Immature Neutrophil Phenotype and Enhanced Myeloperoxidase in Male Patients With Chronic Kidney Disease and Cardiovascular Comorbidity
Sonja Vondenhoff, Alessandra Antwerpen, Carolina Victoria Cruz Junho, Philipp Martin, Sina Hourtz, Jinmi Zou, Berkan Kurt, Carolin Haas, Susanne Fleig, Corinna Schulte, Jane Lauxen, Martina Wessiepe, Ulrike Späte‐Schulze, Rafael Kramann, Jürgen Floege, Oliver Soehnlein, Joachim Jankowski, Claudia Goettsch, Yvonne Döring, Florian Kahles, Nikolaus Marx, Constance C. F. M. J. Baaten, Heidi NoelsABSTRACT
Aim
Patients with chronic kidney disease (CKD) have an increased cardiovascular risk. Since neutrophils and neutrophil‐borne proteins contribute to cardiovascular disease, we analyzed the neutrophil phenotype in patients with CKD who presented with a spectrum of cardiovascular comorbidities.
Methods
Blood from two independent cohorts of male patients with moderate to advanced CKD recruited through the cardiology or nephrology unit was analyzed for neutrophils maturation and activation markers using flow cytometry compared to healthy controls. The formation of neutrophil‐extracellular traps was assessed using isolated neutrophils. Plasma levels of neutrophil‐borne proteins (neutrophil elastase, myeloperoxidase, and S100A8/A9), plasma inflammatory markers and cardiovascular disease characteristics were compared.
Results
Both cohorts of CKD patients showed reduced neutrophil surface expression of maturation marker CD10 and higher plasma levels of myeloperoxidase compared to controls. No significant differences were observed in neutrophil surface activation markers in either baseline or stimulated conditions, or in the formation of neutrophil extracellular traps ex vivo. Although CKD patients presented with variable degrees of systemic inflammation and cardiovascular comorbidities, the immature neutrophil phenotype (low CD10) was not associated with either inflammatory status (CRP, IL6) or NT‐proBNP levels.
Conclusion
Male cardiorenal patients with moderate to advanced CKD do not show altered neutrophil surface activation markers or ex vivo activation potential per se. Yet, they display a more immature neutrophil phenotype and higher circulating neutrophil‐borne myeloperoxidase as observed across a range of systemic inflammation degrees. This could potentially contribute to the overall increased cardiovascular risk in CKD.