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Cyclooxygenase-2 (COX-2) alleles have been associated with allograft outcomes in kidney transplant recipients; however, these alleles may be in linkage with other genes. Human allograft inflammatory factor-1 (AIF-1) is a cytoplasmic protein and is produced by macrophages. Its synthesis is regulated by several cytokines, including interferon gamma. We investigated whether polymorphisms of gene encoding COX-2 and AIF-1 were associated with allograft outcomes among Hispanic renal transplant recipients (RTRs). A total of 527 de novo RTRs of Hispanic ethnicity were included in this study transplanted at St. Vincent Medical Center (SVMC) during 2000–2009. Patients were genotyped for the following: COX-2 (−1195C > T rs689466, intron 6 rs2066826) and AlF1 (rs2269475). Analysis of the results showed that COX-2–1195 CC genotype (OR = 1.92, CI% = 1.00–3.67, p = 0.04) were more frequent, but COX-2–1195 CT genotype was less frequent in kidney allograft acute rejection in comparison with control group (OR = 0.59, CI% = 0.38–0.91, p = 0.017). The genetic variant TT/CT of the AIF-1 gene was associated with a lower risk of rejection (OR = 0.63, CI% = 0.41–0.98, p = 0.038). No association of COX-2 (rs2066826) was observed with allograft rejection. We are unable to find statistically significant association between COX-2 and AIF-1 gene polymorphisms and allograft survival. The −1195C > T in the COX-2 promoter and AIF-1 gene polymorphisms could be a potential predictor of allograft rejection in our Hispanic kidney transplant recipients.

Among prospective kidney transplant recipients, antibodies to HLA-DP are most frequently identified in re-transplant candidates. The significance of these antibodies and their ability to cause rejection is subject to an ongoing debate. The following is a case study of a kidney re-transplant recipient with many HLA-DP antibodies. The patient is a 27 year-old female who had received one prior transplant. Anti-HLA antibodies were determined by Luminex® single antigen beads. Crossmatching was performed by complement-dependent cytotoxicity (CDC) with and without Dithiothreitol (DTT), and flow cytometry (FXM) with and without Pronase®. The patient exhibited only Class II antibodies, including 16 HLA-DP specificities with MFI >10,000. The recipient had a single donor-specific antibody to HLA-DP11 (21,000 MFI) to the potential living donor. The preliminary crossmatch was negative by both CDC and FXM and was reconfirmed with subsequent crossmatches. Post-transplant, the recipient demonstrated good kidney function and a steady decrease in serum creatinine (sCr) to 1.1 mg/dL until developing pyelonephritis two weeks later. The infection was resolved with antibiotics, but the patient’s sCr increased a week later to 3.1 mg/dL, and a kidney biopsy was performed. The biopsy was positive for vasculitis and cellular rejection, with equivocal C4d staining. Following treatment with steroids, IVIG, and thymoglobulin, the patient stabilized with a sCr of 1.6 mg/dL, and the single HLA-DP11 donor-specific antibody persists. Crossmatches performed with current serum and freshly drawn cells from the living donor remained negative. In the presence of negative crossmatches, the recipient experienced cellular and antibody-mediated rejection associated with a donor specific antibody against HLA-DP. The findings suggest that donor-specific HLA-DP antibodies present a risk to kidney transplantation.