Low-fructose diet lowers blood pressure and inflammation in patients with chronic kidney disease.
Nephrol Dial Transplant. 2011 May 25. Epub 2011 May 25. PMID: 21613382
1Department of Nephrology, Hypertension and Internal Medicine, Nicolaus Copernicus University in Toruń, Collegium Medicum of Bydgoszcz, Poland.
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, transforminggrowth 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) orproteinuria 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. CONCLUSIONS: 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.