Dietary Fructose: a New Paradigm in Predicting Metabolic Profile in Kidney Transplant

DIETARY FRUCTOSE: A NEW PARADIGM IN PREDICTING METABOLIC PROFILE IN KIDNEY TRANSPLANT RECIPIENTS Winnie Chan1,2, Jos Bosch2,3, David Jones4, Okdeep Kaur1, Phillip McTernan5, Anna Phillips2, Richard Borrows1,2 1Queen Elizabeth Hospital Birmingham, UK; 2University of Birmingham, UK; 3University of Amsterdam, Netherlands; 4Manchester Metropolitan University, UK; 5University of Warwick, UK

Introduction: Fructose is a monosaccharide foundinfruits, vegetables and honey. Widely used as an industrial sweetener in food and beverages, fructose intake has increased markedly over the last century. Findings from pre-clinical studies and non-transplantation chronic kidney disease (CKD) population suggested that fructose may be associated with CKD progression as well as deranged metabolic syndrome, hyperuricemia, inflammation, and endothelial dysfunction. However, such associations have not been explored in kidney transplant recipients (KTRs). The objective of this study was to investigate the impact of fructose intake on metabolic syndrome and its individual components, hyperuricemia,systemic markers of inflammationand endothelial dysfunction as well as renal function among clinically stable KTRs.

Methods: This single-centre cross-sectional study enrolled 128 clinically stable KTRs. Mean age = 49±15 years; 56% male; and median time post-transplantation = 4 (2-11) years. Fructose intake was estimated by a 3-day food diary. Fasting serum samples were collected for measurements of estimated glomerular filtration rate (eGFR), triglycerides , high-density lipoprotein (HDL), glucose, uric acid, high-sensitivity c-reactive protein (hsCRP), and E- selectin. Metabolic syndrome was defined using the International Diabetes Federation diagnostic criteria: central obesity (waist circumference >94cm for male and >80cm for female) plus two other risk factors including hypertriglyceridemia (≥1.7mmol/L), decreased HDL (<1.03mmol/L for male and <1.29mmol/L for female), elevated blood pressure (systolic ≥130mmHg and diastolic ≥85mmHg), and increased fasting glucose (≥5.6mmol/L). Regression analyses were used to determine the associations between fructose intake and different clinical parameters.

Results: Fructose intake was associated with the presence of metabolic syndrome (OR=1.03, p<0.01), and four out of five of its individual components: increasing waist circumference (OR=1.04, p<0.05), hypertriglyceridemia (OR=1.00, p<0.05), decreased HDL (OR=0.91, p<0.05), and elevated fasting glucose (OR=1.03,p<0.01). Similarly, fructose intake correlated significantly with hyperuricemia (β=0.8, p<0.05), elevated hsCRP (β=0.1, p<0.001), and E- Selectin (β=0.1, p<0.05).All statistical associations persisted after adjustments for body mass index, total intakes of energy, fat, glucose and sucrose. However there was no correlation between fructose intake and eGFR (β=-0.1, p=0.35).

Conclusion: Fructose consumption is highly associated with deranged metabolic profile, inflammation and endothelial dysfunction in KTRs irrespective of renal function. Targeting fructose intake may therefore serve as a novel intervention to improve cardio-metabolic risk profile and ultimately cardiovascular mortality in KTRs.