Impact of Early Blood Transfusion After Kidney Transplantation on the Incidence of Donor-Specific Anti-HLA Antibodies

I. Ferrandiz; N. Congy-Jolivet; A. Del Bello; B. Debiol; K. Trébern-Launay; L. Esposito; D. Milongo; G. Dörr; L. Rostaing; N. Kamar


American Journal of Transplantation. 2016;16(9):2661-2669. 

In This Article

Abstract and Introduction


Little is known about the impact of posttransplant blood transfusion on the sensitization of anti-HLA antibodies and the formation of donor-specific antibodies (DSAs). The aims of our study were to determine the 1-year incidence of DSAs (assessed using a solid-phase assay) and antibody-mediated rejection (AMR) in kidney transplant patients who had or had not received a blood transfusion during the first year after transplantation. Included were 390 non–HLA-sensitized patients who had received an ABO-compatible kidney transplant and had not previously or simultaneously received a nonkidney transplant. Overall, 64% of patients received a red blood cell transfusion within the first year after transplantation, most within the first month. The overall 1-year incidence of DSAs was significantly higher in patients that had undergone transfusion (7.2% vs. 0.7% in patients with no transfusion, p < 0.0001). AMR occurred more often in the transfusion group (n = 15, 6%) compared with the nontransfusion group (n = 2, 1.4%; p = 0.04). Blood transfusion was an independent predictive factor for de novo DSA formation but not for AMR. Patients who had a transfusion and developed DSAs were more often treated with cyclosporin A (n = 10, 55.5%) rather than tacrolimus (n = 45, 19.4%; p = 0.0001). In conclusion, early posttransplant blood transfusion may increase immunological risk, especially in underimmunosuppressed patients.


Anemia is commonly observed after kidney transplantation.[1] Although different definitions of anemia have been used in the literature, its prevalence ranges between 20% and 50% within the first year after transplantation.[1] The causes of anemia are multifactorial. In the early period after kidney transplantation, anemia can be related to bleeding, reduced production of erythropoietin because of impaired kidney function, and resistance to endogenous erythropoietin related to the release of proinflammatory cytokines.[1] Afterward, anemia can be induced by the effects of myelotoxic immunosuppressive drugs, such as mycophenolic acid (MPA), mammalian target of rapamycin (mTOR) inhibitors, and polyclonal antibodies; by the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers; or by impaired kidney function caused by interstitial fibrosis and tubular atrophy.[1] Published data are conflicting on the effect of posttransplant anemia on both patient- and graft-survival rates.[2,3] Correction of anemia relies on giving erythropoietin-stimulating agents and/or blood transfusions.

For patients on a waiting list for a kidney transplant, a history of previous transplantation, pregnancy or blood transfusion has been clearly identified as a risk for developing anti-HLA antibodies.[4] Despite the use of leukodepleted blood components, the risk of anti-HLA sensitization before transplantation persists.[5–8]

After kidney transplantation, it has been clearly shown that the development of anti-HLA antibodies, mainly when they are directed against the donor, is responsible for antibody-mediated rejection (AMR) and increased risk of graft loss.[9] Although blood transfusions are commonly conducted after kidney transplantation, very few studies have assessed the incidence of donor-specific antibodies (DSAs).[10–12] It is thought that the use of immunosuppressive drugs after transplantation reduces the risk of anti-HLA sensitization.[13]

The aims of our study were to determine the 1-year incidence of DSAs (assessed using the highly sensitive Luminex SA assay [Luminex Corp, Austin, TX]) and AMR in a large population of kidney transplant patients who had or had not received at least one red blood cell (RBC) transfusion within the first year after transplantation.