The origin of crescent forming cells in human glomerulonephritis (GN) remains unknown. Some animal studies demonstrated that parietal epithelial cells of Bowman's capsule (PECs) were the main component of proliferating cells and PEC-specific tight junction protein claudin-1 was expressed in crescentic lesions. We investigated the expression of claudin-1 in human GN. Immunohistochemistry for claudin-1 was performed on 17 kidney biopsy samples with crescent formation. Colocalization of claudin-1 with intracellular tight junction protein ZO-1 was also evaluated by immunofluorescence double staining. Claudin-1 is expressed mainly at the cell to cell contact site of proliferating cells in cellular crescentic lesions in patients with these forms of human GN. Small numbers of crescent forming cells showed extrajunctional localization of claudin-1. Colocalization of claudin-1 with ZO-1 was found at cell to cell contact sites of adjacent proliferating cells. In control samples, staining of claudin-1 was positive in PECs, but not in podocytes. Our findings suggest that claudin-1 contributes to crescent formation as a component of the tight junction protein complex that includes ZO-1. Co-localization of claudin-1 with ZO-1 implies the formation of functional tight junction complexes in crescentic lesions to prevent the interstitial damage caused by penetration of filtered molecules from Bowman's space.

Glomerulonephropathy is a rare complication of Takayasu's arteritis (TA). To date, most glomerulonephropathies associated with TA show the histological feature of mesangial proliferation. Membranous glomerulonephropathy (MG) is a form of glomerulonephropathy in which the mesangial proliferation is not conspicuous and its association with TA is extremely rare. A 54-year-old man was referred to our hospital due to progressive edema in the lower limbs and nephrotic range proteinuria. Five years previously, he underwent percutaneous angioplasty for left subclavian artery stenosis. Kidney biopsy revealed stage II MG. General examination including enhanced CT scan confirmed the presence of TA. He started oral prednisolone therapy at a dose of 40 mg daily. The C-reactive protein level normalized 7 days after the prednisolone therapy. Three months later, proteinuria had remitted. Though the true relationship between MG and TA was not revealed in present case, considering the fact that complete remission of nephrotic syndrome occurred following the improvement of C-reactive protein level in response to steroid therapy, TA might be the secondary cause of MG. To our best knowledge, only two case reports described the association of MG and TA previously. Those two patients, however, also demonstrated the feature of systemic lupus erythematosus in addition to TA. This is the first case report that describes a patient who presented as MG associated with TA, but not complicated by systemic lupus erythematosus.

: Even though fibrous wood filler is known to be effective for improving mechanical and water-resistant properties of wood plastic composite (WPC), it has not been commercially adopted because of its high cost and less handling ability. In the present study, with an expectation of similar positive effect of fibrous wood filler, we carried out a fibrillation of a surface of practical wood flour in pre-mixed compound, containing wood flour, polypropylene, and compatibilizer, for producing WPC with high filler content by means of wet disk-milling. Scanning electron micrography revealed a micro-fibrillation on the surface of wood flour in the ground pre-mixed compound. The size of the surface micro-fiber could be controlled by disk-milling conditions. The formation of the micro-fibrous structure affected the melt viscosity of the compounds and improved mechanical properties of molded samples. The positive effect of the surface micro-fiber formation can be attributed to an interaction among the micro-fibers such as hydrogen bonding and entanglement. The observed reinforcement effect by the surface fibrillation was essentially identical to that of wood fiber although fibrillation was attained just in the surface of wood flour.

Short bowel syndrome (SBS) is characterized by a malabsorptive state. It is conceivable that the coexistence of SBS and end-stage renal disease can lead to severe metabolic acidosis; however, such a condition has rarely been documented. We herein describe the case of a 64-year-old man with SBS who required maintenance hemodialysis. Persistent metabolic acidosis and mineral and bone disorders should be of particular concern in hemodialyzed patients with SBS.

Background: Dipeptidyl peptidase-4 inhibitors (DPP-4i) have become widely used in hemodialysis patients with type 2 diabetes mellitus (T2DM). This study aimed at testing the hypothesis that administration of alogliptin, a DPP-4i, soon after hemodialysis initiation improves beta cell function in hemodialysis patients with T2DM. Methods: Patients with end-stage renal disease and T2DM (n = 10) not previously treated with DPP-4i (mean age, 54.2 years) were enrolled. The study end point was the acute insulin response to glucose assessed by a frequently sampled intravenous glucose tolerance test (IVGTT) that was conducted during the hemodialysis session just before lunch using an external circulation circuit. All patients received 6.25 mg alogliptin for 2 weeks. Blood glucose (Glu), serum insulin (IRI), and C-peptide (CPR) were measured before (0 min) in addition to 5 and 15 min after the glucose load. Glucagon-like peptide-1 (GLP-1) was measured before the glucose load. Results: Glu(0) significantly decreased after the 2-week DPP-4i treatment (174 ± 20 vs. 150 ± 27 mg/dL, P = 0.023). IRI(5) significantly increased after the DPP-4i treatment (14.6 ± 31.7 vs. 23.4 ± 16.6 μU/mL, P = 0.038), but IRI(0) and IRI(15) did not change significantly. GLP-1 also significantly increased after the DPP-4i treatment (6.6 ± 4.4 vs. 2.6 ± 0. 8 pmol/L, P = 0.012). Conclusions: Inhibition of DPP-4 with alogliptin improved endogenous insulin secretion in response to intravenous glucose in hemodialysis patients with T2DM.