Cases reported "Glomerulonephritis"

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1/187. IgA antiglomerular basement membrane disease associated with bronchial carcinoma and monoclonal gammopathy.

    Antiglomerular basement membrane (anti-GBM) disease is characterized by a linear deposition of immunoglobulins along the glomerular basement membrane. A 67-year-old man with a recently discovered monoclonal gammopathy of unknown significance (MGUS) presented with microscopic hematuria, nephrotic-range proteinuria, and rapidly deteriorating renal function after a pneumonia. Renal histology showed a crescentic glomerulonephritis; immunohistology showed intense linear staining of the GBM with immunoglobulin a (IgA) and moderate linear staining with kappa and lambda light chains. Screening for systemic disease, including diabetes mellitus, lupus erythematodes disseminatus, cryoglobulinemia, was negative. Serological tests for detection of anti-GBM antibodies were positive for IgA class and negative for IgG. Further examination indicated a bronchial carcinoma T2N2M0. This clinical report adds new information to the spectrum of anti-GBM disease and suggests that neoplasia may be associated with unusual exposure of and/or immune response to epitopes in the GBM.
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2/187. Antiglomerular basement membrane antibody-mediated glomerulonephritis after intranasal cocaine use.

    We report a case of rapidly progressive glomerulonephritis due to antiglomerular basement membrane (anti-GBM) antibodies that progressed to end-stage renal disease in a 35-year-old man who used intranasal cocaine on an occasional basis. In contrast to many prior reports of acute renal failure occurring with cocaine-associated rhabdomyolysis, this patient did not have any evidence of acute muscle damage and myoglobin release. Circulating anti-GBM antibodies and renal biopsy with linear IgG and C3 deposits confirmed the diagnosis of anti-GBM disease. The possibility of anti-GBM must be considered in the differential diagnosis of acute renal failure in cocaine addicts. This unusual combination raises complex questions regarding the pathogenesis of this type of renal injury.
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3/187. Sequential development of anti-GBM nephritis and ANCA-associated Pauci-immune glomerulonephritis.

    The medical history is presented of a 23-year-old man experiencing three episodes of pulmonary-renal syndrome. On the first occasion, a diagnosis of anti-glomerular basement membrane (GBM) disease (with linear deposition of immunoglobulin g [IgG] along the GBM) was made, whereas anti-neutrophil cytoplasmic autoantibodies were also present in serum. On the third occasion, 5 years later, p-ANCA-associated vasculitis (with pauci-immune crescentic glomerulonephritis) was diagnosed, whereas anti-GBM antibodies were absent. The current literature on ANCA-positive anti-GBM disease is briefly reviewed. A substantial proportion (20% to 30%) of patients with histologically and serologically proven anti-GBM nephritis display the presence of ANCA as well. In this group of patients with dual antibodies, clinical and histological findings suggest that ANCA are not merely epiphenomena, but are of pathogenetic importance and might be responsible for an initial vasculitic insult to the kidney with resultant secondary anti-GBM nephritis. The clinical course in our patient lends further support to this concept. Histological demonstration of anti-GBM nephritis followed by ANCA-associated pauci-immune glomerulonephritis in a single patient has not been reported before.
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4/187. Myeloperoxidase antineutrophil cytoplasmic antibody-positive necrotizing crescentic glomerulonephritis and membranous glomerulonephropathy.

    In September 1997, a 68-year-old woman was found to have proteinuria and renal dysfunction. In December 1997, renal biopsy revealed necrotizing crescentic glomerulonephritis and membranous glomerulonephropathy. We diagnosed myeloperoxidase antineutrophil cytoplasmic antibody-positive necrotizing crescentic glomerulonephritis and membranous glomerulonephropathy because of the presence of necrotizing cellular crescents and spike lesions in the subepithelial region of the glomerular basement membrane. After steroid therapy, the antibody level and the incidence of cellular crescents showed a decrease. This is a rare case of myeloperoxidase antineutrophil cytoplasmic antibody-positive necrotizing crescentic glomerulonephritis associated with membranous glomerulonephropathy.
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5/187. Thin basement membrane disease with heavy proteinuria or nephrotic syndrome at presentation.

    Thin basement membrane disease (TBMD) is a condition originally defined as diffuse thinning of the glomerular basement membrane (GBM) associated with hematuria in all patients. Although proteinuria has been described in up to 60% of patients with TBMD, it is almost always mild, with a 24-hour excretion mostly of less than 500 mg. We describe eight patients (four men and four women between 32 and 66 years of age) with TBMD who presented with heavy proteinuria or nephrotic syndrome. Among the seven cases with family history, hematuria was noted in five. All patients had a long history of microscopic hematuria, with episodic gross hematuria in two. Renal biopsies showed diffuse thinning of the GBM in each patient (mean between 185.3 x 29.8 nm and 232.6 x 34.5 nm versus control between 325 x 35 nm and 350 x 15 nm). Three cases showed thinning of GBM only (group I); the remaining five cases showed thinning of GBM associated with focal segmental glomerulosclerosis. All three patients of group I presented with nephrotic syndrome and normal renal function. Treatment with steroids resulted in remission of nephrotic syndrome in two, whereas nephrotic syndrome persisted in the untreated patient. Among the five patients in group II, nephrotic syndrome and normal renal function at presentation were noted in two, whereas the other three had heavy proteinuria (2.2, 2. 5, and 2.6 g/d, respectively) associated with mildly decreased renal function (serum creatinine 1.8, 1.3, and 1.5 mg/dL, respectively). At last follow-up, although the renal function was stable in all five, only the three who received steroid treatment had remission or marked improvement of proteinuria. hematuria, however, persisted in all eight patients of both groups. Whether specific gene mutations are translated into structural changes responsible for both excessive GBM thinning and increased transcapillary permeability remains to be elucidated. Alternatively, the heavy proteinuria/nephrotic syndrome may not be related to TBMD, but rather is the manifestation of associated glomerular diseases. Follow-up, including a response to steroids, supports the latter hypothesis.
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6/187. Spontaneous improvement in a case of C1q nephropathy.

    A 17-year-old girl showed mild proteinuria accompanied by hematuria and mild hypocomplementemia. A light microscopic study of the first renal biopsy specimen showed diffuse mild to moderate mesangial proliferation and thickening of the glomerular basement membrane (GBM). An immunofluorescence study showed dominant positive staining (3 ) of IgG and C1q in the glomerular mesangium and capillary loop. Staining for C3 and fibrinogen was weak or 1 . Staining for IgA and IgM was negative. Electron-dense deposits were present in the mesangial area and also in the subepithelial, subendothelial, and intramembranous space. Urinary findings improved after dipyridamole treatment. The second renal biopsy, which was performed 5 years later, showed histological improvements, and various pictures of washing-out of deposits were also noted in an electron microscopic study. However, dominant positive staining for IgG and C1q was persistent in an immunofluorescence study. The glomerulopathy of this case belongs in the criteria of neither membranoproliferative glomerulonephritis nor lupus nephritis but could be designated as C1q nephropathy. This is the first report of a histological improvement in C1q nephropathy.
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7/187. Membranoproliferative glomerulonephritis in childhood cirrhosis associated with alpha1-antitrypsin deficiency.

    Three alpha1-antitrypsin (alpha1AT) deficient, protease inhibitor type ZZ children who died from cirrhosis and its complications had membranoproliferative glomerulonephritis at postmortem examination. During life, all three had clinical and laboratory evidence of renal disease which became apparent when hepatic decompensation developed. Immunofluorescence studies and electron microscopy performed in one patient revealed subendothelial deposits of alpha1AT, complement, and immune globulins along the glomerular basement membrane. The pathogenesis of these renal lesions is speculative. Glomerular lesions were not observed in kidney sections of 16 children who died from cirrhosis but who were not alpha1AT-deficient. The present study suggests that renal involvement may be yet another manifestation of disease associated with alpha1AT deficiency.
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8/187. Immunotactoid glomerulopathy--an unusual deposition disease: report of the first Malaysian case.

    A 31-year-old Malay female presented with nephrotic syndrome without renal impairment. Renal biopsy features were in keeping with immunotactoid glomerulopathy (ITG). Non-Congophilic deposits were seen causing thickening of the glomerular capillary basement membrane with segmental accentuation, and widening of the mesangium. Immunofluorescence examination showed moderate amounts of IgG and C3 in the glomerular capillary walls with some in the mesangium. Ultrastructurally, 20-nm thick fibrils with microtubular organisation were present predominantly in the subendothelial region with similar fibrils in the mesangium. Although immunotactoid glomerulopathy and fibrillary glomerulonephritis (FG) have been recognised as entities with extracellular fibrillary material in the kidney, to date much remains to be clarified regarding these 2 conditions. While the renal biopsy findings in this patient are consistent with ITG, her clinical presentation is unlike that of usual ITG in that she is of a much younger age and has no associated haemopoietic disorder. Response to initial treatment of 8 weeks of prednisolone therapy was poor.
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9/187. IgA antibasement membrane nephritis with pulmonary hemorrhage.

    Goodpasture's syndrome has characteristically been described as being mediated by IgG antibodies. We have recently seen a 55-year-old man who developed renal failure and hemoptysis; a renal biopsy showed linear deposits of IgA and C3 involving glomerular and tubular basement membrane. serologic tests for detecting (IgG) antiglomerular basement membrane antibodies were negative. Elution studies of kidney and lung showed the presence of an IgA antibasement membrane antibody only. The patient's serum contained IgA, but not IgG, antibodies reactive with glomerular and tubular basement membrane of normal human kidney and alveolar basement membrane of normal human lung. Attempts to transfer disease with the patient's IgA antibody to a monkey and to Lewis and Brown-norway rats were unsuccessful. immunoglobulin a antibasement membrane antibody must be considered in the design of immunoserologic procedures for the diagnosis of Goodpasture's syndrome.
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10/187. A case of fibrillary glomerulonephritis with linear immunoglobulin g staining of the glomerular capillary walls.

    We report a case of crescentic glomerulonephritis that presented with extensive crescent formation and fibrinoid necrosis in the glomeruli. Immunofluorescence staining was strongly positive for linear and pseudolinear staining of the capillary walls for immunoglobulin g (IgG) in the absence of significant mesangial staining. Histologic examination and immunofluorescence staining suggested a diagnosis of anti-glomerular basement membrane disease. However, electron microscopy showed the presence of numerous fibrillary deposits in the subepithelial areas of the glomerular capillary walls, supporting the diagnosis of fibrillary glomerulonephritis. Test results for circulating anti-glomerular basement membrane antibodies were negative. We report this interesting case to illustrate the point that fibrillary glomerulonephritis should be considered in the differential diagnosis of crescentic glomerulonephritis with linear and pseudolinear IgG deposits within the capillary walls. In such cases, electron microscopy is critical in differentiating the cause of crescentic glomerulonephritis.
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