Abstract

BackgroundFructose acutely raises serum uric acid in normal subjects, but the effect in subjects with metabolic syndrome or subjects with chronic kidney disease is unknown. The aim of the study was to evaluate changes in serum uric acid during the fructose tolerance test in patients with chronic kidney disease, metabolic syndrome with comparison to healthy controls.MethodsStudies were performed in 36 subjects with obesity (body mass index >30) and metabolic syndrome, 14 patients with stage 3 chronic kidney disease, and 25 healthy volunteers. The fructose tolerance test was performed in each patient. The change in serum uric acid during the fructose challenge was correlated with baseline ambulatory blood pressure, serum uric acid, metabolic, and inflammatory markers, and target organ injury including carotid intima media thickness and renal resistive index (determined by Doppler).ResultsAbsolute serum uric acid values were highest in the chronic kidney disease group, followed by the metabolic syndrome and then healthy controls. Similar increases in serum uric acid in response to the fructose tolerance test was observed in all three groups, but the greatest percent rise was observed in healthy controls compared to the other two groups. No significant association was shown between the relative rise in uric acid and clinical or inflammatory parameters associated with kidney disease (albuminuria, eGFR) or metabolic syndrome.ConclusionsSubjects with chronic kidney disease and metabolic syndrome have higher absolute uric acid values following a fructose tolerance test, but show a relatively smaller percent increase in serum uric acid. Changes in serum uric acid during the fructose tolerance test did not correlate with changes in metabolic parameters, inflammatory mediators or with target organ injury. These studies suggest that acute changes in serum uric acid in response to fructose do not predict the metabolic phenotype or presence of inflammatory mediators in subjects with obesity, metabolic syndrome or chronic kidney disease.Trial registrationThe study was registered in ClinicalTrials.gov. Identifier : NCT01332526. www.register.clinicaltrials.gov/01332526Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-015-0048-y) contains supplementary material, which is available to authorized users.

Highlights

  • Fructose acutely raises serum uric acid in normal subjects, but the effect in subjects with metabolic syndrome or subjects with chronic kidney disease is unknown

  • Subjects with chronic kidney disease (CKD) had lower estimated glomerular filtration rate (eGFR) and more microalbuminuria than healthy controls, and subjects with metabolic syndromes had worse lipid profiles and higher body mass index (BMI) compared to healthy subjects

  • Levels of inflammatory mediators and target organ injury were greater in the subjects with metabolic syndrome and CKD compare to healthy controls (Additional file 1: Table S1)

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Summary

Introduction

Fructose acutely raises serum uric acid in normal subjects, but the effect in subjects with metabolic syndrome or subjects with chronic kidney disease is unknown. The aim of the study was to evaluate changes in serum uric acid during the fructose tolerance test in patients with chronic kidney disease, metabolic syndrome with comparison to healthy controls. Less is known about the changes of serum uric acid that occur during oral FTT in subjects with CKD and/or the metabolic syndrome. Anderstam analyzed the effect of 75 g of fructose load on serum uric acid in hemodialysis patients in comparison to healthy controls. They reported stable serum uric acid levels during the test in healthy individuals but a significant increase by 10% in hemodialysis patients at 240 minutes after fructose intake [14]. We tested the hypothesis that the change in serum uric acid in response to fructose might correlated with the metabolic phenotype, the degree of renal injury, the presence of inflammation or the presence of target organ injury

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