A behavioral and educational strategy addressing the patient's perceptions and knowledge about the anti-rejection drugs significantly improved the short-term adherence to immunosuppressive therapy.
There is no standardization on the timing of the best approach to treat a non-functioning renal graft.We reviewed the literature and performed a proportional meta-analysis of case series of transplantectomy and embolization for a non-functioning renal graft. The groups were compared for mortality and morbidity outcomes.A total of 2421 patients were included in this review. Of these, 2232 patients underwent transplantectomy and 189 underwent percutaneous embolization. The mortality rate in the nephrectomy group was 4% [95% confidence interval [CI], 2–7%; I2=87%] as compared with 0.1% [95% CI, 0.1–0.5%; I2=0%] in the embolization group. The rates of common morbidities were 18% [95% CI, 13–26%, I2=79.7%] for nephrectomy compared with 1.2% [95% CI, 0.7–2.1%, I2=26.4%] for embolization. The incidence of post-embolization syndrome was 68%, and 20% of patients needed post-embolization nephrectomy.Percutaneous embolization was associated with lower mortality and morbidity rates but also with a high rate of post-embolization syndrome. However, in most cases this complication had easily manageable symptoms. Embolization is a new and attractive technique that can be considered in treating non-functioning renal grafts.
IntroductionThe treatment of choice for Atypical Hemolytic Uremic Syndrome (aHUS) is the monoclonal antibody eculizumab. The objective of this study was to assess the efficacy and safety of eculizumab in a cohort of kidney transplant patients suffering from aHUS.MethodsDescription of the prospective cohort of all the patients primarily treated with eculizumab after transplantation and divided into the therapeutic (onset of aHUS after transplantation) and prophylactic use (patients with previous diagnosis of aHUS undergoing kidney transplantation).ResultsSeven cases were outlined: five of therapeutic use and two, prophylactic. From the five cases of therapeutic use, there was improvement of the thrombotic microangiopathy in the 48 hours following the start of the drug and no patient experienced relapse during an average follow-up of 21 months in the continuous use of eculizumab (minimum of 6 and maximum of 42 months). One patient died at 6 months, due to Aspergillus infection. From the two cases of prophylactic use, one patient experienced relapsed thrombotic microangiopathy after 4 months and another patient remained asymptomatic after 16 months of follow-up, both on chronic treatment.DiscussionThe therapeutic use of eculizumab showed to be effective, with improvement of the microangiopathy parameters and persisting up to the end of the follow-up, without relapses. The additional risk of immunosuppression, leading to opportunistic infections, was well tolerated. The prophylactic use showed to be effective and safe; however, the doses and intervals should be individualized in order to avoid relapsed microangiopathy, especially in patients with factor H mutation.
Background The measurement of native T1 through cardiovascular magnetic resonance (CMR) is a noninvasive method of assessing myocardial fibrosis without gadolinium contrast. No studies so far have evaluated native T1 after renal transplantation. The primary aim of the current study is to assess changes in the myocardium native T1 6 months after renal transplantation. Methods We prospectively evaluated 44 renal transplant patients with 3 T CMR exams: baseline at the beginning of transplantation and at 6 months after transplantation. Results The native T1 time was measured in the midventricular septum and decreased significantly from 1331 ± 52 ms at the baseline to 1298 ± 42 ms 6 months after transplantation ( p = 0.001). The patients were split into two groups through a two-step cluster algorithm: In cluster-1 ( n = 30) the left ventricular (LV) mass index and the prevalence of diabetes were lower. In cluster-2 ( n = 14) the LV mass index and diabetes prevalence were higher. Decrease in native T1 values was significant only in the patients in cluster-1 ( p = 0.001). Conclusions The native myocardial T1 time decreased significantly 6 months after renal transplant, which may be associated with the regression of the reactive fibrosis. The patients with greater baseline LV mass index and the diabetic group did not reach a significant decrease in T1. Electronic supplementary material The online version of this article (10.1186/s12968-019-0531-x) contains supplementary material, which is available to authorized users.
The Brazilian collaborative registry for pediatric renal transplantation began in 2004 as a multicenter initiative aimed at analyzing, reporting, and disseminating the results of pediatric renal transplantation in Brazil. Data from all pediatric renal transplants performed from January 2004 to May 2018 at the 13 participating centers were analyzed. A total of 2744 pediatric renal transplants were performed in the thirteen participating centers. The median age at transplantation was 12.2 years, with the majority being male recipients (56%). The main underlying diseases were CAKUT (40.5%) and glomerulopathy (28%). 1981 (72%) of the grafts were from deceased donors (DD). Graft survival at one year (censored by death) was 94% in the live donor group (LD) and 91% in the DD group (log‐rank test P < 0.01). The patient’s survival at one and 5 years was 97% and 95% for the LD group and 96% and 93% for the DD group (log‐rank test P = 0.02). The graft loss rate was 19% (n = 517), more frequently caused by vascular thrombosis (n = 102) and chronic graft nephropathy (n = 90). DD recipients had 1.6 (1.0‐2.2) times greater chance of death and 1.5 (1.2‐1.8) times greater chance of graft loss compared to LD recipients. The mortality rate was 5.4% (n = 148), mainly due to infection (n = 69) and cardiovascular disease (n = 28). The results of this collaborative pediatric renal transplant record are comparable to other international registries, although we still have a high infection rate as a cause of death.
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