NDT Advance Access published May 10, 2005 Nephrol Dial Transplant (2005) 1 of 6 doi:10.1093/ndt/gfh897
Original Article
The effects of chronic kidney disease and renal replacement therapy on circulating dendritic cells Dennis A. Hesselink, Michiel G. H. Betjes, Martijn A. Verkade, Petros Athanassopoulos, Carla C. Baan and Willem Weimar Erasmus University Medical Center, Internal Medicine, Division of Nephrology and Renal Transplantation, Rotterdam, The Netherlands
Correspondence and offprint requests to: D.A. Hesselink, Department of Internal Medicine, Division of Nephrology and Renal Transplantation, Room Ee 563 A, Erasmus MC, University Medical Center Rotterdam, Dr Molewaterplein 50, 3015 GE Rotterdam, The Netherlands. Email:
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Conclusions. Circulating DC counts are decreased in patients with CKD; for pDCs, this reduction is primarily related to the loss of GFR, whereas the dialysis treatment appears to affect mDC numbers. Keywords: chronic haemodialysis; chronic kidney failure; chronic renal disease; continuous ambulatory peritoneal dialysis; immunodeficiency; renal replacement therapy
Introduction Chronic kidney disease (CKD) induces a state of immunodeficiency. Clinically, this is apparent by the high incidence of infectious complications among patients with CKD, and the excess infection-related mortality in patients on chronic intermittent haemodialysis (CIHD) as compared with the general population [1]. In addition, loss of glomerular filtration rate (GFR) is associated with a decreased vaccination response [2], an increased overall risk of cancer [3] and diminished delayed-type hypersensitivity responses [4]. The exact mechanisms responsible for the impaired immunity of CKD are incompletely understood but several immune abnormalities have been described. First, patients with CKD have low numbers of circulating T-, B- and natural killer (NK) lymphocytes [5]. Second, there is evidence that T-lymphocyte function is aberrant in dialyzing patients. Several studies have demonstrated that phenotypically, T-cells are in an activated state and display altered proliferative responses after stimulation with mitogens or soluble antigens in vitro [5,6]. However, whether CKD causes an intrinsic T-cell defect is still a matter for debate as the observed alterations in T-cell response may have resulted from a defective antigen-presenting capacity of monocytes [7].
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Abstract Background. The mechanisms underlying the immunodeficiency of chronic kidney disease (CKD) are incompletely understood. Recently, we described decreased numbers of myeloid (m) and plasmacytoid (p) dendritic cells (DCs), considered the most important antigen-presenting cells, in peripheral blood of patients on chronic intermittent haemodialysis (CIHD). In this study, we analysed whether this reduction resulted from CKD or from renal replacement therapy (RRT). Methods. Using flowcytometry, we quantified mDCs and pDCs in peripheral blood of patients maintained on CIHD (n ¼ 37), continuous ambulatory peritoneal dialysis (CAPD; n ¼ 29), and patients with CKD not receiving RRT (n ¼ 37). Twenty-nine healthy volunteers served as controls. Results. Patients with CKD (n ¼ 103) had lower pDC and mDC counts compared with volunteers: 4.2 vs 8.3 and 10.0 vs 13.8106 cells/l, respectively (P 0.001). Within the CKD group, pDC counts did not differ between patients on CIHD, CAPD and those not receiving RRT (3.6 vs 5.0 vs 4.9106 cells/l, respectively). In the latter group, pDC numbers correlated with the glomerular filtration rate (GFR; Spearman’s r ¼ 0.49; P
