Rechazo crónico mediado por anticuerpos

Contexto el rechazo crónico mediado por anticuerpos (cABMR, chronic antibody-mediated rejection) se considera una de las principales causas de disfunción crónica del injerto. Objetivo profundizar en la comprensión de los mecanismos que la ocasionan para diseñar tratamientos efectivos, dado que es muy poco lo que se ha avanzado en el tratamiento de esta patología. Metodología en esta revisión narrativa de la literatura, presentamos los factores de riesgo relacionados con la disfunción crónica del injerto, haciendo énfasis en la fisiopatología, el diagnóstico y el tratamiento del cABMR. Resultados el factor de riesgo más relevante para el desarrollo de disfunción crónica del injerto es el desarrollo de anticuerpos donante específicos (DSA) y ABMR. Para el diagnóstico de cABMR activo, se requieren los criterios de Banff 2017 (los tres deben estar presentes: Evidencia histológica de lesión tisular crónica, evidencia de inflamación actual en el endotelio vascular ocasionada por anticuerpos y evidencia serológica de DSA. El cABMR no tiene un tratamiento efectivo. Conclusiones dado que cABMR no tiene un tratamiento efectivo, es importante disminuir la exposición a los factores de riesgo y hacer un diagnóstico y un tratamiento oportuno de los eventos agudos de lesión renal que contribuyen a la progresión de disfunción crónica del injerto.

Context Chronic antibody-mediated rejection (cABMR) is considered one of the main causes of chronic graft. Objective To review the mechanisms that cause cABMR to design effective treatments, since it is very little what has been advanced in it treatment of this pathology. Methodology In this narrative review of the literature, we present the risk factors related to the chronic dysfunction of the injection, emphasizing the pathophysiology the diagnosis and treatment of cABMR. Results The most relevant risk factor for the development of chronic graft dysfunction is the development of specific donor antibodies (DSA) and ABMR. For the diagnosis of active cABMR, the criteria of Banff 2017 are required (three must be present: histological evidence of chronic tissue injury, evidence of current inflammation in the vascular endothelium caused by antibodies and serological evidence of DSA. The cABMR does not have an effective treatment. Conclusions Since cABMR does not have an effective treatment, it is important reduce exposure to risk factors and carry out a diagnosis and treatment of the acute events of kidney injury that contribute to the progression of chronic injection dysfunction.

Linfohistiocitosis hemofagocítica por Histoplasma capsulatum en paciente con trasplante renal / Hemophagocytic Lymphohistiocytosis induced by Histoplasma capsulatum in a kidney transplant patient

La linfohistiocitosis hemofagocítica (LHH) por Histoplasma capsulatum, presentación rara de la histoplasmosis diseminada, es causada por la fagocitosis de las células hematopoyéticas por macrófagos tisulares. Presentamos el caso de un paciente masculino de 44 años con trasplante renal que asiste por fiebre sin otra sintomatología. Inicialmente se obtiene una gota gruesa positiva para P. vivax, iniciando manejo antimalárico. A los 2 días de tratamiento, el paciente presenta disfunción multiórganica, se rectifica diagnóstico en centro de referencia reportando en extendido de sangre periférica la presencia de levaduras de H. capsulatum en polimorfonucleares, resultado confirmado con prueba de inmunodifusión. Se ajusta manejo, pero el paciente fallece. El diagnóstico de infecciones por gérmenes inusuales con presentaciones inespecíficas es un reto en pacientes con inmunosupresión.

Hemophagocytic Lymphohistiocytosis (HLH) induced by Histoplasma capsulatum is a rare entity who is characterized by phagocytosis of hematopoietic cells by tissue macrophages. A 44-year-old male patient with kidney transplantation was admitted to our ambulatory service with fever. Initially, we performed a thick drop test who was positive for P. vivax, so antimalarial therapy was initiated. Patient then progressed to multiple organ dysfunction after 2 days of treatment. Thus, a reference center went back over the blood smear which revealed the presence of yeast cells H. capsulatum within polymorphonuclear cells. This result was confirmed by an immunodifussion assay. Despite of antifungal treatment, patient passed away. The diagnosis for unusual microorganism with unspecific clinical presentation could be a challenge in immunosupressive patients.

Acute Kidney Injury in Hospitalized Kidney Transplant Recipients.

BACKGROUND: Acute kidney injury (AKI) is a main cause of morbidity, hospitalization, and hospital readmission in kidney transplant recipients. We aimed to determine AKI incidence and risk factors following kidney transplant to assess outcomes such as renal function and graft loss after AKI. METHODS: We conducted a retrospective cohort study with hospitalized kidney transplant recipients during 2016 to 2017. Clinical data of 179 patients were reviewed. The primary outcome was AKI incidence and risk factors. To determine AKI occurrence, we based it on creatinine criteria from Acute Kidney Injury Network classification. RESULTS: We documented a total of 179 hospital admissions; AKI was diagnosed in 104 patients (58.1%). Recipients with higher baseline serum creatinine (odds ratio, 2.6; confidence interval [CI], 1.5-4.5; P < .001) and hospital admission because of infections (odds ratio, 2.4; CI, 1.1-5.2; P = .020) were more likely to experience AKI. A total of 19 recipients (10.6%) had graft loss with a significant AKI association (P = .003) at 12 months after admission. Intensive care unit length of stay (P = .63) and hospital stay (P = .55) were not different in patients with AKI compared with the control group. CONCLUSIONS: As a main clinical finding, we concluded that infections and higher serum creatinine baseline level were associated with the development of AKI.