Erythropoietin Effect on Complement Activation in Chronic Kidney Disease
Virginia Athanasiadou,
Kleio Ampelakiotou,
Eirini Grigoriou,
Katherina Psarra,
Alexandra Tsirogianni,
Serena Valsami,
Theodoros Pittaras,
Eirini Grapsa,
Maria G. Detsika
Affiliations
Virginia Athanasiadou
Department of Nephrology, School of Medicine, Aretaieion University Hospital, National and Kapodistrian University of Athens, 11528 Athens, Greece
Kleio Ampelakiotou
Department of Immunology and Histocompatibility, ‘Evangelismos’ General Hospital, 10676 Athens, Greece
Eirini Grigoriou
Department of Immunology and Histocompatibility, ‘Evangelismos’ General Hospital, 10676 Athens, Greece
Katherina Psarra
Department of Immunology and Histocompatibility, ‘Evangelismos’ General Hospital, 10676 Athens, Greece
Alexandra Tsirogianni
Department of Immunology and Histocompatibility, ‘Evangelismos’ General Hospital, 10676 Athens, Greece
Serena Valsami
Hematology Laboratory-Blood Bank, Aretaieion Hospital, National and Kapodistrian University of Athens, 11528 Athens, Greece
Theodoros Pittaras
Hematology Laboratory-Blood Bank, Aretaieion Hospital, National and Kapodistrian University of Athens, 11528 Athens, Greece
Eirini Grapsa
Department of Nephrology, School of Medicine, Aretaieion University Hospital, National and Kapodistrian University of Athens, 11528 Athens, Greece
Maria G. Detsika
1st Department of Critical Care Medicine and Pulmonary Services, GP Livanos and M. Simou Laboratories, Evangelismos Hospital, National and Kapodistrian University of Athens, 10675 Athens, Greece
The complement system is an important part of innate immunity. Despite its known protective role, the complement system may contribute to increased inflammation and tissue injury in cases where its balanced activation is disrupted. The kidneys have been shown to be largely affected by complement dysregulation. The aim of the present study was to investigate the effect of erythropoietin administration, on the complement system, in chronic kidney disease patients. The study involved 20 patients with CKD who received erythropoietin and measurements of levels of complement factors C3a and C5a and complement regulatory proteins (CregPs) CD55, CD46, and CD59. An increase in serum C3a and C5a levels was observed in response to EPO therapy. The increase in C3a was statistically significant (p + T cells (p p + and CD8+ T cells (p < 0.05) at completion of EPO therapy compared with healthy controls. The above observations demonstrate that EPO induces complement activation in patients undergoing EPO therapy with a simultaneous restriction of CRegPs expression, thus possibly allowing the uncontrolled complement activation, which may contribute to tissue injury and disease progression.
