Differences in the Profile of Circulating Immune Cell Subsets in Males with Type 2 Cardiorenal Syndrome versus CKD
Anila Duni1,2, Athanasios Kitsos1,2, Aris Bechlioulis3
1Department of Nephrology, School of Health Sciences, Faculty of Medicine, University of Ioannina and University Hospital of Ioannina, GR 45500 Ioannina, Greece.
Insights
Immune cell differences in cardiorenal syndrome type 2 (CRS-2) patients compared to chronic kidney disease (CKD) patients were identified. Specific immune cells, like CD4+ T-lymphocytes, predict mortality in CRS-2 patients.
Area of Science:
- Immunology
- Nephrology
- Cardiology
Background:
- Chronic kidney disease (CKD) pathogenesis involves maladaptive immune system activation.
- Cardiorenal syndrome type 2 (CRS-2) involves both cardiac and kidney dysfunction.
- Understanding immune cell profiles in CRS-2 is crucial for prognosis.
Purpose of the Study:
- To investigate differences in circulating immune cells between CRS-2 patients and CKD patients without cardiovascular disease (CVD).
- To identify immune cell subsets associated with mortality in CRS-2 patients.
Main Methods:
- Prospective follow-up of 39 stable males with CRS-2 and 24 male CKD patients matched for estimated glomerular filtration rate (eGFR).
- Flow cytometry was used to measure a panel of immune cell subsets.
Main Results:
- CRS-2 patients showed higher proinflammatory CD14++CD16+ monocytes and T regulatory cells (Tregs), but lower lymphocytes and natural killer cells compared to CKD patients.
- Decreased lymphocytes, T-lymphocytes, CD4+ T-cells, CD8+ T-cells, Tregs, and increased CD14++CD16+ monocytes were associated with mortality.
- CD4+ T-lymphocytes were independent predictors of mortality in a multivariate model.
Conclusions:
- CRS-2 patients exhibit distinct immune cell profiles compared to CKD patients with similar kidney function but no CVD.
- CD4+ T-lymphocytes independently predicted fatal cardiovascular events in the CRS-2 cohort.
Abstract:
Maladaptive activation of the immune system plays a key role in the pathogenesis of chronic kidney disease (CKD). Our aim was to investigate differences in circulating immune cells between type 2 cardiorenal syndrome (CRS-2) patients and CKD patients without cardiovascular disease (CVD). CRS-2 patients were prospectively followed up, with the primary endpoint being all-cause and cardiovascular mortality.
Method:
A total of 39 stable males with CRS-2 and 24 male CKD patients matched for eGFR (CKD-EPI) were enrolled. A selected panel of immune cell subsets was measured by flow cytometry.
Results:
Compared to CKD patients, CRS-2 patients displayed higher levels of proinflammatory CD14++CD16+ monocytes (p = 0.04) and T regulatory cells (Tregs) (p = 0.03), lower lymphocytes (p = 0.04), and lower natural killer cells (p = 0.001). Decreased lymphocytes, T-lymphocytes, CD4+ T-cells, CD8+ T-cells, Tregs, and increased CD14++CD16+ monocytes were associated with mortality at a median follow-up of 30 months (p < 0.05 for all). In a multivariate model including all six immune cell subsets, only CD4+ T-lymphocytes remained independent predictors of mortality (OR 0.66; 95% CI 0.50-0.87; p = 0.004).
Conclusion:
Patients with CRS-2 exhibit alterations in immune cell profile compared to CKD patients of similar kidney function but without CVD. In the CRS-2 cohort, CD4+ T-lymphocytes independently predicted fatal cardiovascular events.
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