Anaemia in Renal Transplant Recipients: Is There a Role for Hepcidin?

Abstract

Introduction and aims: Anaemia following renal transplantation is common and multi-factorial, with a prevalence of 20 to 57%. Hepcidin is a peptide hormone produced by hepatocytes in response to iron loading and inflammation. Renal dysfunction is associated with increased hepcidin levels, possibly contributing to the development of anaemia by dysregulation of iron homeostasis. Hepcidin has been investigated with great interest in patients with non-transplant chronic kidney disease, including the dialysis population. However, it has received relatively little attention in renal transplant population. The aims of this study were to evaluate the associations between hepcidin and renal function, iron status and inflammation in renal transplant recipients. Methods: In this cross-sectional study, patients who were at least 1 year post renal transplant were recruited. Haemoglobin (Hb), C-Reactive Protein (CRP), Albumin (Alb), Ferritin (Ferr) and Transferrin Saturation (TSAT) were assessed using standard laboratory methods. Estimated Glomerular Filtration Rate (eGFR) was estimated using MDRD formula. Serum hepcidin-25 levels were determined by mass spectrometry using stable isotope labelled synthetic hepcidin-25 as an internal standard. Results: Sixty-four patients were enrolled. Gender: 55% male and 45% female. Mean age: 51 years (22-77). Ethnicity: Caucasian 81%, Asian 10%, African/Caribbean: 9%. Types of kidney donation: 69% deceased donor and 31% living donor. Mean time post transplantation: 8 years (1-22). Mean eGFR = 44.10 ± 16.81 mL/min. Mean Hb = 12.71 ± 1.44 g/dL. Hepcidin correlated significantly with Hb (r = -0.24, p < 0.05) and eGFR (r = -0.36, p < 0.005). The significant correlation between hepcidin and Hb disappeared when adjusted for eGFR (r = -0.17, p = 0.19). Hepcidin did not correlate with CRP (r = 0.09, p = 0.47), Alb (r = -0.05, p = 0.72), Ferr (r = 0.37, p = 0.32) and TSAT (r = 0.03, p = 0.84). Conclusions: Hepcidin may be of limited utility as an anaemia biomarker in this relatively uninflamed and iron replete population. Nevertheless, the possibility remains that the link between anaemia and reduced eGFR may be mediated by hepcidin, which may potentially give rise to specific therapeutic strategies in this population.