Membranous Nephropathy with Crescents

Basford, Amanda Walton; Lewis, Julia B.; Dwyer, Jamie P.; Fogo, Agnes B.

doi:10.1681/asn.2010090923

Cited by 56 publications

(53 citation statements)

References 30 publications

(18 reference statements)

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“…The first mechanism is associated with anti-GBM antibodies. The coexistence of MN and anti-GBM GN was first reported by Klassen et al [2], and, since then, at least 28 cases have been described [3]. The second mechanism occurs in the absence of anti-GBM antibodies, and most cases are associated with ANCA.…”

Section: Discussionmentioning

confidence: 92%

Combined membranous nephropathy and crescentic glomerulonephritis with concurrent anti-glomerular basement membrane antibody and myeloperoxidase-specific anti-neutrophil cytoplasmic antibody

Iwafuchi¹,

Morita

Oyama³

et al. 2013

CEN Case Rep

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We report a case of a 71-year-old man with rapidly progressive nephritic syndrome and dual positivity for anti-glomerular basement membrane antibody and myeloperoxidase-specific anti-neutrophil cytoplasmic antibody. Renal biopsy revealed crescentic, mainly cellular, glomerulonephritis with granulomatous lesions, and advanced membranous changes. Membranous nephropathy had apparently existed for an extended period before the development of crescentic glomerulonephritis. In some studies reporting the simultaneous occurrence of both diseases, membranous nephropathy might be followed by crescentic glomerulonephritis, presumably from a histological point of view. Although we cannot prove a causal relationship between the two diseases, we caution that precise observations, especially histological, are necessary in similar cases.

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Section: Discussionmentioning

confidence: 92%

Combined membranous nephropathy and crescentic glomerulonephritis with concurrent anti-glomerular basement membrane antibody and myeloperoxidase-specific anti-neutrophil cytoplasmic antibody

Iwafuchi¹,

Morita

Oyama³

et al. 2013

CEN Case Rep

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“…7 Several cases of membranous nephropathy or ANCA vasculitis associated with additional anti-GBM antibody formation and disease have been reported. 8,9 ANCA antibodies may occasionally be produced before anti-GBM antibody formation and clinical disease. 10 HIV infection presents an additional level of complexity in anti-GBM disease.…”

Section: Discussionmentioning

confidence: 99%

AKI in an HIV Patient

Hartle

Carlo

Dwyer

et al. 2013

Journal of the American Society of Nephrology

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The renal manifestations of patients infected with HIV are diverse. Patients may have podocytopathies ranging from a minimal-change-type lesions to FSGS or collapsing glomerulopathy. Furthermore, such patients produce a variety of autoantibodies without clinical signs of the disease. Antiretroviral drugs also cause renal injury, including crystals and tubular injury, acute interstitial nephritis, or mitochondrial toxicity. In these circumstances, it is essential to perform a renal biopsy for diagnosis and to guide treatment. Here we describe a patient with HIV who presented with AKI and hematuria without concomitant systemic manifestations. Renal biopsy elucidated the cause of acute deterioration of kidney function.

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“…mPSL methylprednisolone, PSL prednisolone, UP/Cr spot protein-to-creatinine ratio, Cr serum creatinine, Alb serum albumin, GBM anti-GBM antibody CEN Case Rep (2013) 2:239-247 243 [28]. There have been several reviews of the literature and it has been observed that the chronologic relationship between MN and anti-GBM disease fell into three patterns: (1) MN followed by anti-GBM disease, (2) primary anti-GBM disease followed by granular subepithelial deposits, and (3) simultaneous detection of both lesions [19,24,26,29,30]. Anti-GBM disease is a rare form of autoimmune disorder with significant morbidity and mortality, and is characterized by crescentic glomerulonephritis, often accompanied by pulmonary hemorrhage and the presence of circulating and deposited anti-GBM antibodies [46].…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, in a few patients with primary anti-GBM disease followed by granular subepithelial deposits, immunologic mechanisms involved in the pathogenesis of anti-GBM disease may directly or indirectly lead to the genesis of membranous-type deposits. It has been proposed in analogy to the model of Heymann nephritis that membranoustype deposits may subsequently arise from in situ immune complex formation in the setting of anti-GBM disease in association with increased antigen synthesis by injured podocytes, facilitated by the capping and shedding of antigen-antibody complexes into the subepithelial space [24,27,29,30,49]. Also, anti-GBM antibodies might alter the permeability of GBM, allowing circulating immune complexes to access otherwise inaccessible parts of the GBM [12][13][14]28].…”

Section: Discussionmentioning

confidence: 99%

A case of anti-GBM glomerulonephritis superimposed on HBV-associated membranous nephropathy

et al. 2013

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In September 2010, a 75-year-old hepatitis B virus (HBV)-positive man was admitted to our hospital because of fever, persistent cough, general fatigue, and leg edema. The patient was a hepatitis B surface antigen carrier with detectable HBV DNA level. On admission, laboratory examination revealed severe inflammatory signs, decreased serum albumin, and renal insufficiency with proteinuria. The patient had rapidly progressive renal insufficiency without pulmonary involvement over the few days after admission. Renal biopsy showed membranous nephropathy (MN) with crescent formation. Further serological study revealed a high titer of anti-glomerular basement membrane (GBM) antibody, suggestive of anti-GBM glomerulonephritis superimposed on HBV-associated MN. For both preventing HBV reactivation during immunosuppressive therapy and treating HBV-associated MN, the administration of entecavir was immediately initiated, and then treatment with plasma exchange (PE) and intravenous methylprednisolone administration was performed. Both HBV DNA level and an anti-GBM titer became undetectable, and clinical remission of MN was subsequently achieved. This was a rare case of an elderly patient with anti-GBM glomerulonephritis superimposed on HBVassociated MN, who was successfully treated with PE, corticosteroid, and entecavir combination therapy.

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Membranous Nephropathy with Crescents

Cited by 56 publications

References 30 publications

Combined membranous nephropathy and crescentic glomerulonephritis with concurrent anti-glomerular basement membrane antibody and myeloperoxidase-specific anti-neutrophil cytoplasmic antibody

Combined membranous nephropathy and crescentic glomerulonephritis with concurrent anti-glomerular basement membrane antibody and myeloperoxidase-specific anti-neutrophil cytoplasmic antibody

AKI in an HIV Patient

A case of anti-GBM glomerulonephritis superimposed on HBV-associated membranous nephropathy

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