Alterations to the Gut Microbiota and Their Correlation With Inflammatory Factors in Chronic Kidney Disease Original paper

Researched by:

  • Dr. Umar ID
    Dr. Umar

    User avatarClinical Pharmacist and Clinical Pharmacy Master’s candidate focused on antibiotic stewardship, AI-driven pharmacy practice, and research that strengthens safe and effective medication use. Experience spans digital health research with Bloomsbury Health (London), pharmacovigilance in patient support programs, and behavioral approaches to mental health care. Published work includes studies on antibiotic use and awareness, AI applications in medicine, postpartum depression management, and patient safety reporting. Developer of an AI-based clinical decision support system designed to enhance antimicrobial stewardship and optimize therapeutic outcomes.

    Read More

November 26, 2025

Researched by:

  • Dr. Umar ID
    Dr. Umar

    User avatarClinical Pharmacist and Clinical Pharmacy Master’s candidate focused on antibiotic stewardship, AI-driven pharmacy practice, and research that strengthens safe and effective medication use. Experience spans digital health research with Bloomsbury Health (London), pharmacovigilance in patient support programs, and behavioral approaches to mental health care. Published work includes studies on antibiotic use and awareness, AI applications in medicine, postpartum depression management, and patient safety reporting. Developer of an AI-based clinical decision support system designed to enhance antimicrobial stewardship and optimize therapeutic outcomes.

    Read More

Last Updated: 2019-01-01

Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.

Karen Pendergrass

Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.

Location
China
Sample Site
Feces
Species
Homo sapiens

What was studied?

This original research article examined alterations to the gut microbiota in chronic kidney disease (CKD) and how these changes correlate with inflammatory cytokines, with a particular focus on microbial signatures such as Akkermansia, which is central to the study’s findings. Using 16S rDNA sequencing of fecal samples, the investigators compared microbial diversity, taxonomic composition, and functional predictions between CKD patients and healthy controls. They also quantified serum cytokines (IL-4, IL-6, IL-10) to determine links between microbial shifts and systemic inflammation. The research underscores disruptions in gut microbial ecology—including reduced richness, altered phylum-level abundances, and significant genus-level differences—that may contribute to CKD-related immune activation and disease progression.

Who was studied?

The study analyzed 50 adults with clinically diagnosed CKD and 22 healthy control individuals recruited from Shanxi Provincial People’s Hospital between 2017 and 2018. All participants consented and were screened to exclude confounders such as antibiotic or probiotic use, recent infections, autoimmune disease, cancer, or liver disease. CKD participants demonstrated impaired renal function (mean eGFR ~22 mL/min/1.73 m²) and higher levels of inflammatory cytokines, offering a clear physiological contrast to controls. Demographic characteristics, including age, sex, and BMI, were similar between groups, strengthening the validity of microbial comparisons.

Most important findings

The study identified substantial microbial dysbiosis in CKD, highlighted by reduced alpha and beta diversity, as illustrated by the PD whole-tree and UniFrac PCoA plots on pages 4–5. Key microbiome alterations included reduced Actinobacteria and Verrucomicrobia, with the latter driven by a striking depletion of Akkermansia (0.67% in CKD vs. 3.08% in controls). Genus-level shifts showed enrichment of Lactobacillus, Clostridium IV, Paraprevotella, Clostridium sensu stricto, Desulfovibrio, and Alloprevotella in CKD patients. Conversely, Akkermansia and Parasutterella were significantly enriched in healthy controls.

A table summarizing major taxa shifts is presented below:

Microbial GroupIncreased in CKDIncreased in ControlsNotes
PhylaVerrucomicrobia↓, Actinobacteria↓Verrucomicrobia↑Loss of Verrucomicrobia driven by Akkermansia reduction
GeneraLactobacillus, Clostridium IV, Paraprevotella, Desulfovibrio, AlloprevotellaAkkermansia, ParasutterellaAkkermansia depletion is novel and pronounced
Cytokine CorrelationsAkkermansia (neg. IL-10), others (neg. IL-4/IL-10)Indicates microbiome–inflammation linkage

Key implications

These findings reinforce the concept of a gut–kidney–immune axis in CKD. The marked loss of Akkermansia, a mucin-degrading bacterium that supports barrier integrity and modulates inflammation, suggests a mechanistic pathway through which dysbiosis may worsen CKD-associated systemic inflammation. The negative correlation between Akkermansia and IL-10 adds a layer of complexity, indicating that immune-microbiome interactions may differ in CKD compared with metabolic diseases, where Akkermansia is typically anti-inflammatory. Genus-level associations with renal function markers (eGFR, BUN, SCr) propose that microbial signatures could serve as diagnostic or prognostic biomarkers, while also offering therapeutic targets. Modulating gut microbiota—via prebiotics, probiotics, or dietary intervention—may become a useful strategy to reduce inflammation and slow CKD progression.

Citation

Li F, Wang M, Wang J, Li R, Zhang Y. Alterations to the gut microbiota and their correlation with inflammatory factors in chronic kidney disease. Front Cell Infect Microbiol. 2019;9:206. doi:10.3389/fcimb.2019.00206

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