RESUMO
BACKGROUND: Malignancy is a well-known complication in patients after kidney transplantation (KT), but its effect on posttransplant outcomes, allograft, and patient survival remains unexplored. The aim of this study is to report the impact of the comorbidity on clinical outcome, function, and failure of an allograft kidney. METHODS: This case-control study included 101 KT patients. Twenty-six patients who developed cancer (CA) were assigned to the case group and 75 to the control group. Statistical analysis was performed using logistic regression models, and graft survival was analyzed using the Kaplan-Meier curve. RESULTS: Non-melanoma skin CA was the most common malignancy, accounting for almost 60% of cases, followed by stomach CA, prostate CA, and lymphoproliferative diseases (7.70% each). Difference in graft and patient survival was not significant between the two groups (P > .05). A tumor in nonfunctioning in the first nonfunctioning KT was identified in 1 KT patient with a second allograft and by anatomopathological was detect Fuhrman grade II renal cell carcinoma. This KT patient was in good clinical condition with serum creatinine level of 1.5 mg/dL. CONCLUSIONS: No association was observed between CA development and risk factors, including family history and smoking habit, and no differences in allograft and patient survival were found. Nevertheless, in our data, CA in KT patients occurred early after transplantation. Renal cell carcinoma in allograft failure was identified in a patient; that suggested that nephrectomy of kidney failure must be performed to avoid patient allosensitization and neoplasia. Thus, we suggest continuous screening of malignancy diseases for KT patients.
Assuntos
Carcinoma de Células Renais , Neoplasias Renais , Transplante de Rim , Aloenxertos , Carcinoma de Células Renais/etiologia , Estudos de Casos e Controles , Sobrevivência de Enxerto , Humanos , Neoplasias Renais/etiologia , Transplante de Rim/efeitos adversos , Masculino , Fatores de Risco , Resultado do TratamentoRESUMO
Chronic kidney disease (CKD) is a serious public health problem whose prevalence has increased in the last few years. Its progression is associated with high morbidity and mortality. Several factors are associated with the onset and progression of CKD, such as obesity, hypertension and diabetes mellitus. Beyond these factors, there is evidence of a pathophysiological role for inflammation in CKD. Several cytokines and chemokines have been detected in the plasma and urine of patients at early stages of CKD, and have also been related to CKD complications. The expression of these mediators and renal injury may be influenced by drugs such as angiotensin-converting enzyme inhibitors, statins and antagonists of cytokine receptors. Modulation of the immune-inflammatory response can become a target for CKD treatment. The aim of this study was to review the scientific evidence on the role of inflammation in CKD, especially the effects of cytokines and chemokines.
Assuntos
Citocinas/fisiologia , Inflamação/imunologia , Falência Renal Crônica/imunologia , Biomarcadores , Humanos , Inflamação/etiologia , Falência Renal Crônica/complicações , Glomérulos Renais , Sistema Renina-Angiotensina/fisiologiaRESUMO
A doença renal crônica (DRC) é um grave problema de saúde pública cuja prevalência tem aumentado nos últimos anos. Apresenta caráter progressivo e está associada à elevada morbidade e mortalidade. Inúmeros fatores estão associados à instalação e progressão da DRC, tais como obesidade, hipertensão arterial e diabetes mellitus. Além desses fatores, existem evidências de inflamação na fisiopatologia da DRC. Diversas citocinas e quimiocinas têm sido detectadas no plasma e urina de pacientes em estágios precoces da DRC e também relacionadas às complicações da doença. A expressão desses mediadores e a lesão renal sofrem interferência de fármacos como inibidores de enzima conversora de angiotensina (ECA), estatinas e antagonistas de receptores de citocinas. A modulação da resposta imuno-inflamatória pode se tornar alvo para tratamento da DRC. O objetivo deste artigo de revisão foi resumir as evidências científicas do pa-pel da inflamação na DRC, destacando-se os efeitos de citocinas e quimiocinas.
Chronic kidney disease (CKD) is a serious public health problem whose prevalence has increased in the last few years. Its progression is associated with high morbidity and mortality. Several factors are associated with the onset and progression of CKD, such as obesity, hypertension and diabetes mellitus. Beyond these factors, there is evidence of a pathophysiological role for inflammation in CKD. Several cytokines and chemokines have been detected in the plasma and urine of patients at early stages of CKD, and have also been related to CKD complications. The expression of these mediators and renal injury may be influenced by drugs such as angiotensin-converting enzyme inhibitors, statins and antagonists of cytokine receptors. Modulation of the immune-inflammatory response can become a target for CKD treatment. The aim of this study was to review the scientific evidence on the role of inflammation in CKD, especially the effects of cytokines and chemokines.
Assuntos
Humanos , Citocinas/fisiologia , Inflamação/imunologia , Falência Renal Crônica/imunologia , Biomarcadores , Inflamação/etiologia , Glomérulos Renais , Falência Renal Crônica/complicações , Sistema Renina-Angiotensina/fisiologiaRESUMO
The antiarrhythmogenic effect of the flavonoid dioclein on myocardial ischemia/reperfusion was investigated in isolated perfused rat hearts. Low concentrations of dioclein (30-300 nM) induced a reduction of arrhythmias observed during the reperfusion period. Dioclein also preserved the diastolic tension after reperfusion without affecting the systolic tension. In addition, dioclein (150 nM) dramatically reduced the formation of reactive oxygen species (ROS) observed during reperfusion in hearts. In conclusion, dioclein acts as a potent antiarrhythmogenic and antioxidant drug with an excellent protective effect during reperfusion of ischemic hearts.