Summary

Chronic kidney disease (CKD) is characterised by progressive nephron loss leading to accumulation of metabolic waste and systemic inflammation. Immune dynamics in CKD involve a complex interplay between persistent low-grade activation of innate immune cells and concurrent functional impairment of adaptive responses. Uraemic toxins derived from reduced glomerular filtration alter the phenotype and function of neutrophils, monocytes and dendritic cells, promoting a pro-inflammatory milieu while compromising antimicrobial defence. In parallel, lymphocyte subsets display reduced proliferative capacity and skewed cytokine production, undermining vaccination efficacy and anti-tumour surveillance. These dysregulated immune pathways contribute to heightened susceptibility to infection, accelerated cardiovascular disease and impaired tissue repair. Recent advances have begun to unravel the molecular drivers of immune imbalance, from complement activation on dialysis membranes to cytokine trans-signalling, and are guiding novel therapeutic strategies aimed at restoring immune homeostasis in CKD.

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Immune Dynamics in Chronic Kidney Disease publication trend

The graph below shows the total number of articles in immune dynamics in chronic kidney disease across all publications each year (not limited to Nature Index journals).

Technical terms

Chronic Kidney Disease (CKD): Progressive reduction in renal function leading to retention of waste products and fluid imbalance.

Innate immunity: Non-specific first line of defence involving cells such as neutrophils, monocytes and natural killer cells.

Adaptive immunity: Antigen-specific responses mediated by B and T lymphocytes, characterised by immunological memory.

Uraemic toxins: Waste metabolites that accumulate in the blood due to impaired renal clearance and disrupt cellular functions.

Monocytes: Circulating innate immune cells that differentiate into macrophages or dendritic cells and orchestrate inflammatory responses.

Cytokines: Soluble proteins, including interleukins and tumour necrosis factors, that regulate immune cell communication and inflammation.

References

  1. Anti-staphylococcus aureus adaptive immunity is impaired in end-stage renal disease patients on hemodialysis: one-year longitudinal study. Frontiers in Immunology (2023).
  2. Interleukin-6 as a Director of Immunological Events and Tissue Regenerative Capacity in Hemodialyzed Diabetes Patients. Medical Sciences (2024).
  3. Monocytes as Targets for Immunomodulation by Regional Citrate Anticoagulation. International Journal of Molecular Sciences (2024).
  4. Chronic Kidney Disease-Associated Immune Dysfunctions: Impact of Protein-Bound Uremic Retention Solutes on Immune Cells. Toxins (2020).
  5. The Complement System in Dialysis: A Forgotten Story?. Frontiers in Immunology (2018).

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