Lupus Membranous Nephropathy.

Chronic kidney disease Glomerular diseases Lupus nephritis Membranous nephropathy Nephrotic syndrome

Journal

Glomerular diseases

ISSN: 2673-3633

Titre abrégé: Glomerular Dis

Pays: Switzerland

ID NLM: 101775779

Informations de publication

Date de publication:
Apr 2021

Historique:

received: 19 07 2020

accepted: 09 10 2020

entrez: 8 2 2023

pubmed: 2 3 2021

medline: 2 3 2021

Statut: epublish

Résumé

Lupus membranous nephropathy (LMN) is a rare disease, usually associated with nephrotic syndrome. We reviewed the literature by searching for the following terms on Pubmed.gov: lupus nephritis, membranous nephropathy (MN), lupus membranous nephropathy, nephrotic syndrome, and Class V lupus nephritis. The histology of LMN at light microscopy is similar to that of primary MN. Cases of MN associated with focal or diffuse proliferation are not considered LMN by the International Society of Nephrology/Renal Pathology Society classification. Immunofluorescence study of LMN shows deposits of all immunoglobulins and complement. Tubulo-reticular structures, extraglomerular deposits, subepithelial, and scanty subendothelial deposits can be seen on electron microscopy. Phospholipase A2 receptor deposits are usually but not necessarily absent in LMN. The pathogenesis is still not completely understood. The inflammatory milieu of lupus may favor the development of autoantigens and intraglomerular assembly of immune complexes. These are more often associated with mesangial or endocapillary hypercellular lesions. Alternatively, autoantibodies may bind autoantigens in the glomerular subepithelium, triggering a signaling cascade leading to LMN. A central role in the development of podocyte injury and proteinuria is played by the components of complement C5b-C9. CKD progression in LMN is slow but may be accelerated by the frequency of renal flares. Persistent nephrotic syndrome and/or the frequent use of corticosteroids may lead to a series of life-threatening complications. Treatment of arterial hypertension, dyslipidemia, and diabetes are of paramount importance. Besides specific therapies of these complications, hydroxychloroquine and vitamin D supplementation are recommended. Immunosuppression should be limited to patients with nephrotic proteinuria. The most frequently used drugs are corticosteroids, calcineurin inhibitors, cyclophosphamide, mycophenolate, and rituximab, alone or combined. Early detection and treatment of renal flares is of paramount importance to prevent CKD progression.

Sections du résumé

Background UNASSIGNED

Lupus membranous nephropathy (LMN) is a rare disease, usually associated with nephrotic syndrome.

Methods UNASSIGNED

We reviewed the literature by searching for the following terms on Pubmed.gov: lupus nephritis, membranous nephropathy (MN), lupus membranous nephropathy, nephrotic syndrome, and Class V lupus nephritis.

Results UNASSIGNED

The histology of LMN at light microscopy is similar to that of primary MN. Cases of MN associated with focal or diffuse proliferation are not considered LMN by the International Society of Nephrology/Renal Pathology Society classification. Immunofluorescence study of LMN shows deposits of all immunoglobulins and complement. Tubulo-reticular structures, extraglomerular deposits, subepithelial, and scanty subendothelial deposits can be seen on electron microscopy. Phospholipase A2 receptor deposits are usually but not necessarily absent in LMN. The pathogenesis is still not completely understood. The inflammatory milieu of lupus may favor the development of autoantigens and intraglomerular assembly of immune complexes. These are more often associated with mesangial or endocapillary hypercellular lesions. Alternatively, autoantibodies may bind autoantigens in the glomerular subepithelium, triggering a signaling cascade leading to LMN. A central role in the development of podocyte injury and proteinuria is played by the components of complement C5b-C9. CKD progression in LMN is slow but may be accelerated by the frequency of renal flares. Persistent nephrotic syndrome and/or the frequent use of corticosteroids may lead to a series of life-threatening complications.

Discussion UNASSIGNED

Treatment of arterial hypertension, dyslipidemia, and diabetes are of paramount importance. Besides specific therapies of these complications, hydroxychloroquine and vitamin D supplementation are recommended. Immunosuppression should be limited to patients with nephrotic proteinuria. The most frequently used drugs are corticosteroids, calcineurin inhibitors, cyclophosphamide, mycophenolate, and rituximab, alone or combined. Early detection and treatment of renal flares is of paramount importance to prevent CKD progression.

Identifiants

DOI: 10.1159/000512278 PMID: 36751488 PMC: PMC9677716

pubmed: 36751488

doi: 10.1159/000512278

pii: gdz-0001-0010

pmc: PMC9677716

doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

10-20

Informations de copyright

Déclaration de conflit d'intérêts

C.P. and G.M. have no conflicts of interest to declare. A.F. is an inventor on pending or issued patents (PCT/US11/56272, PCT/US12/62594, PCT/US2019/041730, PCT/US2019/032215, PCT/US13/36484, and PCT 62/674,897) aimed to diagnosing or treating proteinuric kidney diseases. She stands to gain royalties from her future commercialization of these patents. A.F. is the vice president of L&F Health LLC and is a consultant for ZyVersa Therapeutics, Inc. ZyVersa Therapeutics, Inc. has licensed worldwide rights to develop and commercialize hydroxypropyl-beta-cyclodextrin from L&F Research for the treatment of kidney disease.

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