Low-fructose Diet Lowers Blood Pressure and Inflammation in Patients With Chronic Kidney Disease
Posted: 03/14/2012; Nephrol Dial Transplant. 2012;27(2):608-612. © 2012 Oxford University Press
Abstract and Introduction
Background. Fructose has been strongly linked with hypertension, hyperuricemia and inflammation in experimental models and humans. However, the effect of low-fructose diet on inflammation, hyperuricemia and the progression of renal disease has not yet been evaluated in patients with chronic kidney disease (CKD).
Methods. Twenty-eight patients (age 59 ± 15 years, 17 males/11 females) with Stages 2 and 3 CKD were switched from a regular (basal) (60.0 g/24 h) to a low (12.0 g/24 h) fructose diet for 6 weeks, followed by a resumption of their regular diet for another 6 weeks. Diet was monitored by a dietician. At the baseline, low- and regular-fructose diet ambulatory blood pressure (BP) was measured and blood sampled for renal function (creatinine), inflammatory markers, fasting glucose and insulin and serum uric acid. Twenty-four-hour urine collections were also obtained for creatinine, uric acid, monocyte chemotatic protein-1, transforming growth factor-beta and N-acetyl-beta-D-glucosaminidase.
Results. The low-fructose diet tended to improve BP for the whole group (n = 28), while significant reduction of BP was only seen in dippers (n = 20) but not in non-dippers (n = 8). No effects on estimated glomerular filtration rate (eGFR) or proteinuria were observed. Serum uric acid was lowered non-significantly with low-fructose diet (7.1 ± 1.3 versus 6.6 ± 1.0 mg/dL, P < 0.1), whereas a significant decrease in fasting serum insulin was observed (11.2 ± 6.1 versus 8.2 ± 2.9 mIU/mL, P < 0.05) and the reduction persisted after return to the regular diet. A slight but not significant reduction in urinary uric acid and fractional uric acid excretion was observed while the patients were on the low fructose diet. The low-fructose diet also decreased high sensitivity C-reactive protein (hsCRP) (4.3 ± 4.9 versus 3.3 ± 4.5 mg/L; P < 0.01) and soluble intercellular adhesion molecule (sICAM) (250.9 ± 59.4 versus 227 ± 50.5 ng/mL; P < 0.05). The hsCRP returned to baseline with resumption of the regular diet, whereas the reduction in sICAM persisted.
Conclusion. Low-fructose diet in subjects with CKD can reduce inflammation with some potential benefits on BP. This pilot study needs to be confirmed by a larger clinical trial to determine the long-term benefit of a low-fructose diet compared to other diets in subjects with CKD.
Fructose intake from added sugars has increased dramatically over the last century and has recently been implicated as a potential contributor to hypertension, inflammation and kidney disease. Fructose is distinct from other sugars as uric acid is generated during its metabolism. Serum uric acid levels have been found to correlate with the intake of fructose and added sugars. In turn, an elevated serum uric acid has also been shown to be associated with hypertension, inflammation and chronic kidney disease (CKD), and early intervention trials with xanthine oxidase inhibitors such as allopurinol have been found to have benefits on these parameters in both subjects with normal and decreased renal function.[5–8]
To date, there have been no published studies to examine the effect of a low-fructose diet in subjects with or without CKD. In particular, the usefulness of a low-fructose diet in subjects with CKD could theoretically be unhelpful given the fact that decreased glomerular filtration rate (GFR) itself may lead to the retention of uric acid and sodium which can cause hyperuricemia and hypertension, respectively. Furthermore, both inflammation and oxidative stress characterize subjects with reduced renal function and is likely to have multiple causes.
Given how little is known in this area, we performed an open pilot study to determine the effect of a low-fructose diet on serum uric acid, blood pressure (BP) and markers of inflammation [especially high-sensitivity C-reactive protein (hsCRP) and soluble intercellular adhesion molecule (sICAM) 1] in subjects with stable CKD (Stages 2 and 3). For this pilot study, we estimated fructose intake while patients were on their regular diet along with baseline parameters, followed by a 6-week trial of a low-fructose diet. Subjects then resumed to their regular diet for an additional 6 weeks to determine if the effects of the low-fructose diet were persistent.