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Several studies are conducted to determine the causes of renal hypouricemia, an inherited disorder that leads to impaired renal urate (uric acid) and subsequent low serum urate levels. The mutations taking place in the glucose transporter 9 gene, SLC2A9 is shown to be the major factor that leads to the disorder.

The profibrotic effect of plasminogen activator inhibitor-1 (PAI-1) in renal fibrosis is widely recognized, but its mechanism remains controversial especially in chronic progressive kidney disease. In the present study, pioglitazone (Pio) and candesartan (CD), which are reported to inhibit PAI-1, were administered to spontaneously hypercholesterolemic (SHC) rats, a model of chronic progressive kidney disease. Therapeutic effects and effects on the intrarenal plasmin cascade were examined. Eight-wk-old SHC rats were used as controls. Oral administration of vehicle alone, Pio, or CD was performed starting at 8 wk of age and was continued for 24 wk. The degree of renal fibrosis was evaluated by sirius red staining of kidney sections and by total collagen assay of renal homogenates. The renal PAI-1 protein level was assessed by Western blotting, and plasmin activity was analyzed by chromogenic assay and casein gel zymography. Urinary protein and blood urea nitrogen were significantly increased in the vehicle-treated group, but the increase was attenuated in the Pio- and CD-treated groups. This correlated well with the degree of fibrosis as assessed by sirius red staining and total collagen assay. The PAI-1 protein level was also increased significantly in the vehicle-treated group, and the increase was attenuated in the Pio- and CD-treated groups. Despite the presumed plasmin-inhibitory function of PAI-1, plasmin activity changed in parallel with PAI-1. These results suggest that Pio and CD inhibit PAI-1 and exert renoprotective effects against chronic progressive renal disease, but its action is independent of the regulatory function on plasmin activity. angiotensin II type 1 receptor blocker; peroxisome proliferator-activated receptor-[gamma] agonist; plasminogen activator inhibitor-1

A zero-K Monte Carlo simulation is performed for ferro/antiferromagnetic (F/AF) coupled systems of simple cubic structure. By assuming the existence of a plane in the AF-layer across which the AF-spins loosely with each other, it is noticed that a typical 360 degrees symmetry anisotropy appears without assuming any AF-spin constraint in the plane.

It is well known that glomerulonephritis can occur after streptococcal infection, which is classically referred to as acute poststreptococcal glomerulonephritis (APSGN). The pathogenic mechanism of APSGN has been described by so-called immune complex theory, which involves glomerular deposition of nephritogenic streptococcal antigen and subsequent formation of immune complexes in situ and/or the deposition of circulating antigen-antibody complexes. However, the exact entity of the causative antigen has remained a matter of debate. We isolated a nephritogenic antigen for APSGN from the cytoplasmic fractions of group A streptococcus (GAS) depending on the affinity for IgG of APSGN patients. The amino acid and the nucleotide sequences of the isolated protein revealed to be highly identical to those of reported plasmin(ogen) receptor of GAS. Thus, we termed this antigen nephritis-associated plasmin receptor (NAPlr). Immunofluorescence staining of the renal biopsy tissues with anti-NAPlr antibody revealed glomerular NAPlr deposition in essentially all patients with early-phase APSGN. Furthermore, glomerular plasmin activity was detected by in situ zymography in the distribution almost identical to NAPlr deposition in renal biopsy tissues of APSGN patients. These data suggest that NAPlr has a direct, nonimmunologic function as a plasmin receptor and may contribute to the pathogenesis of APSGN by maintaining plasmin activity., 1. Introduction Acute poststreptococcal glomerulonephritis (APSGN) develops after streptococcal infection with the obvious latent period of around 10 days. It is mostly accompanied by decrement in serum complement titer and [...]

A novel approach using the Monte Carlo method and the more realistic spin model of ferro and antiferromagnetic exchange coupling layers has been performed. The results obtained confirm and are comparable to experimental results and give numerical background to previous theories. The feature of our results is two type of oscillational decay of averaged antiferromagnetic spin directions every atomic plane in (111) and (100) crystalline orientation. Such a behavior suggests different exchange anisotropies and their thickness dependencies in the each crystalline orientation.