nephritis/protease

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Effect of FUT-175, a new synthetic protease inhibitor, on the development of lupus nephritis in (NZB x NZW) F1 mice.

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FUT-175 (6-amidino-2-naphthyl p-guanidinobenzoate dimethanesulphonate), a new synthetic protease inhibitor, was administrated to (NZB x NZB) F1 mice in order to examine its influence on the development of autoimmune diseases. A dose (400 mg/kg of body weight) of FUT-175 has both prophylactic and

Acute interstitial nephritis associated with atazanavir, a new protease inhibitor.

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Atazanavir is a new human immunodeficiency virus 1 protease inhibitor that has a favorable side-effect profile and is available in once-daily dosing. We report the case of a young man with human immunodeficiency virus infection who developed acute renal failure after therapy with this drug. Renal

Urine proteome scans uncover total urinary protease, prostaglandin D synthase, serum amyloid P, and superoxide dismutase as potential markers of lupus nephritis.

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To identify potential biomarkers in immune-mediated nephritis, urine from mice subjected to an augmented passive model of anti-glomerular basement membrane (GBM)-induced experimental nephritis was resolved using two-dimensional gels. The urinary proteome in these diseased mice was comprised of at

Pharmacological inhibition of protease-activated receptor-2 reduces crescent formation in rat nephrotoxic serum nephritis.

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Glomerular crescent formation is a hallmark of rapidly progressive forms of glomerulonephritis. Thrombosis and macrophage infiltration are features of crescent formation in human and experimental kidney disease. Protease-activated receptor-2 (PAR-2) is a G-protein coupled receptor that links

Antiphospholipid antibody profiles in lupus nephritis with glomerular microthrombosis: a prospective study of 124 cases.

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BACKGROUND Glomerular microthrombosis (GMT) is a common vascular change in patients with lupus nephritis (LN). The mechanism underlying GMT is largely unknown. Although several studies have reported the association of antiphospholipid antibodies (aPL) with GMT, the relation between GMT and aPL

CR1 stump peptide and terminal complement complexes are found in the glomeruli of lupus nephritis patients.

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The number of CR1 on podocytes is reduced in nephropathies with severe glomerular damage, especially in the diffuse proliferative glomerulonephritis (DPGN) of systemic lupus erythematosus (SLE). Reduction of CR1 number on erythrocytes is due to proteolysis of CR1 by macrophage proteases activated by

Acute interstitial nephritis of HIV-positive patients under atazanavir and tenofovir therapy in a retrospective analysis of kidney biopsies.

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We performed a retrospective analysis on kidney biopsies of 30 human immunodeficiency virus (HIV)-positive patients. Twenty-two of them received highly active antiretroviral therapy (HAART). Tenofovir containing HAART together with atazanavir, a new protease inhibitor, was administered to three

Proteolytic enzyme treatment reduces glomerular immune deposits and proteinuria in passive Heymann nephritis.

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We investigated the effect of proteolytic enzyme treatment on the course of passive Heymann nephritis (PHN). PHN was induced by intravenous injection of Heymann antibody into Sprague Dawley rats. Protease-treated rats received intraperitoneal chymopapain and subtilisin. In rats given

Epitope specificity of anti-gp330 autoantibodies determines the development of proteinuria in active Heymann nephritis.

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In active Heymann nephritis, an experimental autoimmune disease in the rat, gp330 is regarded as the main antigenic target. Immunization with detergent-solubilized renal tubular epithelium (RTE-DOC) has been shown to be less nephritogenic than immunization with crude RTE. In this study immunization

Therapeutic Potential of Thrombomodulin in Renal Fibrosis of Nephrotoxic Serum Nephritis in Wistar-Kyoto Rats.

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Recombinant human soluble thrombomodulin (rhTM) was approved in 2008 and has been used for treatment of disseminated intravascular coagulation in Japan. The antifibrotic effects of rhTM in acute exacerbation of idiopathic pulmonary fibrosis are well established, but the therapeutic

Cloning of rodent megsin revealed its up-regulation in mesangioproliferative nephritis.

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BACKGROUND We recently cloned a new human mesangium-predominant gene, megsin. Megsin is a novel member of the serine protease inhibitor (serpin) superfamily. To elucidate functional roles of this gene, we cloned megsin in rodents and investigated its role in a rat nephritis model. METHODS Megsin

Avian nephritis virus (ANV) as a new member of the family Astroviridae and construction of infectious ANV cDNA.

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The complete RNA genome of the avian nephritis virus (ANV) associated with acute nephritis in chickens has been molecularly cloned and sequenced. Excluding the poly(A) tail, the genome comprises 6,927 nucleotides and contains three sequential open reading frames (ORFs). The first ORF (ORF 1a)

Protease inhibitor therapy in children with perinatally acquired HIV infection.

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OBJECTIVE To review the short-term response and safety of protease inhibitor therapy in HIV-infected children. METHODS Retrospective chart review of open-label protease inhibitor-containing combination therapy. METHODS Two urban pediatric HIV centers. METHODS Twenty-eight HIV-infected children were

[The association of von Willebrand factor and von Willebrand factor-cleaving protease in systemic lupus erythematosus].

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OBJECTIVE To evaluate the clinical significance of plasma von Willebrand factor (vWF) and von Willebrand factor-cleaving protease (vWF-CP) activity in systemic lupus erythematosus (SLE). METHODS vWF antigen (vWF:Ag) and vWF-CP activity were respectively evaluated by using ELISA and residual-collagen

Significance of plasma von Willebrand factor level and von Willebrand factor-cleaving protease activity in patients with chronic renal diseases.

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BACKGROUND von Willebrand factor (vWF) mediates the initial capture of platelets to vascular subendothelium and is essential for platelet aggregation under high fluid shear stress as in arterial stenosis. On release from endothelial cells, vWF is rapidly cleaved by ADAMTS13/vWF-cleaving protease

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Herbal & Natural Medicine

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