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A 66-year-old-man who had undergone partial aortic arch and descending aortic graft replacement for a dissecting aortic aneurysm presented to our hospital with pain and beating swelling of his left back shoulder. Enhanced computed tomography and aortic angiography revealed graft rupture caused by one of the claws of a rib fixation strut. Furthermore, another claw had invaded a lung. We performed emergency thoracic endovascular aortic repair, and removed all of the struts 3 weeks later. Claw-type rib fixation struts have the potential to injure other organs, including prosthetic grafts. Careful follow-up is mandatory after implantation of this type of strut.

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Recent studies have indicated that the detection of urinary podocytes holds major significance for focal segmental glomerulosclerosis (FSGS). We present two cases of FSGS after kidney transplantation, focusing on urinary podocytes. In Case 1, treatment led to incomplete remission with the reduction of urinary podocytes, and his renal function was preserved. Case 2, however, showed continuous increase in proteinuria with loss of renal function despite apheresis. Urinary podocytes remained high throughout. On the basis of this experience, we suggest the significance of the detection of urinary podocytes for determining renal prognosis in FSGS following renal allograft.

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BACKGROUND: For a definitive diagnosis of chronic kidney disease, at least 2 consecutive positive results of proteinuria with an interval of >3 months are required. However, most previous reports were based on single-screening data. PATIENTS AND METHODS: The subjects in this study were participants in an annual health examination held in Ibaraki, Japan, between 1993 and 2003. The follow-up duration with serial urinalysis for 3 years of patients who were negative for proteinuria in the initial year was 330,614 person-years in males and 687,381 person-years in females among 81,854 male and 155,256 female subjects. We evaluated the incidence and risk factor for the incidence of proteinuria and persistent proteinuria. RESULT: The annual incidence of proteinuria and persistent proteinuria was 1.31 and 0.33 % in males and 0.68 and 0.14 % in females. Among the subjects without hypertension and diabetes, the annual incidence was 0.81 and 0.16 % in males and 0.37 and 0.06 % in females, respectively. Risk analysis indicated that hypertension in males [hazard ratio (HR) 2.052] and females (2.477), diabetes in males (3.532) and females (3.534) and reduced renal function in males (3.097) and females (2.827) were significant positive risks for development of persistent proteinuria. CONCLUSION: By annual urinalysis screening of the general population, 1 out of 303 male subjects and 1 out of 725 female subjects developed persistent proteinuria every year. Subjects with diabetes, hypertension and reduced renal function had a 2 or 3 times higher risk for the incidence of persistent proteinuria in both males and females.

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Dysfunction of mitochondria in podocytes is believed to be a trigger of injury and contributes to progressive glomerular sclerosis; however, the mechanisms had not been fully understood. Yuan et al. report involvement of SIRT1 (a homolog of the life-extending gene sir2 in mammals) and PPAR-γ coactivator 1α, a major regulator of oxidative metabolism, in mitochondria during podocyte injury. This information will be important in exploration of the mechanisms and future treatment of glomerular sclerosis.

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Renal involvement is a significant complication of multicentric Castleman's disease (MCD) and various glomerular involvements have been reported. A 45-year-old Japanese man presented with persistent proteinuria, with lymphadenopathy and hypergammaglobulinemia. He had been diagnosed 4 years previously with MCD. As his renal impairment had progressed to renal failure, he underwent a renal biopsy. Histology revealed diffuse and global membranous lesions with large and heterogeneous epimembranous deposits. In addition, mesangial cell proliferation and focal extracapillary lesions were found. Under immunofluorescence, granular staining for anti-IgG, IgG1, IgG2 and IgA was strongly positive in the capillary loop, and weakly positive in the mesangium. As such, there was a diversity of histological features. Our perspective with regard to pathogenesis is that the formation of the immune-complex contributed to the membranoproliferative glomerulonephritis type 3-like lesion. This histological multiform with MCD is valuable for increasing our understanding of the mechanism for onset of immune-complex glomerular deposition and cellular proliferation of glomerulonephritis.

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Human hepatitis B virus (HBV) is well known as a cause of membranous nephropathy (MN). While the association of HBV infection with MN is strong, data regarding its association with other glomerular diseases are conflicting. Here, we report a case of focal segmental glomerulosclerosis (FSGS) with HBV infection. In this case, we have found HBV-DNA in urinary podocytes by real-time PCR methods. After the administration of anti-viral therapy, FSGS improved, paralleling the decreased level of HBV-DNA in podocytes. The refractory FSGS induced by HBV could be effectively treated with appropriate anti-viral agents.

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