Kidney Week

Abstract: TH-PO1074

Progressive Circulating Inflammatory Signatures in CKD Due to Diabetic Kidney Disease

Session Information

• Pathology and Lab Medicine
  October 22, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Pathology and Lab Medicine

• 1700 Pathology and Lab Medicine

Authors

• Piggott, Raymond Simon, University College Dublin Diabetes Complications Research Centre, Dublin, Leinster, Ireland

Raymond Simon Piggott, MBChB

• Andrews, Darrell C., University College Dublin Diabetes Complications Research Centre, Dublin, Leinster, Ireland

Darrell C. Andrews, PhD

• Doyle, Ross, Mater Misericordiae University Hospital, Dublin, Leinster, Ireland

Ross Doyle, MBChB, PhD

• O'Meara, Yvonne M., University College Dublin Diabetes Complications Research Centre, Dublin, Leinster, Ireland

Yvonne M. O'Meara, MD, MBChB

• Redahan, Lynn, Mater Misericordiae University Hospital, Dublin, Leinster, Ireland

Lynn Redahan, MBChB

• Sadlier, Denise M., University College Dublin Diabetes Complications Research Centre, Dublin, Leinster, Ireland

Denise M. Sadlier, MD, PhD

• Godson, Catherine, University College Dublin Diabetes Complications Research Centre, Dublin, Leinster, Ireland

Catherine Godson, PhD

Group or Team Name

• Diabetes Complications Research Centre, School of Medicine, University College Dublin

Background

Diabetic kidney disease (DKD) is characterized by progressive inflammation and immune dysregulation contributing to chronic kidney disease (CKD) progression. However, the relationship between circulating monocyte phenotypes and systemic inflammatory signalling across the spectrum of DKD associated CKD remains incompletely defined. We characterized monocyte subsets and plasma inflammatory mediators in patients with DKD associated CKD.

Methods

Age matched healthy volunteers (n=10), CKD stage III due to DKD (n=15), and CKD stage V due to DKD (n=15) were recruited. Peripheral blood mononuclear cells were isolated, stained and analysed using multiparameter flow cytometry to quantify classical, intermediate, and non
classical monocyte subsets. Plasma inflammatory mediators were quantified using multiplex cytokine profiling. Group comparisons were performed using Kruskal–Wallis testing with Dunn’s post hoc analysis.

Results

DKD associated CKD was associated with significant circulating monocyte remodelling, characterized by reduced classical monocytes (p<0.001) and expansion of intermediate monocyte subsets (p<0.001) compared with healthy volunteers. Multiplex cytokine profiling demonstrated enrichment of monocyte associated inflammatory mediators including CCL2 (p<0.001), CCL3 (p<0.0001), CSF1(p<0.0001), and CXCL9 (p = 0.003) across CKD cohorts. Intermediate monocyte expansion and inflammatory chemokine enrichment were most pronounced in advanced CKD.

Conclusion

DKD associated CKD exhibits progressive circulating innate immune activation, characterized by expansion of intermediate monocytes and enrichment of monocyte associated chemokines. These findings support a role for systemic inflammatory dysregulation in DKD progression and identify circulating inflammatory signatures that may help inform future mechanistic and therapeutic studies.

Acknowledgment

Sinead Kinsella Educational Bursary, Irish Nephrology Society
University College Dublin Foundation