The Clinical Spectrum of Necrotizing Glomerulonephritis

Tj, Furlong; Ls, Ibels; Rp, Eckstein

doi:10.1097/00005792-198705000-00003

Cited by 29 publications

(12 citation statements)

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“…In the absence of drug addiction, allergy history, eosinophilia or disorders like SLE or atrial mixoma, the finding of multiple intraparenchymal saccular aneu rysms demonstrable by renal angiography is virtually diagnostic of classic PAN [15,16]. In our patient, the glomerular lesions consisted in necrotizing glomerulon ephritis, an uncommon histological entity responsible for only 5% of all glomérulonéphrites according to a recent report [17], but the most frequent histological finding in patients with classic PAN. Two cases have been recently reported of renal necrotizing vasculitis with massive glomerular crescentic epithelial proliferation, pulmon ary hemorrhage and death from severe renal failure in 18 months [14].…”

Section: Discussionmentioning

confidence: 53%

Polyarteritis Nodosa and Necrotizing Glomerulonephritis Associated with Long-Standing Silicosis

Arnalich

Lahoz²,

Picazo³

et al. 1989

Nephron

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A 55-year-old white male, with silicosis diagnosed 10 years earlier, presented massive proteinuria with microscopic hematuria, moderate renal failure and distal polyneuropathy. Bilateral renal angiography showed multiple intraparenchymal saccular aneurysms. Renal biopsy disclosed a focal segmental necrotizing glomerulonephritis and arteriolitis. After combined corticosteroid and immunosuppressive treatment, renal function improved and remained stable 6 months later.

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Section: Discussionmentioning

confidence: 53%

Polyarteritis Nodosa and Necrotizing Glomerulonephritis Associated with Long-Standing Silicosis

Arnalich

Lahoz²,

Picazo³

et al. 1989

Nephron

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“…Others have observed correlation of glomerular and interstitial macrophages with serum creatinine at biopsy (19). The extent of glomerular necrosis and crescent formation correlated with the serum creatinine at biopsy in a separate study (33).…”

Section: Discussionmentioning

confidence: 80%

M2 Macrophage Infiltrates in the Early Stages of ANCA-Associated Pauci-Immune Necrotizing GN

Zhao¹,

David

Hyjek

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objectives This study examined kidney biopsies with focal segmental glomerular fibrinoid necrosis to identify early features of pauci-immune necrotizing GN and the primary effector cells mediating initial capillary injury.Design, setting, participants, & measurements Seventeen consecutive kidney biopsies with focal pauci-immune necrotizing GN, obtained over a 6-year period (2007)(2008)(2009)(2010)(2011)(2012), were studied. Neutrophils and CD68 + , CD163 + , CD3 + , CD56 + , and CD20 + cells were scored in paraffin sections counterstained with periodic acid-Schiff. Electron microscopy was performed in 15 of 17 biopsies and additional examples of pauci-immune necrotizing GN (n=25). Biopsies with thin basement membrane nephropathy (n=5) served as immunohistologic normal controls.Results Biopsies with pauci-immune necrotizing GN had a mean of 10 (range=3-25) normal-appearing glomeruli, a mean of 2 (range=1-5) glomeruli with segmental fibrinoid necrosis, and a mean of 2 (range=1-11) glomeruli with cellular crescents. CD68 + and CD163 + macrophages predominated at sites of fibrinoid necrosis in pauci-immune necrotizing GN, exceeding the quantity of neutrophils and T cells (mean scores The quantity of other glomerular infiltrates did not differ from controls. The serum creatinine level at biopsy correlated with the glomerular CD68 and neutrophil scores (r=0.74 and r=0.71, respectively; P=0.001) but did not correlate with the extent of fibrinoid necrosis (r=0.36). Macrophages were localized at minute perforations and attenuations of the capillary basement membrane by electron microscopy.[Conclusions Early pauci-immune necrotizing GN is characterized by a selective localization of CD163 + M2 macrophages at sites of glomerular fibrinoid necrosis and in normal-appearing glomeruli. These observations indicate that alternatively activated macrophages are positioned as potential effectors of glomerular injury in the early stages of pauci-immune necrotizing GN and may be potential targets for therapeutic intervention.

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“…It is seen in up to 5% of patients with glomerulonephritis (3% primary glomerulonephritis) and 7% of glomerulonephritis in as sociation with systemic disease [12]. It usually presents with constitutional symptoms in association with haematuria and proteinuria and is characterized histologi cally by focal and segmental glomerular necrosis with frequent crescent formation, prominent interstitial in flammation and tubular damage [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

Acute Renal Failure due to Focal Necrotizing Glomerulonephritis in a Patient with Non-Hodgkin’s Lymphoma

Pollock

Ibels²,

Levi³

et al. 1988

Nephron

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Renal disease in association with lymphoma is more prevalent than generally recognized. Glomerulonephritis may occur as a paraneoplastic phenomenon. We report a patient who presented with acute renal failure due to focal necrotizing glomerunonephritis in association with non-Hodgkin’s lymphoma in whom the acute renal failure and glomerulonephritis resolved on clinical, biochemical and histological grounds with treatment of the lymphoma. Focal necrotizing glomerulonephritis is extremely uncommon in association with lymphoma and, to our knowledge, this association with follow-up and histological resolution of glomerulonephritis has not previously been reported.

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The Clinical Spectrum of Necrotizing Glomerulonephritis

Cited by 29 publications

References 0 publications

Polyarteritis Nodosa and Necrotizing Glomerulonephritis Associated with Long-Standing Silicosis

Polyarteritis Nodosa and Necrotizing Glomerulonephritis Associated with Long-Standing Silicosis

M2 Macrophage Infiltrates in the Early Stages of ANCA-Associated Pauci-Immune Necrotizing GN

Acute Renal Failure due to Focal Necrotizing Glomerulonephritis in a Patient with Non-Hodgkin’s Lymphoma

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