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Few studies have described the clinical impact of anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines in renal transplant recipients (RTRs) in the context of omicron variant and the third vaccine dose. Antibody titer has been tried to relate to the prediction of outcomes related to SARS-CoV-2, but it results controversially in these populations.All patients with positive SARS-CoV-2 polymerase chain reaction followed at a RTRs reference center from March 15, 2020, to March 15, 2022, were considered for analysis. Cases were analyzed by vaccination status. Breakthrough cases were then analyzed by nonantibodies (20 arbitrary unit [AU]/mL), low (20-100 AU/mL), and high antibody titers (100 AU/mL) against SARS-CoV-2 spike protein. Outcomes included pneumonia and mortality. We used logistic regression multivariable to assess for confounders.Among 186 RTRs with coronavirus disease 2019, 50.5% (n = 94) were vaccinated versus 49.5% (n = 92) unvaccinated. Of the vaccinated patients, 67.02% developed a high antibody titer (100 AU/mL) but 14.89% achieved a low antibody titer and 18.08%. Pneumonia-free survival (day 20) was 95% in high antibody titer but 40% in unvaccinated RTRs. Survival in RTRs at day 60 was similar in the unvaccinated group compared with nonantibodies breakthrough cases (82%) but 92% in the low antibody titer group (relative risk, 0.027; 95% confidence interval, 0.002-0.479; P = 0.014). Only patients with100 AU/mL showed a 100% survival on day 60 postinfection.Vaccinated RTRs who achieve at least a low antibody titer (20 AU/mL) had better results in terms of pneumonia and mortality than unvaccinated RTRs. Antibody titer100 AU/mL associate with even better results than patients with lower antibody titers.

BACKGROUND Hemophagocytic syndrome (HPS) is an infrequent complication of transplantation caused by an inflammatory response with a benign proliferation of macrophages and defective lytic capability of T lymphocytes and NK cells that can lead to multiorgan failure. Transplant patients are particularly exposed as a result of the increased risk of both infections and malignancies derived from immunosuppressive drugs. There is no consensus for therapy or immunosuppression; mortality is high. We report a case and present a review of all cases of HPS occurring in solid organ transplant recipients. CASE REPORT: We report two cases of infection by Toxoplasma gondii transmitted by the kidney allograft. One of the recipients was seronegative before transplantation and developed disseminated primary toxoplasmosis. An immune reaction compatible with an HPS ensued. Both were treated with Trimethoprim/sulfamethoxazole, immunosuppression was tapered, and after a 2-week period a complete response was obtained. CONCLUSION HPS presents therapeutic challenges in the context of transplantation. If HPS is suspected, the search of a very likely underlying infection should be central to the management.

Minimization of immunosuppression and administration of antiretrovirals have been recommended for kidney transplant recipients (KTRs) with coronavirus disease 2019 (COVID-19). However, outcomes remain poor. Given the likely benefit of cyclosporine because of its antiviral and immunomodulatory effect, we have been using it as a strategy in KTRs diagnosed with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We studied 29 kidney transplant recipients (KTRs) who were admitted to our institution with COVID-19 between March 15and April, 24, 2020. Mycophenolate and/or mammalian target of rapamycin inhibitors (mTORi) were discontinued in all patients. Two therapeutic strategies were compared: Group 1, minimization of calcineurin inhibitors (N = 6); and Group 2, cyclosporine-based therapy (N = 23), with 15 patients switched from tacrolimus. Hydroxychloroquine was considered in both strategies but antivirals in none. Six patients died after respiratory distress (20.6%). Five required mechanical ventilation (17.2%), and 3 could be weaned. Nineteen patients had an uneventful recovery (65.5%). In group 1, 3 of 6 patients died (50%) and 1 of 6 required invasive mechanical ventilation (16.7%). In group 2, 3 of 23 patients died (12.5%). Renal function did not deteriorate and signs of rejection were not observed in any patient on the second treatment regime. In conclusion, immunosuppressant treatment based on cyclosporine could be safe and effective for KTRs diagnosed with COVID-19.

Background The incidence of cytomegalovirus (CMV) infection in solid organ transplant recipients may be reduced by antiviral prophylaxis, but this strategy may lead to delayed-onset CMV infection. The proinflammatory cytokine interleukin (IL)-18 plays a major role in viral host defense responses. This study examines the impacts of 2 single-nucleotide polymorphisms (SNPs) in the promoter region of the IL-18 gene, -607C/A (rs1946518) and -137G/C (rs187238), on the incidence of delayed-onset CMV infection in patients undergoing kidney transplant. Methods This retrospective study analyzed 2 IL-18 SNPs in consecutive adult kidney transplant recipients using real-time polymerase chain reaction with TaqMan probes. Participants were enrolled over the period 2005–2013 and stratified according to their IL-18 SNP genotype. The concordance index (Harrell’s c-index) was used as a measure of the discriminatory power of the predictive models constructed with bootstrapping to correct for optimistic bias. Results Seven hundred nine patients received transplants in the study period, and 498 met selection criteria. Cytomegalovirus infection and disease incidence were 38% and 7.5%, respectively. In multivariate competing risk regression models, carriers of the -607C/-137G haplotype who received prophylaxis showed a higher incidence of CMV replication after antiviral agent discontinuation (hazard ratio = 2.42 [95% confidence interval, 1.11–5.26]; P = .026), whereas CMV disease was not observed in those given prophylaxis who were noncarriers of this polymorphism (P = .009). Conclusions Our findings suggest that the -607C/-137G IL-18 haplotype is associated with a higher incidence of postprophylaxis CMV replication. The prior identification of this polymorphism could help select alternative measures to prevent delayed-onset CMV infection in these patients.