Department of Nephrology, Hypertension and Internal Medicine, Nicolaus Copernicus University in Toruń, Collegium Medicum of Bydgoszcz, Poland.
Nephrol Dial Transplant. 2012 Feb;27(2):608-12. doi: 10.1093/ndt/gfr223. Epub 2011 May 25.
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).
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.
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.
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.
果糖在实验模型和人类中与高血压、高尿酸血症和炎症密切相关。然而,低果糖饮食对慢性肾脏病(CKD)患者炎症、高尿酸血症和肾脏疾病进展的影响尚未得到评估。
28 名年龄为 59 ± 15 岁(17 名男性/11 名女性)的 CKD 2 期和 3 期患者从常规(基础)(60.0 g/24 h)饮食改为低(12.0 g/24 h)果糖饮食 6 周,然后再恢复常规饮食 6 周。饮食由营养师监测。在基线时,测量低果糖和常规果糖饮食的动态血压(BP)并采集血液样本来检测肾功能(肌酐)、炎症标志物、空腹血糖和胰岛素以及血清尿酸。还收集 24 小时尿液样本来检测肌酐、尿酸、单核细胞趋化蛋白-1、转化生长因子-β和 N-乙酰-β-D-氨基葡萄糖苷酶。
低果糖饮食倾向于改善全组的 BP(n = 28),而仅在夜间血压下降者(n = 20)中观察到 BP 的显著降低,而非夜间血压下降者(n = 8)中则未观察到。低果糖饮食对估计肾小球滤过率(eGFR)或蛋白尿没有影响。血清尿酸水平略有但无统计学意义的降低(7.1 ± 1.3 与 6.6 ± 1.0 mg/dL,P < 0.1),而空腹血清胰岛素水平显著降低(11.2 ± 6.1 与 8.2 ± 2.9 mIU/mL,P < 0.05),且在恢复常规饮食后仍持续降低。在患者接受低果糖饮食时,尿液尿酸和尿酸排泄分数略有但无统计学意义的降低。低果糖饮食还降低了高敏 C 反应蛋白(hsCRP)(4.3 ± 4.9 与 3.3 ± 4.5 mg/L;P < 0.01)和可溶性细胞间黏附分子(sICAM)(250.9 ± 59.4 与 227 ± 50.5 ng/mL;P < 0.05)。恢复常规饮食后 hsCRP 恢复至基线水平,而 sICAM 的降低则持续存在。
CKD 患者的低果糖饮食可降低炎症,对血压可能有一定益处。这项初步研究需要通过更大规模的临床试验来证实,以确定与其他饮食相比,低果糖饮食在 CKD 患者中的长期益处。