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Improving long-term graft survival remains one of the critical challenges facing kidney transplantation since a great portion of kidney grafts are lost by 10 years after transplantation. Understanding the causes of chronic allograft injury and providing timely therapeutic interventions are essential for improving these outcomes. In this review, we will discuss the recent data that emerged turning down calcineurin inhibitors as the primary cause of long-term graft injury and highlighting the increased importance of non-compliance, antibody-mediated injury, disease recurrence, and BK nephropathy as culprits. We suggest a number of different strategies to better manage kidney transplant recipients that, ultimately, may improve long-term graft survival.  相似文献   

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BackgroundMicrovascular invasion is the strongest prognostic factor of survival in patients with hepatocellular carcinoma. We therefore developed a predictive model for microvascular invasion of hepatocellular carcinoma to help guide treatment strategies in patients scheduled for either hepatic resection or liver transplantation.MethodsPatients with hepatocellular carcinoma who underwent hepatic resection or liver transplantation from 1994 to 2016 were divided into training and validation cohorts. A predictive model for microvascular invasion was developed based on microvascular invasion risk factors in the training cohort and validated in the validation cohort.ResultsA total of 910 patients (425 having received hepatic resection, 485 having received liver transplantation) were included in the training (n = 637) and validation (n = 273) cohorts. Multivariate analysis identified α-fetoprotein ≥100 ng/mL (relative risk 3.05, P < .0001), tumor size ≥40 mm (relative risk 1.98, P = .0002), nonboundary hepatocellular carcinoma type (relative risk 1.91, P = .001), neutrophil-to-lymphocyte ratio (relative risk 1.86, P = .002), and aspartate aminotransferase (relative risk 1.53, P = .02) as associated with microvascular invasion. The estimated probability of microvascular invasion ranged from 17.0% in patients with none of these factors to 86.9% in the presence of all factors. This model achieved a C-index of 0.732 in the validation cohort. The 5-year overall survival of patients with ≥50% probability of microvascular invasion was poorer than that of patients with <50% probability (hepatic resection; 39.1% vs 61.2%, P < .0001, liver transplantation; 5-year overall survival, 54.8% vs 79.0%, P = .05).ConclusionThis model developed from preoperative data allows reliable prediction of microvascular invasion in candidates for either hepatic resection or liver transplantation.  相似文献   

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Background

Recurrence of focal segmental glomerulosclerosis (FSGS) in renal allograft recipients after first transplant occurs in the second graft in virtually all patients. There is little evidence regarding optimal treatment.

Case presentation

A 55-year-old man with primary FSGS and disease recurrence in both the first and the second kidney grafts is presented. In 1999, the patient developed FSGS 3 years after transplant, which was treated with plasmapheresis and cyclophosphamide. Hemodialysis was started at 8 years from the onset of relapse. In February 2014, the patient received a second kidney transplant, and after 2 weeks laboratory analysis showed nephrotic proteinuria (5.9 g/d) with increased serum creatinine. Biopsy results revealed recurrence of FSGS. At that time, he was treated with steroids and plasmapheresis with partial efficacy, achieving a serum creatinine level of 1.1 mg/dL with decreased proteinuria (1 g/d). After 4 months, creatinine worsened (1.6 mg/dL) with new evidence of proteinuria. Second biopsy results showed evidence of FSGS progression. The patient then received plasmapheresis and 2 doses of rituximab. Follow-up was characterized by progressive remission up to complete resolution. The patient is currently free from relapses after 3 years with good renal function and almost no proteinuria.

Conclusions

More evidence and prospective studies are needed to better understand the role of rituximab in FSGS in order to obtain an optimized therapeutic protocol for recurrence of FSGS in renal transplant recipients.  相似文献   

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