of dietary interventions: Calorie restriction and fasting, purine-low diets, Mediterranean-style diets, and supplements. Overall, fasting resulted in an increase of SUA, whilst small (SUA change +0.3 to −2.9 mg/dL) but significant effects were found after low-calorie, purine-low, and Mediterranean-style diets. Studies investigating the effect on cardiovascular risk factors were limited and inconclusive. Since Mediterranean-style diets/DASH (Dietary Approach to Stop Hypertension) have shown to be effective for the reduction of cardiovascular risk factors in other at-risk populations, we recommend further investigation of such diets for the treatment of gout.

Regulation of serum uric acid with canagliflozin monotherapy in type 2 diabetes: A potential link between uric acid and pancreatic β-cell function .

This aim of this study is to investigate the regulation of serum uric acid (SUA) levels with canagliflozin in relation to diabetic parameters. Drug-naïve subjects with type 2 diabetes (T2DM) received 50-100 mg/day canagliflozin monotherapy (n = 40) for 3 months. Levels of SUA and some diabetic parameters were monitored. In the overall subjects, significant negative correlations were observed between the changes (Δ) of SUA and the baseline SUA levels (R = -0.392, p &lt; 0.02). The subjects were divided into two subgroups (n = 20 each) according to the changes of SUA levels (above the median (group A): from 4.79 ± 1.22 to 5.34±1.39 mg/dL; and below the median (group B): from 5.80±1.08 to 4.98±0.97 mg/dL). Significant increases of SUA levels were observed in group A (11.4%, p<0.0002), while significant decreases of SUA levels were seen in group B (-14.1%, p<0.00001). Significant correlations were seen between the baseline levels of SUA and those of homeostasis model assessment (HOMA)-B (R=0.463, p<0.04) and between the changes of SUA and those of HOMA-B (R=0.420, p<0.05) only in group A. Higher degrees of elevations of HOMA-B and decreases of HbA1c/fasting blood glucose (FBG) were seen in group A versus group B. These results suggest that 1) high SUA levels decreased while low SUA levels increased with canagliflozin; 2) better glycemic efficacies and higher degrees of enhancement of β-cell function were observed in those with elevated SUA levels with canagliflozin; 3) SUA might be linked to modulation of β-cell function.

Improvement of hyperuricemia in chronic hepatitis C patients receiving directly acting antiviral agents.

Hepatitis C virus eradication via the use of antivirals ameliorates metabolic profiles. The changes in serum uric acid (SUA) levels in chronic hepatitis C patients who receive antivirals are not well understood. We aimed to address this issue by comparing the SUA changes before and after the achievement of a sustained virological response (which is defined as hepatitis C virus RNA seronegativity at 12weeks after the end of treatment). Two hundred and thirteen sustained virological response patients who were treated by directly acting antivirals were consecutively enrolled. Pretreatment and post-treatment SUA levels were compared. Hyperuricemia was defined as a uric acid level >7.0mg/dL in men and >6.0mg/dL in women. The SUA levels significantly decreased after treatment, as compared to the pretreatment levels (5.6±1.5 vs 6.0±1.7mg/dL, respectively; P<0.001). The proportion of hyperuricemia incidences significantly decreased after treatment (25.8% vs 35.7%, respectively; P=0.001). The improvement was only observed in patients with a fibrosis-4 index (FIB-4)<6.5 (25.7% vs 37.1%, P=0.001) but not in those patients with a FIB-4≧6.5 (26.3% vs 28.9%, P=1.00). A multivariate analysis revealed that the factor that was associated with significantly decreased SUA levels was FIB-4<6.5 (odds ratio [OR]/95% confidence interval [CI]: 3.22/1.04-9.95, P=0.04) and estimated glomerular filtration rate <60mL/min/1.73m2 (OR/CI: 4.34/1.94-9.73, P<0.001). There existed a trend of a higher proportion of patients with significant SUA improvement along with the decrement of FIB-4 (29.7%, 25%, and 10.5% in patients with FIB-4<3.25, 3.25-6.5, and >6.5, respectively; trend P=0.03). SUA levels were significantly decreased in chronic hepatitis C patients after viral eradication. The improvement was particularly enhanced in patients with mild liver disease.

Serum uric acid increases in patients with systemic autoimmune rheumatic diseases after 3months of treatment with TNF inhibitors.

In patients with gout, the serum uric acid (SUA) is usually lower during acute gouty attacks than during intercritical periods. It has been suggested that systemic inflammatory response can cause this phenomenon. The objective is to determine whether therapy with TNF inhibitors (TNFis) affects SUA levels in patients with systemic autoimmune rheumatic diseases (SARDs) and whether SUA changes correlate with pro-inflammatory cytokines or with the oxidative stress marker allantoin. In this study, SUA, CRP, creatinine, MCP-1, IFN-α2, IFN-γ, Il-1β, IL-6, IL-8, IL-10, IL-12, IL-17a, IL-18, IL-23, IL-33, TNF-α, and allantoin levels were measured prior to and after 3months of TNFis treatment in patients with SARDs. The values obtained in the biochemical assays were then tested for associations with the patients' demographic and disease-related data. A total of 128 patients (rheumatoid arthritis, n = 44; ankylosing spondylitis, n = 45; psoriatic arthritis, n = 23; and adults with juvenile idiopathic arthritis, n = 16) participated in this study. Among the entire patient population, SUA levels significantly increased 3months after starting treatment with TNFis (279.5 [84.0] vs. 299.0 [102.0] μmol/l, p < 0.0001), while the levels of CRP, IL-6, IL-8, and MCP-1 significantly decreased. Male sex was the most powerful baseline predictor of ΔSUA in univariate and multivariate models. None of the measured laboratory-based parameters had statistically significant effects on the magnitude of ΔSUA. 3months of anti-TNF therapy increased the levels of SUA in patients with SARDs, but neither the measured pro-inflammatory cytokines nor the oxidation to allantoin appeared responsible for this effect.

Decline in serum uric acid predicts higher risk for mortality in peritoneal dialysis patients-a propensity score analysis.

The level of serum uric acid (SUA) in treatment follow-up is associated with mortality in peritoneal dialysis (PD) patients, but it remains unknown if the longitudinal change in SUA affects mortality. 309 PD patients who were not using UA-lowering agents were enrolled. The longitudinal change in SUA was estimated by comparing the values between the run-in and follow-up periods. Based the calculated values, the patients were divided into SUA decliner and SUA non-decliner. A propensity score (PS) was calculated using the parameters measured in run-in period. After PS matching, the time-to-event analysis was performed for all-cause death. After PS matching, 86 patients of each group were left. A higher mortality of 19/86 existed in SUA decliner compared with SUA non-decliner which is 3/86 (p < 0.001). Kaplan-Meier analysis in sub-cohort showed worse survival in the SUA decliner. Standard and stratified Cox regression analysis both showed SUA decline to be an independent risk factor for all-cause death in PD patients. The decline in SUA in the follow-up may predict the all-cause mortality of PD patients, the reason of which may result from reducing scavenging effects of SUA or may reflect general condition. More studies need to be done.

2071-P: Changes in Serum Uric Acid Correlated with Sex Hormones Variations for Chinese Obese Patients Undergoing Sleeve Gastrectomy

Background: Hyperuricemia (HUA) and sex hormone imbalance in obese patients can be reversed by bariatric surgery. However, the relationships between changes in serum uric acid (SUA) and sex hormones variations after bariatric surgery is unexplored. We aimed to investigate the correlations between changes in SUA and sex hormones variations after laparoscopic sleeve gastrectomy (LSG) in Chinese obese patients in relation to gender. Methods: We enrolled 133 severely obese patients who underwent LSG in this study. SUA, sex hormones, and relevant metabolic parameters were compared pre- and 12 months post-LSG. Results: At baseline, HUA was more common in males than in females. Twelve months after LSG, significant improvements in BMI and glucolipid metabolic indices were noted. SUA levels and the prevalence of HUA were declined significantly in both gender while the changes in SUA and percentage of SUA variations were significantly greater in females than in males (all P&amp;lt;0.01). In addition, we observed significant increase in estradiol (E2) and decrease in total testosterone (TT) in females and increase in TT in males (P=0.018, P=0.006, P &amp;lt;0.001, respectively). In a multiple regression model, after adjusting for age and changes in BMI, fasting insulin (FINS), and HOMA-IR, SUA reduction correlated significantly with increased E2 (β=-0.645, P=0.001) and decreased TT (β=0.503, P=0.014) in females, and increased TT (β=-0.909, P=0.008) in males. Conclusion: LSG promotes more profound improvement of SUA levels in female obese patients than in males, and SUA reduction after surgery correlated significantly with different sex hormones changes in males and females. Disclosure C. Zhu: None. J. Gao: None. F. Mei: None. X. Wang: None. D. Zhou: None. S. Qu: None. Funding Shanghai Municipal Science and Technology Commission (17DZ1910603); Fundamental Research Funds for the Central Universities (1501219107); National Natural Science Foundation of China (81500650, 81700752, 81570782)

High–Resistant Starch, Low-Protein Flour Intervention on Patients With Early Type 2 Diabetic Nephropathy: A Randomized Trial

The objective of this study is to explore the effect of high-resistant starch (RS), low-protein flour as a source of RS on patients with early type 2 diabetic nephropathy (DN) through the clinical intervention trial. This was a single center, randomized, comparative, open-label trial. Seventy-five patients with early DN, aged 18 to 80y, were recruited and randomly assigned to two groups. During the 12-week intervention, the control group patients (38 cases) followed protein-restriction diet daily with a common staple. The intervention group (37 cases) received 50 g of high-RS, low-protein flour instead of a common staple of equal quality at lunch and dinner each day. The blood glucose, blood lipids, nutritional parameters, indicators of renal function, oxidative stress, and inflammatory markers were measured. Compared with the control group, high-RS, low-protein flour intake led to a significant reduction in fasting blood glucose, HbA1c, total cholesterol, and triglycerides levels (P<.05 for all). The changes in serum uric acid (UA) and β2-microglobulin (β2-MG) level were observed after high-RS, low-protein flour intervention (uric acid [mean±standard deviation]: -24.7±38.5μmol/L, P=.001; β2-MG: 0.5±0.9 mg/L, P=0.018). In addition, high-RS, low-protein flour intake increased serum superoxide dismutase level by 10.1±27.7 U/mL (P<.05); however, it did not change the interleukin-6 and Tumor Necrosis Factor α (TNF-α) concentration. Twelve-week intervention with high-RS, low-protein flour improved the blood glucose and blood lipid levels, decreased the serum uric acid (UA) and urine β2-MG, and enhanced the ability to prevent antioxidative stress in patients with early DN.

High Levels of Serum Uric Acid, Cystain C and Lipids Concentration and their Clinical Significance in Primary Gouty Arthritis Patients.

To investigate the changes of serum Uric Acid (sUA), lipids and Cystatin C (CysC) in primary gout patients, and to explore the clinical significance in gout patients. sUA, CysC, high-sensitivity C-reactive Protein (hsCRP) and other biochemical parameters were measured in 326 gout patient and 210 healthy control subjects, blood cell counts were also detected. Clinical data were collected from gout patients. sUA, CysC, hsCRP, Body Mass Index (BMI), White Blood Cell (WBC) counts, neutrophil Granulocyte (GR), Monocyte (Mo), Triglycerides (TG), plasma Total Cholesterol (TC), Very Low Density Lipoprotein (VLDL), apolipoprotein B100 (apoB100), Blood Glucose (GLU), serum Creatinine (sCr) and Urea Nitrogen (BUN) were significantly increased in gout patients compared with HC subjects (P<0.01, respectively), while lymphocyte counts and High Density Lipoprotein- Cholesterol (HDL-C) were significantly decreased in gout patients compared with HC subjects (P<0.01, respectively). Positive correlations were observed between concentration of sUA and age, TG, VLDL, sCr and CysC (P<0.05, respectively). While negative correlations were observed between the concentration of sUA and HDL-C(P<0.01). Besides, Positive correlations were observed between concentration of CysC and WBC, GR, Mo, apoA1, GLU, sCr, BUN, sUA, hsCRP (P<0.05, respectively). While negative correlations were observed between the concentration of CysC and TC, LDL-C(P<0.01, respectively). Blood lipid profile changes in gout patients. Gout patients who suffer from lipid metabolism disorder and vascular diseases might be associated with hyperuricemia, which leads to endothelial cell damage and vascular smooth muscle cell proliferation. CysC might be a marker for renal function damage and inflammation. Hyperuricemia is the risk factor of renal disorder in gout patients.

Association of serum uric acid levels with the incident of kidney disease and rapid eGFR decline in Chinese individuals with eGFR > 60mL/min/1.73m2 and negative proteinuria.

Epidemiological studies suggest that higher serum uric acid (SUA) level is significantly associated with kidney disease development. However, it remains debatable whether higher SUA is independently associated with new-onset kidney disease and rapid eGFR decline in individuals with estimated glomerular filtration rate (eGFR) ≥ 60mL/min/1.73m2 and negative proteinuria. This was a large, single-center, retrospective 6-year cohort study at People's Hospital of Tonglu County, Zhejiang, from 2001 to 2006. We enrolled 10,677 participants (19-92years) with eGFR ≥ 60mL/min/1.73m2 and without dipstick proteinuria at baseline. The association between SUA change and the occurrence of renal outcomes and annual eGFR decline were evaluated using Cox models with adjustment for confounders. Higher quartiles (2.51%) of SUA levels were associated with greater prevalence of kidney disease compared with quartile 1 (0.52%), 2 (1.13%) and 3 (1.76%), respectively. In addition, greater baseline SUA levels [OR (95% CI) 3.29(1.68-6.45), p < 0.001] and increased SUA [1.36(1.23-1.50), p < 0.001] were all associated with greater odds of renal disease progression when comparing the 4th quartile of annual eGFR decline rate with the 1st quartile. In addition, both of higher baseline SUA levels and increased SUA change were the risk factors of rapid annual eGFR decline along with male gender, lower albumin, hematocrit and creatinine levels, higher hemoglobin levels and hyperlipidemia after multivariable adjustments when compared with each quartile group. Increasing SUA were independent risk factor for the prevalent of kidney disease and rapid eGFR decline and reduced SUA over time could abate kidney disease development in a Chinese community.

Association of serum uric acid change with mortality, renal function and diuretic dose administered in treatment of acute heart failure

Background and aimsHyperuricemia is reportedly associated with poor outcome in acute heart failure (AHF). The association between changes in Uric acid (UA) levels with renal function change, diuretic doses, and mortality in patients with AHF were studied. Methods and resultsConsecutive patients hospitalized with AHF were reviewed (n = 535). UA levels were measured at admission and either at discharge or on approximately the seventh day of admission. Patients with an UA change in the top tertile were defined as having an increase (UA-increase) and were compared to those outside the top tertile (non-UA-increase). The endpoint was all-cause mortality, with a mean follow-up duration of 22.2 months. Patients in the UA-increase group presented with greater creatine increase (P < 0.001), and were administered a higher average daily dose of loop diuretic (P = 0.016) compared with the non-UA-increase group. In-hospital UA-increase was associated with higher risk of mortality even after adjusting for confounding variables including creatine change and diuretic dosage [harzard ratio (HR) 1.53, 95% confidence interval (CI) 1.02–2.30, P = 0.042]. In patients with hyperuricemia on admission, UA-increase was associated with increased mortality (adjusted HR 2.21, 95% CI 1.38–3.52, P = 0.001). Whereas, in those without admission hyperuricemia, UA-increase had no significant association with mortality. ConclusionsAn increase in UA during in-hospital treatment is associated with an increase in creatine levels and daily diuretic dose. Mortality associated with increased UA is restricted to patients who already have hyperuricemia at admission. A combination of UA levels at admission and UA changes on serial assessment during hospitalization may be additional value in the risk stratification of AHF patients.