Membranous glomerulopathy

Author(s):  
C. D. Short
Author(s):  
Satoru Kudose ◽  
Miroslav Sekulic ◽  
Collette J. Mehring ◽  
Dominick Santoriello ◽  
Ibrahim Batal ◽  
...  

2010 ◽  
Vol 55 (4) ◽  
pp. B36
Author(s):  
Sana Akbar ◽  
Melvin Goldblat ◽  
Sadanand Palekar ◽  
Sachin Sachdev ◽  
Adeem Akbar

Proteinuria ◽  
1985 ◽  
pp. 175-193
Author(s):  
Jerome G. Porush ◽  
Pierre F. Faubert

2020 ◽  
pp. 46-53
Author(s):  
Maurizio Salvadori ◽  
Aris Tsalouchos

Membranous nephropathy (MN) is the major cause of nephrotic syndrome in adults, accounting for 20% of cases with an annual incidence of 1 per 100,000 population. In the past 10 years, the role of podocytes has been identified. Environmental triggers in genetically predisposed patients can activate podocytes to exhibit antigenic epitopes, including PLA2R, THBS1, and NELL1, which become targets of specific autoantibodies with subsequent complement activation. The discovery of these mechanisms has opened a new horizon in the treatment of MN, and novel drugs are available with more specific mechanisms of action. Rituximab, a monoclonal antibody directed against CD20 expressed on B lymphocytes, has been used in several trials and appears to induce remission of nephrotic syndrome in 60% of patients (GEMRITUX trial). The recently published results of the MENTOR trial documented the superior efficacy of rituximab in patients observed for up to 24 months. In MN, the concept of targeting disease control has introduced novel therapies with specific blocking mechanisms, such as belimumab; nonspecific blocking mechanisms, such as those against adrenocorticotropic hormone; and new therapeutic options, such as ofatumumab, bortezomib, and eculizumab, which have recognised the pathological processes involved in the glomerular diseases.


Author(s):  
A. Meyrier ◽  
P. Niaudet ◽  
J. Brodehl

Nephron ◽  
1988 ◽  
Vol 50 (3) ◽  
pp. 263-264 ◽  
Author(s):  
Silvio Garattini ◽  
Tullio Bertani ◽  
Giuseppe Remuzzi

2015 ◽  
Vol 2015 ◽  
pp. 1-5
Author(s):  
Yasuyuki Nakada ◽  
Nobuo Tsuboi ◽  
Yasuto Takahashi ◽  
Hiraku Yoshida ◽  
Yoriko Hara ◽  
...  

We report a case in which antineutrophil cytoplasmic antibody- (ANCA-) associated glomerulonephritis and membranous glomerulopathy (MGN) were detected concurrently. The patient showed rapidly progressive renal deterioration. A renal biopsy showed crescentic glomerulonephritis, together with marked thickening and spike and bubbling formations in the glomerular basement membranes. Indirect immunofluorescence examination of the patient’s neutrophils showed a perinuclear pattern. Enzyme-linked immunosorbent assays revealed that the ANCA in this case did not target myeloperoxidase (MPO) or proteinase 3 (PR3) but bactericidal-/permeability-increasing protein, elastase, and lysosome. The relationship between these two etiologically distinct entities, MPO-/PR3-negative ANCA-associated glomerulonephritis and MGN, remains unclear.


Author(s):  
James Carton

This chapter discusses renal pathology, including acute kidney injury (AKI), chronic kidney disease (CKD), nephrotic syndrome, hereditary renal diseases, Alport’s syndrome and thin basement membrane lesion, hypertensive nephropathy, diabetic nephropathy, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulopathy, glomerulonephritis, IgA nephropathy, post-infectious glomerulonephritis, C3 glomerulopathy, anti-glomerular basement membrane disease, monoclonal gammopathy-associated kidney disease, acute tubular injury, acute tubulointerstitial nephritis, reflux nephropathy, and obstructive nephropathy.


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