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1/6. Focal segmental glomerulosclerosis and hepatitis c virus: a case report.

    Focal segmental glomerulosclerosis (FSGS) is a renal disease characterized by sclerotic segmentary lesions, involving a few glomeruli. Male-female ratio is >1 and, in the majority of cases, the patients are aged between 25 to 35 years. The clinical picture is similar to a nephrotic syndrome with non-selective proteinuria poorly sensitive to steroids and often associated with microhematuria. The etiology is still unknown, even in a prevalence in drug addicts, patients with AIDS and subjects with recurrent urological infections with vesico-ureteral reflux was observed. Recent reports showed that chronic infection hepatitis c Virus (HCV)-related may be associate with or responsible for onset of some syndrome involving the kidney but not the liver. We report the case of a young woman with HCV-Ab positive chronic hepatitis that, during the disease, showed clinical findings of renal involvement, histologically related to a FSGS. We administered to her alpha-IFN at doses of 3 Mega Units thrice-a-week for six months. Serum HCV-rna, proteinuria and hematuria disappeared simultaneously after the treatment. We underline that the lack of finding of HCV antigens or HCV-rna in glomerular lesions (as occurred in our patient) does not rule out the virus role in pathogenesis of immunological nephritis. The recovery of our patient as well as the disappearance of proteinuria and hematuria during IFNalpha treatment may be further evidence that FSGS and chronic hepatitis HCV-related are not associated by chance. Further observations and perfectioning of diagnostic techniques are required to clarify the pathogenetic relationship between HCV and renal immunological syndromes.
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2/6. Focal-segmental glomerulosclerosis associated with herpes simplex viral encephalitis.

    A 5-month-old boy presented nephrotic syndrome associated with severe viral encephalitis. From his various body fluids herpes simplex virus (HSV) type 1 and anti-HSV antibodies could be isolated. Renal biopsy showed focal-segmental glomerulosclerosis and cytomegaly within the mesangial region in a single glomerulus. Immunohistology demonstrated mesangial and segmental depositions of IgM and C3. HSV antigen could be detected in two of the glomeruli. Osmiophilic mesangial deposits, segmental sclerosis and foot process fusion of podocytes could be seen by electron microscopy. In the nucleoplasm of a mesangial cell of a single glomerulus typical viral particles were observed. To the best of the author's knowledge this is the first reported case in the literature on human herpes glomerulopathy confirmed by histological examination.
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3/6. IgA nephropathy associated with disseminated tuberculosis.

    A 59-year-old man had disseminated tuberculosis and microscopic hematuria, red cell casts, and normal renal function. Renal biopsy revealed focal mesangial proliferation with exclusively IgA deposits, diagnostic of IgA nephropathy. After institution of antituberculous therapy, the urinary abnormalities resolved. There is evidence to suggest that tuberculosis, in addition to other conditions associated with mucosal exposure to antigens producing an IgA immune response, can result in IgA nephropathy. This glomerulopathy is reported as a potential renal complication of concurrent mycobacterial infection.
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4/6. recurrence of de novo graft membranous glomerulonephritis.

    Graft membranous nephropathy (MN) appears mainly de novo or, less frequently, develops in patients whose original disease was MN. The rarity of the latter occurrence contrasts with the frequency of MN as the original disease: the existence of renal recurrence may thus be questioned. We report a patient with terminal renal failure due to focal glomerulosclerosis; typical MN developed de novo in the first and recurred in the third graft. This observation establishes that recurrence of MN is a real phenomenon and demonstrates that the factor(s) determining recurrence may appear only after transplantation. Neither HBs nor antilymphocyte serum antigens were found along the basement membrane. The late onset of proteinuria after the third demonstrates that the delayed appearance of clinical signs of glomerular disease does not rule out the occurrence of MN.
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5/6. A case of nephrotic syndrome associated with hepatic glomerulosclerosis and diabetic nephropathy.

    We report here an adult case of nephrotic syndrome associated with hepatic glomerulosclerosis with the hepatitis c virus (HCV) antigen and diabetic nephropathy. To clarify the etiology of the nephrotic syndrome, we performed a renal biopsy and obtained the histological findings of hepatic glomerulosclerosis, glomerular mesangial cell proliferation and mesangial expansion. Electron dense deposits and deposits of IgA and C3 were also noted in the glomerular mesangial areas. Histological findings of diabetic nephropathy included thickening of the glomerular basement membrane and aneurysmal change of glomerular capillary walls in light microscopy. In immunofluorescence, linear staining of IgG was observed in the glomerular capillary walls, Bowman's capsules and tubular basement membranes. HCV was also detected focally in the glomerular capillary walls by immunofluorescence. association of these two diseases has not been reported in any of the previous manuscripts that we reviewed. Thus, this patient seems to be a case of very rare association of the two diseases.
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6/6. hepatitis c--associated glomerular disease in liver transplant recipients.

    hepatitis c virus (HCV) infection may be associated with extrahepatic illness including renal disease. We investigated the clinical and virological characteristics of three patients who developed a mesangial proliferative and sclerosing glomerulopathy alone or in association with membranoproliferative glomerulonephritis after liver transplantation for end-stage liver disease secondary to HCV infection. Using polymerase chain reaction technology and the IgM RIBA assay, viral load, genotype and IgM antibody response to HCV in the setting of glomerulonephritis was evaluated. Within 1 year of transplantation, the patients showed decreased renal function, proteinuria and recurrent hepatitis c liver disease. Likewise, HCV viral load increased following transplantation, whereas the viral genotypes remained unchanged. Although the first patient presented with classic type II cryoglobulinemia in association with glomerulonephritis, the second patient developed an IgM directed specifically against the hepatitis c core antigen. The third patient developed a low-titered IgM directed against the hepatitis c core antigen with rheumatoid factor activity but without cryoglobulinemia. All of the patients show IgM in glomerular capillary walls by biopsy. One patient has shown a clinical response to interferon (IFN) alfa-2b therapy without evidence of hepatic allograft rejection. The second and third patients have not responded to IFN or developed hepatic rejection. This study suggests that HCV-associated glomerulonephritis may complicate liver transplantation in conjunction with the production of increased amounts of IgM of variable specificity. The posttransplant setting may provide a unique situation in which to investigate the specific requirements for the onset of renal disease.
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