Journal
CLINICAL SCIENCE
Volume 133, Issue 17, Pages 1857-1870Publisher
PORTLAND PRESS LTD
DOI: 10.1042/CS20190171
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Funding
- National Natural Science Foundation of China (NSFC) [81570480, 81770529]
- National High Technology Research and Development Program of China (863 Program) [2015AA020701]
- Special Scientific Research Fund of Public Welfare Profession of National Health and Family Planning Commission [201502026]
- Guangdong Gastrointestinal Disease Research Center [2017B02029003]
- Key Scientific and Technological Program of Guangzhou City [201607020016]
- Nanchong City-School Cooperative Scientific Research Project [18SXHZ0547]
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Chronic kidney disease (CKD) affects 10-15% of the population worldwide, results in high morbidity and mortality, and requires costly treatment and renal replacement therapy. Glomerulosclerosis, tubulointerstitial fibrosis, and persistent intestinal flora disturbance are common in CKD. Short-chain fatty acids (SCFAs), produced by the intestinal microbiota, have been previously reported to ameliorate kidney injury; however, the specific concentrations and types that are required to improve renal function remain unknown. The present study aims to evaluate the levels of SCFAs in healthy and CKD patients, and to test the hypothesis that SCFAs play a critical role in delaying CKD progression. One hundred and twenty-seven patients with CKD and 63 healthy controls from China were enrolled in the present study. Butyrate, which is considered beneficial to humans, was almost three-times higher in healthy volunteers than that in CKD5 subjects (P=0.001). Moreover, the serum SCFA levels in controls were significantly higher than that in CKD patients (P< 0.05), and the butyrate level among CKD5 patients (1.48 +/- 0.60 mu mol/l) was less than half of that in controls (3.44 +/- 2.12 mu mol/l, P< 0.001). In addition, we observed an inverse correlation between butyrate level and renal function (P< 0.05). A CKD rat model transplanted with microbiota obtained from CKD patients exhibited accelerated CKD progression via increased production of trimethylamine N-oxide (TMAO), which was reversed by supplementation with extra butyrate. Our results showed that SCFA levels were reduced in CKD patients and that butyrate supplementation might delay CKD progression.
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