Donderski Rafał, Miśkowiec-Wiśniewska Ilona, Kretowicz Marek, Grajewska Magdalena, Manitius Jacek, Kamińska Anna, Junik Roman, Siódmiak Joanna, Stefańska Anna, Odrowąż-Sypniewska Grażyna, Pluta Agnieszka, Lanaspa Miguel, Johnson Richard J
Department of Nephrology, Hypertension and Internal Medicine, Collegium Medicum, Bydgoszcz, Nicolaus Copernicus University, Toruń, Poland.
Department of Diabetology and Endocrinology, Collegium Medicum, Bydgoszcz, Nicolaus Copernicus University, Toruń, Poland.
BMC Nephrol. 2015 May 3;16:68. doi: 10.1186/s12882-015-0048-y.
Fructose 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.
Studies 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).
Absolute 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.
Subjects 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.
The study was registered in ClinicalTrials.gov. Identifier : NCT01332526. www.register.clinicaltrials.gov/01332526.
果糖可使正常受试者的血清尿酸水平急性升高,但对代谢综合征患者或慢性肾脏病患者的影响尚不清楚。本研究旨在评估慢性肾脏病、代谢综合征患者在果糖耐量试验期间血清尿酸的变化,并与健康对照者进行比较。
对36名肥胖(体重指数>30)且患有代谢综合征的受试者、14名3期慢性肾脏病患者和25名健康志愿者进行了研究。对每位患者进行果糖耐量试验。果糖激发试验期间血清尿酸的变化与基线动态血压、血清尿酸、代谢及炎症标志物以及包括颈动脉内膜中层厚度和肾阻力指数(通过多普勒测定)在内的靶器官损伤相关。
慢性肾脏病组的血清尿酸绝对值最高,其次是代谢综合征组,然后是健康对照组。在所有三组中均观察到果糖耐量试验后血清尿酸有类似升高,但与其他两组相比,健康对照组的升高百分比最大。尿酸相对升高与肾病(蛋白尿、估算肾小球滤过率)或代谢综合征相关的临床或炎症参数之间未显示出显著关联。
慢性肾脏病和代谢综合征患者在果糖耐量试验后血清尿酸绝对值较高,但血清尿酸升高的百分比相对较小。果糖耐量试验期间血清尿酸的变化与代谢参数、炎症介质的变化或靶器官损伤无关。这些研究表明,肥胖、代谢综合征或慢性肾脏病患者对果糖的反应导致血清尿酸的急性变化并不能预测其代谢表型或炎症介质的存在。
本研究已在ClinicalTrials.gov注册。标识符:NCT01332526。网址:www.register.clinicaltrials.gov/01332526 。