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ABSTRACT Introduction: Anemia is frequent in patients undergoing replacement therapy for kidney failure. Anemia in the pre- and post-transplantation period might be related to kidney transplant outcomes. The current study therefore sought to assess the relationship between anemia, delayed allograft function (DGF), chronic kidney allograft dysfunction (CAD), and death from any cause following kidney transplantation from a deceased donor. Methods: This was a retrospective study with 206 kidney transplant patients of deceased donors. We analyzed deceased donors' and kidney transplant patients' demographic data. Moreover, we compared biochemical parameters, anemia status, and medicines between DGF and non-DGF groups. Afterward, we performed a multivariate analysis. We also evaluated outcomes, such as CAD within one year and death in ten years. Results: We observed a lower frequency of pre-transplant hemoglobin concentration (Hb) but higher frequency of donor-serum creatinine and red blood transfusion within one week after transplantation in the group with DGF. In addition, there was an independent association between Hb concentration before transplantation and DGF [OR 0.252, 95%CI: 0.159-0.401; p < 0.001]. There was also an association between Hb concentration after six months of kidney transplantation and both CAD [OR 0.798, 95% CI: 0.687-0.926; p = 0.003] and death from any cause. Conclusion: An association was found between pre-transplantation anemia and DGF and between anemia six months after transplantation and both CAD and death by any cause. Thus, anemia before or after transplantation affects the outcomes for patients who have undergone kidney transplantation from a deceased donor.
RESUMO Introdução: A anemia é frequente em pacientes submetidos à terapia substitutiva para insuficiência renal. A anemia nos períodos pré e pós-transplante pode estar relacionada aos desfechos do transplante renal. Portanto, o presente estudo buscou avaliar a relação entre anemia, função retardada do enxerto (FRE), disfunção crônica do enxerto renal (DCE) e óbito por qualquer causa após transplante renal de doador falecido. Métodos: Este foi um estudo retrospectivo com 206 pacientes transplantados renais de doadores falecidos. Analisamos dados demográficos de doadores falecidos e pacientes transplantados renais. Além disso, comparamos parâmetros bioquímicos, status de anemia e medicamentos entre os grupos FRE e não-FRE. Posteriormente, realizamos uma análise multivariada. Também avaliamos desfechos, como DCE em um ano e óbito em dez anos. Resultados: Observamos menor frequência de concentração de hemoglobina (Hb) pré-transplante, mas maior frequência de creatinina sérica do doador e transfusão de hemácias no período de uma semana após o transplante no grupo FRE. Além disso, houve associação independente entre a concentração de Hb antes do transplante e a FRE [OR 0,252; IC 95%: 0,159-0,401; p < 0,001]. Houve também associação entre a concentração de Hb após seis meses de transplante renal e ambos, DCE [OR 0,798; IC95%: 0,687-0,926; p = 0,003] e óbito por qualquer causa. Conclusão: Encontrou-se uma associação entre anemia pré-transplante e FRE e entre anemia seis meses após o transplante e ambos, DCE e óbito por qualquer causa. Assim, a anemia antes ou após o transplante afeta os desfechos de pacientes que foram submetidos a transplante renal de doador falecido.
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BACKGROUND: Prolonged donor hepatectomy time may be implicated in early and late complications of liver transplantation. AIM: To evaluate the impact of donor hepatectomy time on outcomes of liver transplant recipients, mainly early allograft dysfunction. METHODS: This multicenter retrospective study included brain-dead donors and adult liver graft recipients. Donor-recipient matching was obtained through a crossover list. Clinical and laboratory data were recorded for both donors and recipients. Donor hepatectomy, cold ischemia, and warm ischemia times were recorded. Primary outcome was early allograft dysfunction. Secondary outcomes included need for retransplantation, length of intensive care unit and hospital stay, and patient and graft survival at 12 months. RESULTS: From January 2019 to December 2021, a total of 243 patients underwent a liver transplant from a brain-dead donor. Of these, 57 (25%) developed early allograft dysfunction. The median donor hepatectomy time was 29 (23-40) min. Patients with early allograft dysfunction had a median hepatectomy time of 25 (22-38) min, whereas those without it had a median time of 30 (24-40) min (P = 0.126). CONCLUSION: Donor hepatectomy time was not associated with early allograft dysfunction, graft survival, or patient survival following liver transplantation.
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PURPOSE: New-onset diabetes after transplantation (NODAT) is a frequent metabolic complication associated with podocyte damage and renal allograft dysfunction. Thus, Wilm's tumor-1 (WT-1) protein, as a podocyte marker, holds promise as an option to evaluate renal allograft dysfunction in NODAT. Therefore, the study aimed to investigate urinary WT-1 levels in NODAT patients during the first year after kidney transplantation (KTx). MATERIALS AND METHODS: KTx patients were categorized into non-NODAT and NODAT groups. Fasting blood glucose, glycated hemoglobin (HbA1c), urinary albumin/creatinine ratio (ACR), serum creatinine, estimated glomerular filtration rate (eGFR), and urinary WT-1 were measured at 3, 6, 9, and 12-months post-KTx. RESULTS: The NODAT group manifested elevated levels of blood glucose and HbA1c during the first year post-KTx. Also, exhibited elevations in ACR and serum creatinine levels at 6, 9, and 12-months post-KTx when compared to non-NODAT group. Conversely, eGFR values in the NODAT group demonstrated significant declines at 3, 6, and 9-months post-KTx relative to non-NODAT. Furthermore, NODAT group exhibited a median annual eGFR of 47 âmL/min/1.73 âm2. Urinary WT-1 levels at 3, 6, 9, and 12-months post-KTx were significantly higher in the NODAT group compared to non-NODAT. Additionally, noteworthy positive correlations were identified between urinary WT-1 and HbA1c levels, along with significant negative correlations between urinary WT-1 and eGFR at the 3, 6, 9, and 12-months post-KTx. CONCLUSION: The increased urinary WT-1 levels from 3-months post-KTx in NODAT patients may indicate the first sign of podocyte injury, predicting a renal allograft dysfunction in these patients.
Subject(s)
Diabetes Mellitus , Glomerular Filtration Rate , Kidney Transplantation , WT1 Proteins , Humans , Kidney Transplantation/adverse effects , Male , Female , Middle Aged , Adult , WT1 Proteins/urine , Diabetes Mellitus/urine , Biomarkers/urine , Biomarkers/blood , Allografts , Prognosis , Follow-Up Studies , Glycated Hemoglobin/metabolismABSTRACT
Abstract Background: Adenine phosphoribosyl transferase (APRT) deficiency has great implications on graft survival in kidney transplant patients. This systematic review investigated the diagnostic pattern, treatment approach, and kidney transplant outcomes among kidney transplant patients with adenine phosphoribosyl transferase deficiency. Material and methods: Articles reporting the APRT enzyme deficiency and kidney allograft dysfunction were retrieved from PubMed/Medline, ScienceDirect, Cochrane library and Google scholar databases. Descriptive analysis was used to draw inferences. Results: The results from 20 selected studies covering 30 patients receiving 39 grafts had an average age of 46.37 years are presented. Graft survival time of more than 6 months was reported in 23 (76.7%) patients, while other 7 (23.3%) patients had graft survival time of less than 6 months. Only 4 (13.3%) patients had APRT deficiency before transplantation. After follow-up, one-third of the patients 10 (33.3%) had stable graft function, 1 patient had allograft loss, 8 (26.6%) patients had delayed graft function while the remaining 11 (36.6%) patients had chronic kidney graft dysfunction. Conclusions: APRT deficiency is an under-recognized, treatable condition that causes reversible crystalline nephropathy, leading to loss of allograft or allograft dysfunction. The study results showed that inclusion of genetic determination of APRT deficiency in the differential diagnosis of crystalline nephropathy, even in the absence of a history of nephrolithiasis, can improve renal outcomes and may improve allograft survival.
Resumo Antecedentes: A deficiência de adenina fosforibosiltransferase (APRT) tem grandes implicações na sobrevida do enxerto em pacientes transplantados renais. Esta revisão sistemática investigou o padrão diagnóstico, a abordagem de tratamento e os desfechos do transplante renal entre pacientes transplantados renais com deficiência de adenina fosforibosiltransferase. Material e métodos: Os artigos que relatam sobre a enzima APRT e a disfunção do aloenxerto renal foram recuperados do PubMed/Medline, ScienceDirect, Biblioteca Cochrane e bancos de dados do Google Acadêmico. Utilizou-se a análise descritiva para extrair inferências. Resultados: Foram incluídos participantes que receberam 39 enxertos, a maioria dos quais provenientes de doadores vivos seguidos por doadores falecidos e doadores cadáveres. Foi relatado tempo de sobrevida do enxerto superior a 6 meses em 23 (76,7%) pacientes, enquanto outros 7 (23,3%) pacientes tiveram tempo de sobrevida do enxerto inferior a 6 meses. Apenas 4 (13,3%) pacientes apresentaram deficiência de APRT antes do transplante. Após acompanhamento, um terço dos pacientes, 10 (33,3%) apresentaram função do enxerto estável, 1 paciente teve perda do aloenxerto, 8 (26,6%) pacientes apresentaram função retardada do enxerto, enquanto os 11 (36,6%) pacientes restantes tiveram disfunção crônica do enxerto renal. Conclusões: A deficiência de APRT é uma causa subestimada e reversível de nefropatia cristalina que leva à disfunção do aloenxerto renal ou à perda total do aloenxerto. Os resultados deste estudo pedem a inclusão desta condição no diagnóstico diferencial de nefropatia cristalina, mesmo na ausência de um histórico de nefrolitíase.
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Resumen El trasplante pulmonar implica una serie de desafíos, que como lo ha demostrado la historia, no sólo depende de un adecuado desarrollo de técnicas quirúrgicas, sino también de la comprensión de una serie de complejas interacciones inmunológicas celulares y humorales que serán las responsables del tipo de respuesta (innata y/o adquirida) fisiológica y que pudiesen desencadenar las complicaciones asociadas al trasplante (rechazo hiperagudo, agudo o crónico). Cada una de las cuales tiene su potencial prevención y/o tratamiento. El poder conocer esta serie de respuestas, permite al clínico anticiparse a algunos de estos eventos y evitar de mejor forma el daño y las consecuencias que pueden producir en los casos de trasplante pulmonar.
Lung transplantation involves a series of challenges, which as history has shown, depends not only on an adequate development of surgical techniques, but also on the understanding of a series of complex cellular and humoral immunological interactions that will be responsible for the type of physiological response (innate - acquired) and that could trigger the complications associated with transplantation (hyperacute, acute or chronic rejection). Each of which has its potential prevention and treatment. Being able to know this series of responses, allows the clinician to anticipate some of these events and to avoid in a better way the damage and the consequences that can occur in cases of lung transplantation.
Subject(s)
Humans , Transplantation Immunology/immunology , Lung Transplantation , Graft Rejection/immunology , T-Lymphocytes/immunology , Autoimmunity , Nuclear Factor 45 Protein , Graft Rejection/prevention & control , Immunity, Cellular , Immunity, Innate , Immunosuppressive AgentsABSTRACT
This special article focuses on the highlights in cardiothoracic transplantation literature in the year 2020. Part I encompasses the recent literature on lung transplantation, including the advances in preoperative assessment and optimization, donor management, including the use of ex-vivo lung perfusion, recipient management, including those who have been infected with coronavirus disease 2019, updates on the perioperative management, including the use of extracorporeal membrane oxygenation, and long-term outcomes.
Subject(s)
Anesthesia, Cardiac Procedures , COVID-19 , Extracorporeal Membrane Oxygenation , Lung Transplantation , Humans , Lung Transplantation/adverse effects , SARS-CoV-2ABSTRACT
BACKGROUND: In chronic kidney disease, intensive systolic blood pressure (SBP) control reduces mortality at a cost of greater acute kidney injury risk. Kidney transplantation involves implantation of denervated kidneys and immunosuppressive medications that increase acute kidney injury risk. The optimal blood pressure (BP) target in kidney transplant recipients (KTRs) is uncertain. Prior observational studies from the Folic Acid for Vascular Outcome Reduction in Transplantation (FAVORIT) trial demonstrate associations of lower SBP levels and reduced mortality risk, but the relationship of BP with kidney allograft function remains unknown. Thus, in FAVORIT, we investigated the relationship of SBP and diastolic blood pressure (DBP) with risk of kidney allograft failure and estimated glomerular filtration rate (eGFR) slope among stable KTRs. METHODS: Cox proportional hazards and multivariable linear regression models adjusted for demographics, transplant characteristics, comorbidities, baseline eGFR, and urine albumin-to-creatinine ratio were used to determine associations of SBP and DBP with time to a composite kidney outcome of ≥50% eGFR decline or dialysis dependence, and with annualized eGFR change, respectively. Multivariable restricted cubic spline plots were developed to evaluate the functional form of the relationships. RESULTS: Among 3,598 KTRs, mean age was 52 ± 9 years, SBP was 136 ± 20 mm Hg, DBP was 79 ± 12 mm Hg, and eGFR was 49 ± 18 ml/minute/1.73 m2. There were 369 events of ≥50% eGFR decline or dialysis dependence during a mean follow-up of 4.0 ± 1.5 years. There was no association of either SBP (compared with SBP 120 to <130 mm Hg, hazard ratio (HR) for the SBP < 110 was 1.01 (95% confidence interval (CI) 0.60 to 1.70) and 130 to <140 was 0.89 (0.64 to 1.24)) or DBP (compared with DBP 70 to <80 mm Hg, HR for the DBP 60 to <70 was 1.00 (95% CI 0.74 to 1.34) and 80 to <90 was 0.90 (0.68 to 1.18)) with the kidney failure outcome or annualized eGFR slope, and, when examined using restricted cubic splines, there was no evidence of "J"- or "U"-shaped relationships. CONCLUSIONS: In a large sample of stable KTRs, we found no evidence of thresholds at which lower BPs were related to higher risk of allograft failure or eGFR decline. In light of prior findings of mortality benefit at low SBP, these observational findings suggest lower BP may be beneficial in KTRs. This important question requires confirmation in future randomized trials in KTRs.
Subject(s)
Blood Pressure , Glomerular Filtration Rate , Hypertension/etiology , Kidney Transplantation/adverse effects , Kidney/physiopathology , Renal Insufficiency, Chronic/etiology , Adult , Aged , Brazil , Canada , Disease Progression , Female , Humans , Hypertension/diagnosis , Hypertension/physiopathology , Male , Middle Aged , Randomized Controlled Trials as Topic , Renal Dialysis , Renal Insufficiency, Chronic/diagnosis , Renal Insufficiency, Chronic/physiopathology , Renal Insufficiency, Chronic/therapy , Risk Assessment , Risk Factors , Time Factors , Treatment Outcome , United StatesABSTRACT
BACKGROUND: BK polyomavirus-associated nephropathy is an important cause of post-transplantation renal failure. We present two cases of BK polyomavirus-associated nephropathy who were submitted to contrasting strategies of clinical follow-up to BK polyomavirus reactivation, but progressed to a similar final outcome. CASE PRESENTATION: Case 1 is a 37-year-old white man whose graft had never presented a good glomerular filtration rate function, with episodes of tacrolimus nephrotoxicity, and no urinary monitoring for BK polyomavirus; stage B BK polyomavirus-associated nephropathy was diagnosed by biopsy at 14 months post-transplant. Despite clinical treatment (dosage decrease and immunosuppressive drug change), he progressed to stage C BK polyomavirus-associated nephropathy and loss of graft function 30 months post-transplant. Case 2 is a 49-year-old mulatto man in his second renal transplantation who was submitted to cytological urinary monitoring for BK polyomavirus; he presented early, persistent, and massive urinary decoy cell shedding and concomitant tacrolimus nephrotoxicity. Even with decreasing immunosuppression, he developed BK polyomavirus-associated nephropathy 1-year post-transplant. Loss of graft function occurred 15 months post-transplant. CONCLUSIONS: Cytological urinary monitoring was an efficient strategy for monitoring BK virus reactivation. Decoy cell shedding may be related to BK polyomavirus-associated nephropathy when extensive and persistent. The presence of associated tacrolimus nephrotoxicity may be a confounding factor for the clinical diagnosis of BK polyomavirus-associated nephropathy.
Subject(s)
BK Virus/isolation & purification , Immunocompromised Host/immunology , Kidney Diseases/virology , Kidney Transplantation , Polyomavirus Infections/diagnosis , Polyomavirus Infections/virology , Postoperative Complications/diagnosis , Postoperative Complications/virology , Adult , Dose-Response Relationship, Drug , Graft Rejection/immunology , Humans , Immunosuppressive Agents/adverse effects , Kidney Diseases/complications , Kidney Diseases/diagnosis , Kidney Diseases/urine , Male , Middle Aged , Polyomavirus Infections/immunology , Polyomavirus Infections/urine , Postoperative Complications/drug therapy , Postoperative Complications/immunology , Renal Dialysis , Tacrolimus/adverse effects , Transplant Recipients , Treatment Outcome , Virus Activation/drug effects , Virus Activation/immunologyABSTRACT
Objective: To assess the long-term impact (minimum of 3 years follow-up) of polymorphisms in cytokine genes in donor: recipient pairs on the results of the transplant. Methods: We compared genetic cytokine polymorphisms and the primary factors of risk for the development of chronic rejection in paired groups of renal transplant patients with and without chronic allograft nephropathy [CAN]. Results: Multivariate analysis indicated that the presence of the high-production TT genotype (codon 10) of the transforming growth factor beta-1 (TGFB1) was protective in receptors (p=0.017), contrasting with the increased risk when present in donor samples (p=0.049). On the other hand, in the case of the gamma interferon studied, the greater frequency of the high production allele was protective in the analysis of the donor group (p=0.013), increasing the risk of chronic nephropathy of the allograft when present in the recipients (p=0.036). Conclusion: Our results highlight the importance of TGFB1 genotyping in donors, and indicate that polymorphisms in the gene of this cytokine in donor cells might contribute to the development of chronic allograft nephropathy.
Objetivo: Avaliar o impacto de longo prazo (com seguimento mínimo de 2 anos) de polimorfismos em genes de citocinas em pares doador:receptor sobre os resultados do transplante. Métodos: Comparamos os polimorfismos genéticos das citocinas e os principais fatores de risco para o desenvolvimento de rejeição crônica em grupos pareados de pacientes transplantados renais com e sem nefropatia crônica do aloenxerto [CAN]. Resultados: A análise multivariada indicou que a presença do genótipo TT (códon 10) de alta produção do fator de crescimento transformador beta-1 (TGFB1) era protetor nos receptores (p=0,017), em contraste com o risco aumentado quando presente nas amostras de doadores (p=0,049). Por outro lado, no caso do interferon gama estudado, a maior frequência do alelo de alta produção foi protetora na análise do grupo de doadores (p=0,013), mas aumentava o risco de nefropatia crônica do aloenxerto quando presente nos receptores (p=0,036). Conclusão: Nossos resultados ressaltam a importância da genotipagem de TGFB1 também em doadores, e indicam que polimorfismos no gene desta citocina em células do doador podem contribuir no desenvolvimento da nefropatia crônica do aloenxerto.