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Membranoproliferative Glomerulonephritis (membranoproliferative + glomerulonephritis)
Selected AbstractsHepatitis C virus and lichen planusJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2004YUMIKO NAGAO Abstract Hepatitis C virus (HCV) is an important factor in the development of chronic liver disease and hepatocellular carcinoma. In recent years it has become known that HCV induces various extrahepatic manifestations including mixed cryoglobulinemia, membranoproliferative glomerulonephritis, Sjögren's syndrome, autoimmune thyroiditis, malignant lymphoma, porphyria cutanea tarda and lichen planus. Although the mechanisms of extrahepatic manifestations remain unclear, it is known that interferon (IFN) therapy and coadministration of IFN with ribavirin are effective in promoting the disappearance or alleviation of such extrahepatic lesions, which have tended to be overlooked. The present review focuses on lichen planus, one of the major extrahepatic manifestations. © 2004 Blackwell Publishing Asia Pty Ltd [source] Mesangial cell proliferation inhibitors for the treatment of proliferative glomerular diseaseMEDICINAL RESEARCH REVIEWS, Issue 1 2003Yasuhisa Kurogi Abstract Mesangial cells (MC) serve a number of functions in the renal glomerular capillary including structural support of the capillary tuft, modulation of glomerular hemodynamics, and a phagocytic function allowing removal of macromolecules and immune complexes. The proliferation of MC is a prominent feature of glomerular disease including IgA nephropathy, membranoproliferative glomerulonephritis, lupus nephritis, and diabetic nephropathy. In experimental animal models of nephritis, MC proliferation frequently precedes and is linked to the increase of extracellular matrix in the mesangium and glomerulosclerosis. Reduction of MC proliferation in glomerular disease models by treatment with heparin, low-protein diet, or antibodies to platelet-derived growth factor (PDGF), have been shown to reduce extracellular matrix expansion and glomerulosclerotic changes. Therefore, MC proliferation inhibitors may offer therapeutic opportunities for the treatment of proliferative glomerular disease. It is also known that the MC proliferation is inhibited by many kinds of pharmacological drugs, for example, angiotensin converting enzyme (ACE) inhibitors, leukotriene D4 (LTD4) antagonists, PDGF inhibitors, matrix metalloproteinases (MMP) inhibitors, 3-hydroxy-3 methyl glutaryl-coenzymeA (HMG-CoA) inhibitors, cyclin-dependent kinases (CDK) inhibitors, and others. This review summarizes the recently reported MC proliferation inhibitors with their pharmacological properties on the basis of their chemical structures. © 2002 Wiley Periodicals, Inc. Med Res Rev, 23, No. 1, 15,31, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/med.10028 [source] School urinalysis screening in KoreaNEPHROLOGY, Issue 2007BYOUNG-SOO CHO SUMMARY: Since 1998, by law, all school children in Korea must have an annual urinalysis. The first early morning urine specimen is examined by a simple dipstick method for the detection of proteinuria, haematuria and glucose. If a urine test is positive, a second test is performed by paediatric nephrologists. We analysed urinalysis data of school urinalysis screening. We also analysed the results of clinical data and the renal biopsy findings of patients referred to our medical centre due to abnormal urinalysis result. To date, about five million students have been screened since annual school urinalysis started in January 1998. Among them, isolated proteinuria was about 0.2%, occult blood was about 0.8%, and glucosuria was about 0.07% from January 1998 to December 2004. Among referred patients, renal biopsy was taken in 63.1% of isolated haematuria, 10.5% of isolated proteinuria and 69.9% of haematuria combined with proteinuria. Histopathological findings are IgA nephropathy in 43.8%, mesangial proliferative glomerulonephritis in 38.4%, Henoch,Schönlein nephritis in 2.7%, membranoproliferative glomerulonephritis in 1.6% and lupus nephritis in 0.5%. Alport disease showed 0.6% as a hereditary disease. In conclusion, the school urinalysis screening could detect chronic renal disease in its early stage. Early detection using school urinalysis screening and confirmatory diagnosis by renal biopsy seems to be helpful for assessment of prognosis and intervention of chronic renal disease progression. [source] Complement analysis in children with idiopathic membranoproliferative glomerulonephritis: A long-term follow-upPEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 3 2001Rainer Schwertz Fifty children with idiopathic membranoproliferative glomerulonephritis (MPGN), aged 2,14 years at apparent onset, were monitored for the presence of C3 nephritic factor (C3 NeF) and signs of complement activation in serum. In addition, C3 allotyping was performed in 32 patients. Observation time ranged from 2 to 20 (median 11) years. C3 NeF activity was detected at least once in 60% of the patients (in 11 of 26 with type I, in 15 of 17 with type II, and in four of seven with type III). C3 NeF-positive patients had significantly reduced levels of CH50 and C3 and elevated levels of C3dg/C3d. During follow-up, C3 levels were persistently normal in 62% of the patients with MPGN type I and in 43% with type III but in only 18% with type II. C3 allotype frequencies differed from those found in healthy controls with a significant shift to the C3F/C3FS variants in C3 NeF-positive patients. C3b(Bb)P as a marker for alternative pathway activation was not increased in C3 NeF-positive patients. Despite the presence of C3 NeF activity, C3 levels remained normal in six patients throughout the observation period. C3 NeF became undetectable in six patients, whereas seven developed C3 NeF activity during follow-up. There was no significant difference in renal survival probability in patients with or without C3 NeF activity. Neither C3 variants nor continous low C3 or low CH50 levels had any prognostic value for the clinical outcome. No factor H deficiency was detected. [source] Glomerular and tubular induction of the transcription factor c-Jun in human renal disease,THE JOURNAL OF PATHOLOGY, Issue 2 2007MH De Borst Abstract The transcription factor c-Jun regulates the expression of genes involved in proliferation and inflammation in many cell types but its role in human renal disease is largely unclear. In the current study we investigated whether c-Jun activation is associated with human renal disease and if c-Jun activation regulates pro-inflammatory and pro-fibrotic genes in renal cells. Activation of c-Jun was quantified by scoring renal expression of phosphorylated c-Jun (pc-Jun) in control human renal tissue and in biopsies from patients with various renal diseases (diabetic nephropathy, focal glomerulosclerosis, hypertension, IgA nephropathy, membranous glomerulopathy, minimal change disease, membranoproliferative glomerulonephritis, systemic lupus erythematosus, acute rejection, and Wegener's granulomatosis); this was correlated with parameters of renal damage. Furthermore, we studied the functional role of c-Jun activation in human tubular epithelial cells (HK-2) stimulated with TGF-,. Activated c-Jun was present in nuclei of glomerular and tubular cells in all human renal diseases, but only sporadically in controls. Across the diseases, the extent of pc-Jun expression correlated with the degree of focal glomerulosclerosis, interstitial fibrosis, cell proliferation, kidney injury molecule-1 (Kim-1) expression, macrophage accumulation, and impairment of renal function. In HK-2 cells, TGF-, induced c-Jun activation after 1 h (+40%, p < 0.001) and 24 h (+160%, p < 0.001). The specific c-Jun N-terminal kinase (JNK) inhibitor SP600125 abolished c-Jun phosphorylation at all time points and blunted TGF-,- or BSA-induced procollagen-1, 1 and MCP-1 gene expression in HK-2 cells. We conclude that in human renal disease, the transcription factor c-Jun is activated in glomerular and tubular cells. Activation of c-Jun may be involved in the regulation of inflammation and/or fibrosis in human renal disease. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Translational Mini-Review Series on Complement Factor H: Genetics and disease associations of human complement factor HCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2008S. Rodríguez De Córdoba Summary Factor H is an abundant plasma glycoprotein that plays a critical role in the regulation of the complement system in plasma and in the protection of host cells and tissues from damage by complement activation. Several recent studies have described the association of genetic variations of the complement factor H gene (CFH) with atypical haemolytic uraemic syndrome (aHUS), age-related macular degeneration (AMD) and membranoproliferative glomerulonephritis (MPGN). This review summarizes our current knowledge of CFH genetics and examines the CFH genotype,phenotype correlations that are helping to understand the molecular basis underlying these renal and ocular pathologies. [source] Recurrent nephrotic syndrome after living-related renal transplantation resistant to plasma exchange: report of two casesCLINICAL TRANSPLANTATION, Issue 2005Kohsuke Masutani Abstract:, We encountered two patients of recurrent nephrotic syndrome (NS) after renal transplantation that was resistant to plasma exchange (PEX). Case 1 was a 34-year-old man with a living-related renal transplant for type-I membranoproliferative glomerulonephritis (MPGN) related end-stage renal disease (ESRD). He developed overt proteinuria 7 months post-transplant and presented with NS 5 months later. Biopsy of the transplant kidney revealed recurrent type I MPGN, but no features of acute rejection (AR) or chronic allograft nephropathy (CAN). He was treated with cyclophosphamide (CP), oral prednisolone (40 mg/d), an anti-platelet agent, heparin sulfate, and PEX, but the nephrotic state persisted and renal function was deteriorated. He recommenced hemodialysis 3 yr and 9 months after renal transplant. Case 2 was a 47-year-old male who underwent living-related renal transplant for ESRD due to focal segmental glomerulosclerosis (FSGS). He presented with proteinuria shortly after renal transplantation. He also had frequent episodes of AR. Graft biopsy revealed recurrent FSGS. Treatment of pulse methylprednisolone and PEX was transiently effective, but NS relapsed shortly after PEX. Graft biopsy at our hospital showed features of CAN with moderate interstitial fibrosis and tubular atrophy, presence of intraglomerular foam cells but no segmental sclerosis. Treatment with 12 courses of low-density lipoprotein apheresis (LDL-A) reduced proteinuria from 9.6 to 2.0 g/d, and incomplete remission has been maintained for more than 1 yr after LDL-A with slowly progressive renal dysfunction. Despite recent therapeutic advances, including the use of immunosuppressants and PEX, treatment of recurrent disease remains difficult. The LDL-A might be useful in cases with recurrent FSGS resistant to PEX. [source] | ||||||||||