6 months after the onset were referred to our clinic. Closed manipulation by careful manipulation under general anesthesia followed by external immobilization with a halo vest was performed in all cases. Radiographic findings and clinical courses were retrospectively reviewed with approvals by the institutional review board.

Results. Three-dimensional

computed tomography images before reduction revealed persistent atlantoaxial subluxation and the C2 facet deformity in the dislocated side in all cases. Follow-up three-dimensional computed tomographic scans demonstrated the remodeling of the C2 facet deformity at an average of 2.8 months after successful reduction of subluxation. Subsequently, the halo vests were removed and gentle neck range of motion exercise was started in all cases. The normal cervical range of motion was obtained 2 weeks after the removal of halo vests in five cases, whereas the range Sirtuin inhibitor of motion remained limited in two cases. At a mean follow-up of 17.4 months, neither symptoms nor recurrence of subluxation occurred in all cases.

Conclusion. Chronic irreducible and recurrent unstable AARF can be managed successfully by careful closed manipulation followed by halo fixation, if the C1 and C2 have not been osseously fused. The remodeling of the C2 facet deformity detected on follow-up

CT scans can be a useful radiographic parameter to determine the appropriate period of halo fixation in this new treatment TPCA-1 order strategy obviating the need for surgical intervention.”
“Focal segmental glomerulosclerosis (FSGS) is a clinicopathologic syndrome of proteinuria, usually of nephrotic range, associated with focal and segmental

sclerotic glomerular lesions. Therefore, FSGS is diagnosed by clinical features and histopathological examination of renal biopsy. The natural history of the condition varies, and although it may respond RGFP966 in vivo to treatment, FSGS is an important disease in the etiology of end-stage renal disease (ESRD). Furthermore, after kidney transplantation, approximately 30% of patients with FSGS develop recurrent FSGS. The risk factors for recurrence of FSGS include childhood onset and age < 15 yr, rapid progression of the primary FSGS to ESRD, recurrence of FSGS in a previous allograft, diffuse mesangial hypercellularity in the native kidney, collapsing FSGS, and podocin gene mutation. In addition, after kidney transplantation, de novo FSGS also develops in approximately 10-20% of allografts, associated with a complication of hyperfiltration injury, chronic transplant glomerulopathy, and calcineurin inhibitor toxicity. FSGS is considered a podocyte disease, and the pathology is characterized by segmental FSGS lesion with glomerular epithelial hypercellularity. The pathological diagnosis of FSGS is based on the 2004 Columbia classification system. In the present minireview, we discuss the pathology of recurrence and de novo FSGS after kidney transplantation.”
“Study Design.