Kidney Week

Abstract: TH-PO0245

Bifidobacterium longum BB536 Ameliorates Kidney Dysfunction and Alters Gut Microbiota in an Adenine-Induced CKD Mouse Model

Session Information

• CKD: Mechanisms of Injury and Fibrosis - 1
  October 22, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

• 2203 CKD (Non-Dialysis): Mechanisms

Authors

• Chiba, Miya, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Miya Chiba

• Noguchi, Yuji, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Yuji Noguchi, MD

• Kinomura, Sosuke, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Sosuke Kinomura, MD

• Kujirai, Ryota, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Ryota Kujirai, PhD

• Watanabe, Shun, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Shun Watanabe, MD, PhD

• Kikuchi, Koichi, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Koichi Kikuchi, MD, PhD

• Suzuki, Chitose, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Chitose Suzuki

• Suzuki, Takehiro, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Takehiro Suzuki, MD, PhD

• Soga, Tomoyoshi, Keio Gijuku Daigaku, Minato, Tokyo, Japan

Tomoyoshi Soga, PhD

• Toyohara, Takafumi, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Takafumi Toyohara, MD, PhD

• Tanaka, Tetsuhiro, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Tetsuhiro Tanaka, MD, PhD, FASN

• Abe, Takaaki, Tohoku Daigaku, Sendai, Miyagi Prefecture, Japan

Takaaki Abe, MD, PhD

Background

Chronic kidney disease (CKD) is closely associated with dysbiosis of the gut microbiota, which promotes the accumulation of gut-derived uremic toxins and may exacerbate renal dysfunction. Some probiotics have been reported to modulate the gut microbiota and ameliorate renal dysfunction; however, the specific strains involved and the precise mechanisms remain unclear. Bifidobacterium longum BB536 (BB536) has been shown to improve bowel habits and modulate immune responses, suggesting its potential to influence the intestinal environment. The aim of this study is to evaluate the effects of BB536 on renal dysfunction and to explore its mechanisms via the gut–kidney axis.

Methods

A renal failure model was established by feeding mice with an adenine-containing diet for 6 weeks. BB536 treatment was initiated 5 weeks after the start of adenine intake. Clinical symptoms were evaluated, and plasma and fecal metabolomic analyses, as well as RNA sequencing of kidney and colon tissues, were performed.

Results

BB536 administration reduced the serum creatinine levels and decreased plasma trimethylamine-N-oxide (TMAO), a gut–derived uremic toxin, compared with the renal failure (RF) group. Gut microbiota analysis revealed compositional changes with a significant difference in beta diversity between the BB536-treated and RF groups. At the genus level, the abundance of Alistipes was decreased in the RF group, and this decrease was restored by BB536 treatment. Plasma metabolomic analysis showed that BB536 attenuated increases in TCA cycle–related and amino acid/nitrogen metabolites observed in the RF group. Fecal metabolomic analysis revealed that BB536 restored decreases in metabolites related to arginine and beta-alanine metabolism in the RF group. Enrichment analysis of kidney RNA-seq data showed reduced enrichment of inflammation-related pathways, including MAPK signaling, and increased enrichment of fatty acid and organic acid metabolism pathways after BB536 treatment. Enrichment analysis of colon RNA-seq data showed reduced immune-related pathways and increased ion transport- and zinc response–related pathways after BB536 treatment.

Conclusion

These findings suggest that BB536 may ameliorate renal dysfunction through modulation of the gut microbiota, metabolic pathways, and tissue transcriptomic responses in renal failure.