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1/29. alpha-Interferon therapy for HBV-related glomerulonephritis.

    We report a case of a patient with hepatitis b virus (HBV)-related membranous glomerulonephritis (MGN) who showed improvement after interferon-alpha (IFN-alpha) therapy. A 35-year-old man with nephrotic syndrome and HBV antigens received a 24-week course of IFN-alpha. At the end of therapy there was an elevation in the level of plasma aminotransferase and an increase in proteinuria, which were followed by antigen/antibody seroconversion. This "flare-up" before seroconversion suggests an increase in disease activity in the liver and kidney, demonstrating in vivo HBV involvement in MGN.
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2/29. Diffuse glomerular basement membrane lamellation in renal allografts from pediatric donors to adult recipients.

    The transplantation of kidneys from pediatric cadaveric donors into adult recipients is performed in many centers. However, some studies indicate that the outcome of such renal transplants may be inferior compared with that of adult donors, particularly if the donor is an infant. Morphologic studies of failed pediatric donor kidneys in adult recipients describe various degrees of segmental or global glomerular sclerosis. The authors have performed ultrastructural examinations on such transplants and have identified six cases with diffuse irregular lamellation of the glomerular basement membrane (GBM), a change that may develop as early as 10 weeks after transplantation. The age of all donors was < or =6 years; three were infants. The incidence of the lesion was 9% at our institution in renal transplant patients who received a graft from donors <10 years old. Diffuse GBM lamellation has not been found in renal transplants from adult donors. light microscopy showed various degrees of diffuse mesangial expansion, usually with segmental glomerular sclerosis. The patients had severe proteinuria. While recurrent focal segmental glomerular sclerosis (FSGS) has to be excluded, such diffuse GBM lamellation is generally not seen in recurrent FSGS cases. The pathogenesis of the lesion is most likely related to hyperperfusion injury of small pediatric donor kidneys grafted into adult recipients.
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3/29. Possible associations of rectal carcinoma with schistosoma japonicum infection and membranous nephropathy: a case report with a review.

    We report the first case of rectal carcinoma associated with S. japonicum and membranous nephropathy. A 57-year-old Japanese man noticed narrowing of his feces. He had lived in Yamanashi prefecture, an endemic area of S. japonicum. He had suffered from nephrotic syndrome for about 1 year. barium enema study showed a severe stricture in the upper rectum and biopsy specimens from the tumor demonstrated well differentiated adenocarcinoma and many ova of S. japonicum. Sonography of the liver showed a network pattern and a linear high echoic area. Low anterior resection with incisional biopsy of the liver and the right kidney was performed. Histopathological findings showed well differentiated adenocarcinoma and schistosomal ova. The total number of ova in the resected colon amounted to 15,133, consisting of 2243 inside and 12,890 outside the carcinoma. The nearer to the carcinoma the area was, the higher was the density of ova. The findings of light microscopy and electron microscopy of the biopsy specimen from the kidney were compatible with membranous nephropathy (stage II). This case suggests that schistosomal ova have some effect on carcinogenesis and nephrotic syndrome. In patients with nephrotic syndrome of unknown cause, especially in inhabitants of endemic areas of S. japonicum, gastrointestinal malignancy should be ruled out as an etiological factor. sigmoidoscopy would be useful for colorectal carcinoma surveillance in S. japonicum patients.
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4/29. Lymphatic tumor emboli of perirenal fat in patient with nephrotic syndrome receiving renal biopsy, ultimately revealed gastric adenocarcinoma with membranous glomerulonephritis.

    The association of malignancy with nephrotic syndrome and renal histopathologic abnormalities is well documented. Paraneoplastic proteinuria caused by membranous glomerulonephritis usually is made simultaneously with the diagnosis of a malignant tumor, or the two conditions are diagnosed within a year of each other. We reported a patient who presented with nephrotic syndrome initially. Incidentally, in kidney specimens, pathologic findings showed perirenal fatty tissue with malignancy tumor emboli in lymphatics. Thereafter, gastric adenocarcinoma was diagnosed by gastrointestinal panendoscopy with gastric biopsy under impression of malignancy associated with glomerulonephritis. Patient died of complications of malignancy-related disseminated intravascular coagulation without chemotherapy after confirming diagnosis was made three months later.
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5/29. Membranous glomerulonephritis associated with renal cell carcinoma: failure to detect a nephritogenic tumor antigen.

    A 57-year-old man with renal cell carcinoma associated with membranous glomerulonephropathy (MGN) developed a transient amelioration of the nephrotic syndrome after excision of the tumor. We tried to identify a nephritogenic tumor antigen using the immunoblotting technique in this patient with MGN, since previous studies examined the interaction between tumor antigens and IgG eluted from the kidney tissue using immunofluorescence or immunodiffusion techniques, and no studies have identified the specific tumor antigen with the immunoblotting method. In the present study, no significant immunoreactivity was noted between the IgG eluted from renal cortical tissues of the patient and renal cell carcinoma proteins. Further studies are necessary to establish the pathogenic mechanism of MGN associated with malignancy.
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6/29. nephrotic syndrome associated with agnogenic myeloid metaplasia.

    Extramedullary hematopoiesis being an important feature of agnogenic myeloid metaplasia (AMM), a chronic myeloproliferative disease of clonal origin, may affect the kidneys, but this condition is usually asymptomatic. Until now, there is only one reported case of nephrotic syndrome associated with AMM. We present a patient with AMM who had nephrotic syndrome and whose renal biopsy revealed membranous glomerulonephritis together with renal extramedullary hematopoiesis.
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7/29. Membranous glomerulonephritis, antiphospholipid syndrome, and persistent low C3 levels associated with meningococcal disease.

    A young male patient with a recent history of meningococcemia was referred to our hospital in his recovery period. He had signs suggesting deep venous thrombosis in the legs but no other abnormalities on physical examination at admission. Laboratory results showed proteinuria (3.1 g/day), prolonged activated partial thromboplastin time (56.3 s), low level of C3c (0.19 g/l), high titers of both IgM (27.04 MPLU/ml) and IgG (74.88 GPLU/ml) anticardiolipin antibodies and recanalized thrombotic changes in the deep veins of the lower extremities on venography. Histopathological diagnosis of the kidney disease was membranous glomerulonephritis. He was started on an angiotensin-converting enzyme inhibitor to reduce proteinuria and an oral anticoagulant to prevent thromboembolic events. Since no reduction in proteinuria was observed at the 10th month of therapy, the angiotensin-converting enzyme inhibitor was discontinued. On his last follow-up, approximately 1.5 years after meningococcemia, he had no complaints and no abnormal findings on physical examination. While both IgM and IgG anticardiolipin antibody titers returned to the normal range, he still had persistent proteinuria and hypocomplementemia.
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keywords = kidney disease, kidney
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8/29. Membranous glomerulonephritis associated with follicular B-cell lymphoma and subepithelial deposition of IgG1-kappa paraprotein.

    A case is described of B-cell lymphoma/chronic lymphocytic leukaemia associated with membranous glomerulonephritis in which the subepithelial deposits of immunoglobulin showed kappa light chain restriction by immunofluorescence. Surface IgG-kappa immunoglobulin was demonstrated on the malignant B cells, and a monoclonal protein of the same type was eluted from kidney. The mechanism of membranous glomerulonephritis in this type of lymphoid malignancy is clearly different from that in epithelial malignancies.
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9/29. Collapsing glomerulopathy coexisting with membranous glomerulonephritis in native kidney biopsies: a report of 3 hiv-negative patients.

    Collapsing glomerulopathy (CG), a variant of idiopathic focal segmental glomerulosclerosis (FSGS), can occur in both human immunodeficiency virus (hiv)-positive and hiv-negative patients. Idiopathic membranous glomerulonephritis (MGN) has been reported to coexist with FSGS, but rarely with CG. We report 3 hiv-negative patients (2 men, 1 woman) who developed nephrotic syndrome secondary to MGN complicated by CG, with relatively rapid disease progression despite aggressive therapy.
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10/29. Presence of circulating antibodies against brush border antigens (Fx1A) in a patient with membranous nephropathy and bilateral pyeloureteral stenosis. Comparison with idiopathic membranous nephropathy.

    In a patient with membranous nephropathy and bilateral pyeloureteral stenosis with hydronephrosis, we examined the possibility that an increase in the intratubular pressure could facilitate the passage of the Fx1A antigens to the circulation. Elevated serum anti-Fx1A antibodies were detected in this particular patient by ELISA on three occasions during the disease follow-up, even though he was in clinical remission. These antibodies reacted in vitro with the tubular brush border of a normal human kidney. The anti-Fx1A antibodies isolated from the patient's sera by affinity chromatography competed with the rabbit anti-Fx1A antisera binding to plates coated with human Fx1A antigen. In immunoblotting studies the isolated specific IgG antibodies from that patient reacted with a 180 kDa antigen of the human Fx1A and with less intensity with 75 kDa and 50-55 kDa polypeptides. In none of 12 patients with idiopathic membranous nephropathy could the circulating anti-Fx1A antibodies be demonstrated. On the whole, this particular case suggests that on some occasions increased intratubular pressure could cause the release of Fx1A antigens, facilitating an autologous immunocomplex nephritis. These antigens, by contrast, do not seem to play any role in most cases of membranous nephropathy in man.
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