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Blood Microbiome Profile in CKD : A Pilot Study 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.

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November 28, 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
United States of America
Sample Site
Blood
Species
Homo sapiens

What was studied?

This pilot study investigated the blood microbiome profile in chronic kidney disease (CKD), focusing on how circulating microbial DNA differs between CKD patients and healthy individuals. Because the blood microbiome profile in CKD may reflect gut-blood barrier dysfunction and systemic inflammation, the study examined both the quantity and composition of bacterial DNA in buffy coat samples using quantitative 16S PCR and 16S targeted metagenomic sequencing. The aim was to characterize diversity, taxonomic patterns, and associations between microbial signatures and kidney function. This work helps clarify whether altered microbial communities in the bloodstream correspond to CKD severity and known dysbiosis-related inflammatory pathways.

Who was studied?

The study included 20 adults with nondiabetic CKD and 20 healthy controls. Participants in the CKD group represented a range of reduced kidney function, enabling analysis of microbiome shifts along gradients of glomerular filtration rate (GFR). All samples were collected in a cross-sectional design, and no participants had diabetes, which reduced potential confounding from metabolic disease. Healthy controls were matched to represent a baseline circulating microbiome for comparison. The intention was to assess microbiome patterns attributable to CKD physiology rather than unrelated comorbidities.

Most important findings

The analysis revealed significant qualitative differences in circulating microbial DNA. CKD patients exhibited lower α diversity, indicated by a reduced Chao1 index (127±18 vs. 145±31), suggesting diminished richness of detectable blood-associated taxa. A total of 22 operational taxonomic units (OTUs) differed significantly between groups. The CKD blood microbiome was enriched in Proteobacteria, especially Gammaproteobacteria, with overrepresentation of Enterobacteriaceae and Pseudomonadaceae—families commonly linked to gut permeability, systemic inflammation, and pathobiont expansion in dysbiosis. Although total 16S copy numbers did not differ between CKD and controls, the microbial composition shifted toward these inflammation-associated taxa. Importantly, GFR correlated inversely with Proteobacteria abundance (r = −0.54), implying that worsening kidney function accompanies escalating dysbiosis signatures in circulating blood. These findings align with research showing that CKD-associated gut barrier dysfunction promotes translocation of Proteobacteria-rich communities, potentially contributing to endotoxemia and chronic inflammation.

Key implications

The study underscores that CKD is associated not only with gut dysbiosis but also with distinct alterations in the circulating microbiome. Reduced α diversity and increased Proteobacteria-rich taxa suggest systemic microbial imbalance that parallels disease severity. These microbial patterns may serve as biomarkers for CKD progression or inflammatory burden and reinforce the pathogenic link between gut permeability, bacterial translocation, and renal decline. Although pilot in scale, the work provides strong rationale for integrating blood microbiome signatures into broader microbiome–kidney interaction research. Future studies with larger cohorts could validate these microbial markers and explore therapeutic interventions targeting gut–blood microbial dynamics to alleviate CKD-related inflammation.

Citation

Shah NB, Allegretti AS, Nigwekar SU, et al. Blood microbiome profile in CKD: a pilot study. Clin J Am Soc Nephrol. 2019;14(5):692-701. doi:10.2215/CJN.12161018

Chronic Kidney Disease (CKD)

Dysbiosis in chronic kidney disease (CKD) reflects a shift toward reduced beneficial taxa and increased pathogenic, uremic toxin-producing species, driven by a bidirectional interaction in which the uremic environment disrupts microbial composition and dysbiotic metabolites accelerate renal deterioration.

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