us-map.html ¶ A list of severe manifestations of monkeypox can be found at https://emergency. cdc.gov/han/2022/han00475.asp. ** During the study period and as of October 21, 2022, CDC was notified by state and local jurisdictions of five decedents whose death certificates included monkeypox as a cause of death or contributing factor, six decedents whose cause of death is still under active investigation, and one decedent in whom the death was not monkeypox-related. Additional monkeypox cases involving severe disease or death might not be included in this report if CDC has not yet been notified about the case or if the case occurred outside of the study period.
In current practice HIV+ candidates with CD4 >200 cells/mm3 are eligible for kidney transplantation. However, the optimal pre-transplant CD4 count above this threshold remains to be defined. We evaluated clinical outcomes in patients with baseline CD4 >350 and <350 cells/mm3 among 38 anti-thymocyte globulin (ATG)-treated HIV- to HIV+ kidney transplants performed at our center between 2006 and 2013. Median follow-up was 2.6 years. Rates of acute rejection, patient and graft survival were not different between groups. However, occurrence of severe CD4 lymphopenia (<200 cells/mm3) was more common among individuals with a baseline CD4 count 200–349 cells/mm3 compared to those transplanted at higher counts (75% vs 30% at 4 weeks [p=0.04] and 71% vs 5% at 52 weeks [p=0.001] post-transplant, respectively). After adjusting for age, baseline CD4 count of 200–349 cells/mm3 was an independent predictor of severe CD4 lymphopenia at 4 (RR, 2.6; 95% CI, 1.3–5.1) and 52 weeks (RR, 14.3; 95% CI, 2–100.4) post-transplant. Patients with CD4 <200 cells/mm3 at 4 weeks had higher probability of serious infections during first 6 months post-transplant (19% vs. 50%; log-rank 0.05). These findings suggest that ATG must be used with caution in HIV+ kidney allograft recipients with a pre-transplant CD4 count <350 cells/mm3.
Background
HIV infection is associated with high rates of acute rejection following kidney transplantation. The underlying mechanisms for such predisposition are incompletely understood. Pathological immune activation is a hallmark of chronic HIV infection that persists despite effective antiretroviral therapy. We hypothesized that the baseline levels of T cell activation in HIV+ candidates would correlate with their risk of acute rejection following kidney transplantation.
Methods
Single-center retrospective cohort analysis of HIV+ adult kidney transplants performed between October 2006 and September 2013. The frequency of CD3+HLA-DR+ cells measured by flow cytometry served as a surrogate marker of immune activation. Patients were categorized into tertiles of activation, and the rates of biopsy-proven acute rejection were compared across groups.
Results
(1) Compared to matched HIV− controls, the baseline number of CD3+HLA-DR+ cells was higher in HIV+ kidney transplant candidates. (2) Abnormally high levels of activation did not decrease with transplant-associated immunosuppression. (3) Patients categorized within the lower and middle CD3+HLA-DR+ tertiles had higher probability of rejection during the first 3 years post-transplant compared to those in the higher activation tertile (36.9% vs. 0%; log-rank P= .04).
Conclusions
Pathological immune activation in HIV+ transplant candidates does not explain their increased susceptibility to allograft rejection. Paradoxically, those with the highest levels of immune activation seem to be less prone to rejection.
Background: Antiretroviral therapy (ART) poses challenging drug-drug interactions with immunosuppressant agents in transplant recipients. We aimed to determine the impact of specific antiretroviral regimens in clinical outcomes of HIV
+ kidney transplant recipients.
Methods: A single-center, retrospective cohort study was conducted at a large academic center. Subjects included 58 HIV
- to HIV
+ adult, first-time kidney transplant patients. The main intervention was ART regimen used after transplantation. The main outcomes assessed at one- and three-years were: patient survival, death-censored graft survival, and biopsy-proven acute rejection; we also assessed serious infections within the first six months post-transplant.
Results: Patient and graft survival at three years were both 90% for the entire cohort. Patients receiving protease inhibitor (PI)-containing regimens had lower patient survival at one and three years than patients receiving PI-sparing regimens: 85% vs. 100% (
p=0.06) and 82% vs. 100% (
p=0.03), respectively. Patients who received PI-containing regimens had twelve times higher odds of death at 3 years compared to patients who were not exposed to PIs (odds ratio, 12.05; 95% confidence interval, 1.31-1602;
p=0.02). Three-year death-censored graft survival was lower in patients receiving PI vs. patients on PI-sparing regimens (82 vs 100%,
p=0.03). Patients receiving integrase strand transfer inhibitors-containing regimens had higher 3-year graft survival. There were no differences in the incidence of acute rejection by ART regimen. Individuals receiving PIs had a higher incidence of serious infections compared to those on PI-sparing regimens (39 vs. 8%,
p=0.01).
Conclusions: PI-containing ART regimens are associated with adverse outcomes in HIV
+ kidney transplant recipients.
Adverse drug reactions most frequently affected the central nervous system. No ADR was life threatening. The frequency of ADRs in this Nicaraguan patient population was less than that reported from other studies in resource-limited settings.
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