2006
DOI: 10.1136/ard.2004.033464
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Collapsing glomerulopathy in systemic autoimmune disorders: a case occurring in the course of full blown systemic lupus erythematosus

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Cited by 17 publications
(27 citation statements)
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“…IVIg, intravenous immunoglobulins; CVVH, continuous venovenous hemofiltration; MMF, mycophenolate mofetil. or death during therapy (9)(10)(11)(12)(15)(16)(17)(18). Only 25% progression to ESRD or death in this group is a surprising finding, and it may be related to a shorter follow-up period or less-stringent criteria for the diagnosis of CG.…”
Section: Discussionmentioning
confidence: 93%
See 1 more Smart Citation
“…IVIg, intravenous immunoglobulins; CVVH, continuous venovenous hemofiltration; MMF, mycophenolate mofetil. or death during therapy (9)(10)(11)(12)(15)(16)(17)(18). Only 25% progression to ESRD or death in this group is a surprising finding, and it may be related to a shorter follow-up period or less-stringent criteria for the diagnosis of CG.…”
Section: Discussionmentioning
confidence: 93%
“…Anecdotal CG in autoimmune diseases including SLE, SLE-like disease, and mixed connective tissue disease has been previously reported (1,2,(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). The aim of this study is to report an analysis of the clinicopathologic findings and the possible association of renal lesions with CG in the setting of SLE and lupuslike disease and review the literature of the reported cases.…”
Section: Introductionmentioning
confidence: 99%
“…What is apparent from the increased reporting of CG is, however, that it is not a single disease but rather a unique pattern of renal parenchymal injury, which may result from a multitude of causes Amoura et al 2006). Indeed, one outcome from the growing awareness of the lesion has been the exponential increase in reporting its association with disorders other than human immunodeficiency virus (HIV)-1 infection or idiopathic.…”
Section: The Etiology and The Associated Conditionsmentioning
confidence: 99%
“…The pathogenesis of the remaining cases of CG in patients with SLE presented by Salvatore et al, as well as in prior reports (8)(9)(10)(11)(12)(13)(14), remains unclear, although it should be noted that the great majority of these patients had active systemic disease (often a lupus flare) and a significant number had concurrent lupus nephritis, albeit usually mild (most often International Society of Nephrology/Renal Pathology Society class II). This certainly suggests involvement of humoral and/or cell-mediated immunity, both of which have been implicated in the pathogenesis of podocytopathies and of SLE (15)(16)(17)(18)(19).…”
mentioning
confidence: 92%
“…Unlike the case with CG in patients with SLE, patients with lupus podocytopathy most often show some therapeutic response to steroids and/or other immunosuppressive therapy and only infrequently progress to ESRD within the first few months to years after biopsy, although the responses are often only partial remissions, even in patients with minimal histologic lesions (8,9,20,21). The relationship between lupus podocytopathy and the CG lesions described by Salvatore et al and others (7)(8)(9)(10)(11)(12)(13)(14) remains unclear, much as is the case with collapsing and noncollapsing forms of idiopathic FSGS, although in all of these lesions the primary target of injury is likely to be the podocyte, and indeed CG may represent an extreme form of lupus podocytopathy.…”
mentioning
confidence: 99%