The fructose tolerance test in patients with chronic kidney disease and metabolic syndrome in comparison to healthy controls

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.

Effects of acute fructose loading on levels of serum uric acid—a pilot study

“…As expected, baseline values of serum uric were higher in CKD. 27 In all groups, serum uric acid levels changed over time following intakes with most pronounced responses after interventions with fructose drink, whereas blueberry drink resulted in the lowest concentrations. Further, CKD who had the highest baseline levels of uric acid increased less than T2D and HS after interventions with fructose drink.…”

“…The main findings of this study were that fructose load increased uric acid levels, postprandial serum fructose differed between drinks and disease category, and postprandial changes in serum uric acid were dependent on both the source of fructose and the disease. As expected, baseline values of serum uric were higher in CKD …”

“…32 In CKD, higher uric acid AUC was found 2 hours following intake (1 g/kg) when compared to controls, while controls had higher uric acid % after 60 minutes. Inhibited generation and increased gut excretion of uric acid in CKD was suggested, 27 meaning a delayed reaction could be present in CKD. In T2D, 30 g of fructose added to regular diet for 2 months did not affect serum uric acid levels.…”

Shortage of Cellular ATP as a Cause of Diseases and Strategies to Enhance ATP

“…Previous results suggest that serum UA is a biomarker of ATP consumption, since rapid ATP consumption can lead to purine degradation and an increased rate of UA production in humans. For example, intense muscular exercise (Hellsten et al, 1999; Stathis et al, 1994, 1999), fructose challenge (Budillon et al, 1992; Donderski et al, 2015), alcohol intake (Lieber, 1965; Schmidt et al, 2013), and high brain activity (Salvadore et al, 2010; Goodman et al, 2016) can lead to energy crisis and resultant hyperuricemia. In addition, vascular regions undergoing ischemia-reperfusion may produce increased purine degradation products; a sign that a local energy crisis has occurred.…”

Nutritional Status, Selected Nutrients Intake and Their Relationship with the Concentration of Ghrelin and Adiponectin in Patients with Diabetic Nephropathy

“…It is estimated that >24% of CKD cases in industrialized countries can be attributed to nutritional factors, the most important of which are calorie dense diet, high in animal protein and sodium but low fruit and vegetable consumption [3]. In recent years, there is a growing body of evidence of the role of fructose (derived from fruits, honey, high-fructose corn syrup) in the pathogenesis and course of chronic kidney disease, because excessive fructose consumption has been shown to promote hypertension and insulin resistance [4][5][6][7][8][9][10][11].…”