Background:The clinical significance of low-level donor-specific anti-HLA antibody (low-DSA) remains controversial. We investigated the impact of low-DSA on posttransplant clinical outcomes in kidney transplant (KT) recipients.Methods: We retrospectively reviewed 1,027 KT recipients, namely, 629 living donor KT (LDKT) recipients and 398 deceased donor KT (DDKT) recipients, in Seoul St. Mary's Hospital (Seoul, Korea) between 2010 and 2018. Low-DSA was defined as a positive anti-HLA-DSA result in the Luminex single antigen assay (LABScreen single antigen HLA class I -combi and class II -group 1 kits; One Lambda, Canoga Park, CA, USA) but a negative result in a crossmatch test. We compared the incidence of biopsy-proven allograft rejection (BPAR), changes in allograft function, allograft survival, patient survival, and posttransplant infections between subgroups according to pretransplant low-DSA. Results:The incidence of overall BPAR and T cell-mediated rejection did not differ between the subgroups. However, antibody-mediated rejection (ABMR) developed more frequently in patients with low-DSA than in those without low-DSA in the total cohort and the LDKT and DDKT subgroups. In multivariate analysis, low-DSA was identified as a risk factor for ABMR development. Its impact was more pronounced in DDKT (odds ratio [OR]: 9.60, 95% confidence interval [CI]: 1.79-51.56) than in LDKT (OR: 3.76, 95% CI: 0.99-14.26) recipients. There were no significant differences in other outcomes according to pretransplant low-DSA.Conclusions: Pretransplant low-DSA has a significant impact on the development of ABMR, and more so in DDKT recipients than in LDKT recipients, but not on long-term outcomes.

No abstract

A 49-year-old female who underwent deceased donor kidney transplantation 1 month prior visited the outpatient clinic complaining of pitting edema. The patient's endstage kidney disease was caused by immunoglobulin A nephropathy, and hemodialysis had been performed for 7 years before the transplantation. Her serum creatinine level was 1.1 mg/dL one week previous at discharge. She received basiliximab as inductive immunosuppressive therapy and was maintained on triple immunosuppressive agents, including tacrolimus, mycophenolate mofetil, and prednisolone. The patient was given nystatin and sulfamethoxazole/trimethoprim as antifungal and antibacterial prophylaxis, respectively. Upon admission, the laboratory findings were as follows: serum creatinine, 2.6 mg/dL; C-reactive protein, 6.11 mg/dL; and pyuria. Ultrasonography revealed hydronephrosis of the graft kidney, suggesting ureteral stent obstruction. Percutaneous nephrostomy was inserted to relieve the obstruction and infection, and antegrade pyelography showed several radiolucent filling defects in the transplant ureter (Fig. 1A). Piperacillin-tazobactam empirical antibiotic therapy was initiated. Blood and urine cultures grew Candida albicans, so the initial antibiotics therapy was transitioned to intravenous flu-