Prospective study of infectious complications in a cohort of pediatric renal transplant recipients

Abstract

In pediatric RT recipients, UTI is the most frequent syndrome. Bacterial infections are the most common, with a high rate of ESBL producer strains. Despite their good prognosis, infections are a cause of morbidity that could potentially be reduced by decreasing cold ischemia times.

Children after renal transplantation hospitalized for fever: Is empirical antibiotic treatment always justified?

“…UTI infection was the most common bacterial infection in our cohort and the most common source of bacteremia. This finding is in concert with previous studies reporting a high (35%‐80%) incidence of UTI in renal transplant recipients . Similar to Their et al .…”

“…Similar to Their et al . and Martin‐Pena et al., we noted no significant difference in the incidence of UTI during and after TMP/SMX prophylaxis, possibly because of the high rates of resistance to this antimicrobial agent in our geographic area . As frequent UTIs may trigger graft rejection and lead to decreased graft survival, early diagnosis and treatment are important.…”

“…Infections are a leading cause of death in pediatric renal transplant recipients, although mortality rates are generally low . In our study, there were no cases of in‐hospital mortality.…”

Infectious Complications in Pediatric Renal Transplant Patients

“…Both nosocomial and opportunistic infection ratios were 39.4% in this period. These results were incompatible with those of other studies [11]. We believe that this higher ratio after the decrease in infectious episodes observed between 7 and 12 months arises mostly from patient care.…”

L’ischémie reperfusion

“…Impact de l'ischémie reperfusion sur les autres mécanismes lésionnels survenant lors de la transplantation Différentes études ont montré que le temps d'ischémie froide était directement corrélé au risque de résurgence d'infections par le CMV (cytomégalovirus), et que tout incrément de 30 min du temps de préservation favorisait ce processus [21,22]. D'un point de vue mécanistique, la relation entre ischémie et activation du CMV a été localisée au niveau du promoteur du virus qui possède des séquences spécifiques de fixation d'intermédiaires de la voie du TNF (tumor necrosis factor a) et de NFB [23], mais également de la voie de AP1 (activator protein 1) qui peut être activée par le stress oxydant produit en réponse à l'IR [23].…”