Abstract:Background: Some children with chronic kidney disease (CKD) develop hypertension faster than others. This may be attributable to endothelial dysfunction, among other reasons. Short-chain fatty acids (SCFAs), that is, acetate, butyrate, and propionate, are known for reducing cardiovascular risks via preserving endothelial function. This study aimed to investigate the association between changes in plasma SCFA concentrations and in cardiovascular and endothelial parameters in children with CKD.Methods: In total,… Show more
“…Several of these genera ( Feacalibacterium, Fusicatenibacter and Anaerostipes ), known to produce short-chain fatty acids, were present in lower abundance in the CKD_Ss+ group. Previously, it was shown that serum SCFAs were reduced in patients infected with S. stercoralis [ 21 ] and in CKD patients [ 38 ]. SCFAs are known for their effects not only on the healthy gut microbiome but also on renal function [ 39 , 40 ].…”
“…Several of these genera ( Feacalibacterium, Fusicatenibacter and Anaerostipes ), known to produce short-chain fatty acids, were present in lower abundance in the CKD_Ss+ group. Previously, it was shown that serum SCFAs were reduced in patients infected with S. stercoralis [ 21 ] and in CKD patients [ 38 ]. SCFAs are known for their effects not only on the healthy gut microbiome but also on renal function [ 39 , 40 ].…”
“…Currently, research on SCFAs in diabetic nephropathy and CKD is underway, but few studies have reported the efficacy of SCFAs in IgAN. A number of studies have found that serum SCFA levels in patients with CKD are significantly lower than those in healthy volunteers and that the administration of SCFAs could reduce the level of urinary toxins in patients and could delay the progression of the disease [17,[40][41][42][43]. SCFAs could also reduce the gene and/or protein expression of inflammatory cytokines, chemokines and profibrotic factors in the kidney tissue of diabetic mice and could protect diabetic mice from kidney disease [16].…”
Background
Recently, a few studies have indicated a relationship between the gut microbiota and IgA nephropathy (IgAN). Whether the gut microbiota participates in the pathogenesis of IgAN and whether probiotics are effective in treating IgAN are still controversial. Therefore, this study aimed to identify the differences in the structure of the gut microbiota between IgAN and controls and to evaluate the efficacy and mechanism of probiotics in the treatment of IgAN.
Methods
To address this question, 35 IgAN patients and 25 healthy volunteers were enrolled, and a mouse IgAN model was also constructed. The stool microbes were analyzed by 16S rRNA high-throughput sequencing to identify the differential strains between IgAN and healthy controls. The impact of probiotics on the structure of the intestinal flora and the efficacy of the probiotics in the treatment of IgAN were evaluated.
Results
Although the microflora structure of mice and humans was not the same, both patients and mice with IgAN exhibited gut microbiota dysbiosis, with all subjects presenting an evident decrease in Bifidobacterium levels. The Bifidobacterium proportion was negatively correlated with proteinuria and hematuria levels, indicating that the decreased Bifidobacterium abundance could be related to IgAN severity. Probiotic treatment containing Bifidobacterium in IgAN mice could significantly alleviate gut dysbiosis, specifically by increasing the proportion of beneficial bacteria and reducing the abundance of potentially pathogenic bacteria. Moreover, both probiotics and their metabolites, short-chain fatty acids (SCFAs), could attenuate IgAN clinicopathological manifestations by inhibiting the NLRP3/ASC/Caspase 1 signaling pathway.
Conclusions
Supplementation with probiotics mainly containing Bifidobacterium could markedly improve gut dysbiosis in IgAN. Moreover, both probiotics and their SCFA metabolites could attenuate the clinicopathological manifestations of IgAN by inhibiting the NLRP3/ASC/Caspase 1 signaling pathway. Therefore, probiotics have potential as an adjunctive therapy for IgAN.
“…An investigation that enrolled 105 children and adolescents with CKD found a difference in plasma acetate between children with and without hypertension, suggesting its preventive role for hypertension in children with CKD. In addition, reduced plasma butyrate was found in the advanced and stable blood pressure groups at the 1-year follow up, which may potentially be caused by the decline in eGFR [80]. In addition, Chai et al identified substantially lower production of SCFAs, including acetic acid, propionic acid, butyric acid, and iso-butyric acid, in IgAN patients compared with those in the control group [53].…”
Section: Gut Microbial Metabolites and Ckdmentioning
Faecal microbiota transplantation (FMT) has attracted increasing attention as an intervention in many clinical conditions, including autoimmune, enteroendocrine, gastroenterological, and neurological diseases. For years, FMT has been an effective second-line treatment for Clostridium difficile infection (CDI) with beneficial outcomes. FMT is also promising in improving bowel diseases, such as ulcerative colitis (UC). Pre-clinical and clinical studies suggest that this microbiota-based intervention may influence the development and progression of chronic kidney disease (CKD) via modifying a dysregulated gut–kidney axis. Despite the high morbidity and mortality due to CKD, there are limited options for treatment until end-stage kidney disease occurs, which results in death, dialysis, or kidney transplantation. This imposes a significant financial and health burden on the individual, their families and careers, and the health system. Recent studies have suggested that strategies to reverse gut dysbiosis using FMT are a promising therapy in CKD. This review summarises the preclinical and clinical evidence and postulates the potential therapeutic effect of FMT in the management of CKD.
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