Cases reported "Glomerulonephritis, IGA"

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1/47. IgA nephropathy in cystic fibrosis.

    The kidney does not usually present specific lesions in cystic fibrosis (CF), although in recent years renal involvement has been reported, particularly amyloidosis and immune complex glomerulonephritis. IgA nephropathy is rare. We report four cases of IgA nephropathy out of five renal biopsies performed in the last three years in patients with CF and renal involvement and discuss the possibility of a relationship between IgA nephropathy and CF.
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2/47. A case of aortitis syndrome and IgA nephropathy: possible role of human leukocyte antigens in both diseases.

    A 51-year-old woman, who had both aortitis syndrome (takayasu arteritis) and IgA nephropathy, presented with hypertension, fever, a high erythrocyte sedimentation rate, high c-reactive protein and serum IgG levels, proteinuria, and renal dysfunction. Renal arteriography showed stenosis and poststenotic dilatation at the origin of the right renal artery, as well as tortuosity of the left renal artery branches and marked atrophy of the left kidney. Renal biopsy showed IgA nephropathy with deposits of IgA, C3, and fibrinogen in the glomeruli and arteriolosclerosis. The present patient had human leukocyte antigen (HLA)-B 52, which is reported to be related to the aortitis syndrome, as well as HLA-DR 4, which is possibly related to IgA nephropathy, suggesting that HLA status may be involved in the pathogenesis of both diseases.
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3/47. Post transplant CD8 gammadelta T-cell lymphoma associated with human herpes virus-6 infection.

    Gammadelta T-cell lymphoma is a rare T-cell lymphoproliferative disorder that has been reported in both immunocompetent and immunocompromised persons. This report describes a forty eight year old patient who developed gammadelta T-cell lymphoma four years after undergoing living-related kidney transplantation. The lymphoma expressed CD2, CD3, CD7, CD8 and CD56, and the gammadelta T-cell receptor and did not express CD5, CD4 and the alphabeta T-cell receptor. In addition, HHV-6 was cultured from the patient's bone marrow, marking the first time that this virus has been associated with gammadelta T-cell lymphoma. Since all patients with gammadelta T-cell lymphoma described to date have responded poorly to standard combination chemotherapies, the patient was treated with the purine analogue 2-chlorodeoxyadenosine. While he responded transiently to treatment, long term remission was not achieved indicating that additional therapeutic approches still need to be developed, for the management of this disorder.
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4/47. A case of IgA nephropathy after ABO-incompatible living kidney transplantation.

    A 39-yr-old Japanese man underwent living related kidney transplantation. Because the graft was ABO-incompatible, he was treated with double filtration plasmapheresis before transplantation and his immunosuppressive therapy was stronger than usual. However, immunoglobulin a nephropathy, accompanied by cellular crescents and necrotizing lesions, developed after 18 months. To our knowledge, the association of IgA nephropathy with ABO-incompatible kidney transplantation has not been reported previously.
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5/47. recurrence of IgA nephropathy 17 months after renal transplantation in the allograft transmitted thin basement membrane disease (TBMD) from donor.

    recurrence of IgA nephropathy (IgAN) following renal transplantation has been described in 40-50% of such patients and it usually has a good outcome. We present the case of a 20-yr-old woman with IgAN who developed end-stage renal failure in 1995. In November 1996, she received a kidney from a living-related donor and was treated with tacrolimus, azathioprine and steroids. Zero- and one-hour biopsies were performed, which revealed minor glomerular abnormalities in light microscopy, thin basement membrane disease (TBMD) in electron microscopy. Eight months later she developed microscopic hematuria and proteinuria; however, the graft function was normal. Renal biopsy revealed an IgAN that is thought to be due to recurrence of the original disease.
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6/47. Primary antiphospholipid antibody syndrome and mesangial IgA glomerulonephritis.

    The antiphospholipid antibody syndrome (APS) is characterized by recurrent thrombosis, fetal loss, multiorgan involvement, and the presence of lupus anticoagulant and/or anticardiolipin antibody. When not associated with systemic lupus erythematosus, other collagen diseases, or ingestion of medications, the condition is called primary APS. The kidney may be involved in the APS syndrome with acute nephritis and renal failure. The cases with renal biopsy studies have shown variable glomerular morphology, ranging from mild mesangial changes to a diffuse endocapillary proliferative glomerulonephritis. The most frequent lesion is thrombotic microangiopathy or features seen in the hemolytic uremic syndrome. Apart from fibrin thrombus deposition, only a few cases have shown focal and segmental deposits of IgG and/or IgM and/or C3. We describe a patient with primary APS who had thrombosis with lower limb amputation and acute renal failure. The renal biopsy specimen showed a focal proliferative glomerulonephritis with endothelial proliferation and damage, with diffuse heavy mesangial deposits of IgA and fibrinogen. This case with diabetes mellitus, but without diabetic nephropathy, represents the occurrence of primary APS and mesangial IgA nephropathy which potentiated the renal injury, leading to acute renal failure. The relationship to the Henoch-Schonlein syndrome is discussed.
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7/47. A case of rapid progressive glomerulonephritis with IgA deposits after renal transplantation.

    A 46-yr-old Japanese male who underwent a second cadaveric kidney transplantation on 31 October 1996 after suffering Type II diabetic mellitus for 25 yr was admitted to our institute on 23 January 1999, because of colicky abdominal pain and abdominal discomfort. Elevated levels of serum creatinine, severe proteinuria and microscopic haematuria were observed. The allograft biopsy specimen disclosed crescentic glomerulonephritis. Immunofluorescence showed granular deposits of mainly IgA and C3 along glomerular capillary walls and mesangial areas. Electron microscopy showed extensive subepithelial and mesangial electron dense deposits. Rapid and irreversible worsening of graft function led to resumption of haemodialysis on 31 May 1999. We speculated that this case was an atypical form of de novo Henoch-Schonlein purpura nephritis (HSPN) in transplanted kidney because of the histopathological findings of the allograft biopsy and clinical symptoms.
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8/47. Diffuse glomerular basement membrane lamellation in post-transplant IgA nephropathy.

    Diffuse glomerular basement membrane (GBM) lamellation, reminiscent of Alport's syndrome, has rarely, and exclusively, been reported in renal allografts from pediatric donors to adult recipients. We report on a similar lesion, identified in a 42-year-old male, who received a kidney from an unrelated 21-year-old living male donor. The disease of the recipient was unknown. Renal allograft biopsies were performed 3.5 and 4.8 years after the renal transplantation, due to massive proteinuria and serum creatinine elevation. The histological features of both biopsies were similar, but more advanced in the second biopsy. glomerular mesangium was widened and had an IgA deposit in the first biopsy. In addition to the presence of mesangial electron dense deposits, the GBM showed diffuse lamellation and splintering on the subepithelial side, but no definite deposits. In the second biopsy, IgA deposits were extended to the peripheral capillary walls, but electron microscopic examination was not available. Two months after the second biopsy, the patient returned for hemodialysis.
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9/47. Henoch-Schonlein IgA glomerulonephritis complicating myeloma kidneys: case report.

    Myeloma kidney is the principal pathological substrate of rapidly progressive renal failure in multiple myeloma. We report the unusual case of a 72-year-old male diagnosed with kappa Bence Jones myeloma with renal failure which needed dialysis. After treatment with vincristine, doxorubicin (Adriamycin), dexamethasone (VAD), and plasmapheresis, the renal function was recovered until serum creatinine level was <2 mg/dl. Six months later, the pathological counterpart of rapidly progressive renal failure was crescentic IgA proliferative glomerulonephritis as a manifestation of Henoch-Schonlein syndrome associated with sepsis caused by coagulase-negative staphylococci. This case suggests that mesangial IgA deposition should be considered within the spectrum of consequent glomerular lesion-associated chemotherapy occurring in multiple myeloma.
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10/47. Successful treatment of mucormycosis peritonitis with liposomal amphotericin b in a patient on long-term peritoneal dialysis.

    A 42-year-old man, with a history of immunoglobulin a nephropathy, underwent a living-related kidney transplant. Allograft function progressively deteriorated secondary to chronic rejection and recurrence of IgA nephropathy, and he returned to peritoneal dialysis after 5 years of the transplant. Fifteen months after the discontinuation of immunosuppressive therapy, Eschericia coli peritonitis developed, which was treated with ceftazidime intraperitoneally; he received fluconazole as prophylactic antifungal therapy during this period. After completing his course of treatment, abdominal pain occurred with an increased peritoneal fluid white blood cell count. Peritoneal fluid cultures were negative. He received broad-spectrum antibiotics and fluconazole with no appreciable response. After removal of the Tenckoff catheter, peritoneal fluid cultures grew a zygomycete. The patient was treated with liposomal amphotericin b (AmBisome) intravenously for 6 weeks. He had episodes of recurrent intraabdominal abscesses requiring surgical drainage and antibiotics. A second course of liposomal amphotericin b was administered for histopathologic evidence of filamentous fungal recurrence. After 5 months, the patient remains well without any evidence of infection.
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