Determining the level of subpopulations of peripheral blood lymphocytes for the diagnosis of chronic renal allograft rejection
Background. One of the main causes of renal allografts (RA) failure in the long-term period after transplantation is progressive chronic allograft dysfunction (CAD), the cause of which in 20 to 60 % of cases is chronic rejection (CR). Diagnosis of the causes of graft dysfunction is based on a morphological study, which has several disadvantages through invasiveness. Therefore, of great interest is the search for non-invasive methods for diagnosing the state of RA, in particular, the study of the cellular link of the immune response. To this end, we decided to investigate the relative number of subpopulations of peripheral blood lymphocytes and their ratio in recipients in the long-term period after kidney transplantation and to assess the informative value of these parameters for the diagnosis of CR RA. Materials and methods. The levels of lymphocyte subpopulations (T-cells, T-helpers, T-cytotoxic, T-activated, T-NK-cells, B-cells, NK-cells) were studied in 43 RA recipients depending on the course of the long-term postoperative period and allograft state 1–9 years after transplantation, who were divided into two groups depending on the morphological verification of the diagnosis. Group 1 — 23 patients with satisfactory RA function without signs of rejection; group 2 — 20 patients with CAD caused by a CR according to a puncture biopsy. The control group consisted of 23 healthy donors, whose parameters made up the reference corridor. Results. The analysis showed an increase in the average levels of T-activated lymphocytes in the groups 1 and 2 relative to the control one (8.9 ± 2.0, 8.4 ± 2.4, 6.8 ± 2.1, respectively). There was also a decrease in the mean levels of T-NK cells (2.4 ± 2.0) and B-cells (9.6 ± 2.0) in group 2 as compared to indicators of group 1 (5.6 ± 1.8 and 12.4 ± 2.4, respectively). Analysis of the correlation between specific subpopulation units of lymphocytes showed a statistically significant difference between the T-cell/T-NK-cell index (22.53 vs. 46.89 in the groups 1 and 2, respectively, p < 0.05) and the index of T-activated/β-cell (1.14 vs 4.17 in the groups 1 and 2, respectively, p < 0.05). The sensitivity of the T-cell/T-NK-cell index was 70 %, and the specificity — 60 %. The sensitivity of the T-activated/B-cell index was 55 %, the specificity — 50 %. Conclusions. The decrease in the level of T-NK-cells closer to the lower threshold value of the reference corridor and, accordingly, the ratio of T-cells/T-NK-cells within 44.49–49.29 (46.89 ± 2.40) in the long-term post-transplant period can be an additional sign of a chronic rejection reaction as a cause of progressive renal allograft dysfunction.
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Horvath P, Capobianco I, Rolinger J, Königsrainer A, Nadalin S, Königsrainer I. Kidney graft salvage strategies for vascular complications during kidney transplantation: a single-center experience. Transplant Proc. 2017;49(6):1331-1335. doi: 10.1016/j.transproceed.2017.02.057.
Delgado JF, Serrano M, Morán L, et al. Early mortality after heart transplantation related to IgA anti-β2-glycoprotein I antibodies. Heart Lung Transplant. 2017;pii: S1053-2498(17)31797-7. doi: 10.1016/j.healun.2017.05.016.
Mohan M, Buros A, Mathur P, et al. Clinical characteristics and prognostic factors in multiple myeloma patients with light chain deposition disease. Am J Hematol. 2017;92(8):739-745. doi: 10.1002/ajh.24756.
Kır O, Zeytinoğlu A, Arda B, Yılmaz M, Aşçı G, Töz H. Impact of prophylaxis vs pre-emptive approach for cytomegalovirus infection in kidney transplant recipients. Transplant Proc. 2017;49(3):537-540. doi: 10.1016/j.transproceed.2017.01.027.
Almardini RI, Salita GM, Farah MQ, Katatbeh IA, Al-Rabadi K. Renal impairment and complication after kidney transplant at Queen Rania Abdulla children's hospital. Exp Clin Transplant. 2017;15(Suppl 1):99-103. doi: 10.6002/ect.mesot2016.O95.
Chinnakotla S, Verghese P, Chavers B, et al. Outcomes and risk factors for graft loss: lessons learned from 1,056 pediatric kidney transplants at the University of Minnesota. J Am Coll Surg. 2017;224(4):473-486. doi: 10.1016/j.jamcollsurg.2016.12.027.
Ayar Y, Ersoy A, Ocakoglu G, et al. Risk factors affecting graft and patient survivals after transplantation from deceased donors in a developing country: a single-center experience. Transplant Proc. 2017;49(2):270-277. doi: 10.1016/j.transproceed.2016.12.009.
de Castro Rodrigues Ferreira F, Cristelli MP, Paula MI, et al. Infectious complications as the leading cause of death after kidney transplantation: analysis of more than 10,000 transplants from a single center. J Nephrol. 2017;30(4):601-606. doi: 10.1007/s40620-017-0379-9.
Kamel M, Kadian M, Srinivas T, Taber D, Posadas Salas MA. Tacrolimus confers lower acute rejection rates and better renal allograft survival compared to cyclosporine. World J Transplant. 2016;6(4):697-702. doi: 10.5500/wjt.v6.i4.697.
Brakemeier S, Dürr M, Bachmann F, Schmidt D, Gaedeke J, Budde K. Risk evaluation and outcome of pneumocystis jirovecii pneumonia in kidney transplant patients. Transplant Proc. 2016;48(9):2924-2930. doi: 10.1016/j.transproceed.2016.05.017.
Ban TH, Yu JH, Chung BH, et al. Clinical outcome of rituximab and intravenous immunoglobulin combination therapy in kidney transplant recipients with chronic active antibody-mediated rejection. Ann Transplant. 2017;22:468-474. PMID: 28775248.
Abu Jawdeh BG, Govil A. Acute kidney injury in transplant setting: differential diagnosis and impact on health and health care. Adv Chronic Kidney Dis. 2017;24(4):228-232. doi: 10.1053/j.ackd.2017.05.005.
Yan Q, Luo H, Wang B, et al. Correlation between PKB/Akt, GSK-3β expression and tubular epithelial-mesenchymal transition in renal allografts with chronic active antibody-mediated rejection. Exp Ther Med. 2017;13(5):2217-2224. doi: 10.3892/etm.2017.4261.
Ghinnagow R, Cruz LJ, Macho-Fernandez E, Faveeuw C, Trottein F. Enhancement of adjuvant functions of natural killer T cells using nanovector delivery systems: application in anticancer immune therapy. Front Immunol. 2017;8:879. doi: 10.3389/fimmu.2017.00879.
Klatka J, Grywalska E, Hymos A, et al. Cyclooxygenase-2 inhibition enhances proliferation of NKT cells derived from patients with laryngeal cancer. Anticancer Res. 2017;37(8):4059-4066. doi: 10.21873/anticanres.11791.
Batista VG, Moreira-Teixeira L, Leite-de-Moraes MC, Benard G. Analysis of invariant natural killer T cells in human paracoccidioidomycosis. Mycopathologia. 2011;172(5):357-63. doi: 10.1007/s11046-011-9451-5.
Goubier A, Vocanson M, Macari C, et al. Invariant NKT cells suppress CD8(+) T-cell-mediated allergic contact dermatitis independently of regulatory CD4(+) T cells. J Invest Dermatol. 2013;133(4):980-7. doi: 10.1038/jid.2012.404.
Zhang G, Nie H, Yang J, et al. Sulfatide-activated type II NKT cells prevent allergic airway inflammation by inhibiting type I NKT cell function in a mouse model of asthma. Am J Physiol Lung Cell Mol Physiol. 2011;301(6):L975-84. doi: 10.1152/ajplung.00114.2011.
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