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1 glomeruli is also elevated in patients with membranous nephropathy.
2 and segmental glomerulosclerosis (FSGS) and membranous nephropathy.
3 mmune deposits in glomeruli of patients with membranous nephropathy.
4 erlying disease and seems to be greatest for membranous nephropathy.
5 diseases, with highest induction observed in membranous nephropathy.
6 omerulonephritis, and severe skin lesions or membranous nephropathy.
7 anomalies play a role in the pathogenesis of membranous nephropathy.
8 lie the loss of podocyte barrier function in membranous nephropathy.
9 eymann nephritis (PHN), a rat model of human membranous nephropathy.
10 ce active Heymann nephritis (HN), a model of membranous nephropathy.
11 Heymann nephritis (HN), a rat model of human membranous nephropathy.
12 glomerulonephritis and less frequently with membranous nephropathy.
13 tients met the criteria for NSAID-associated membranous nephropathy.
14 AID intake should be sought in patients with membranous nephropathy.
15 hamide regimen is the first-line therapy for membranous nephropathy.
16 nditions including inflammation, cancer, and membranous nephropathy.
17 detectable in ~75% of patients with primary membranous nephropathy.
18 may serve as a novel therapeutic target for membranous nephropathy.
19 hropathy, fibrillary glomerulonephritis, and membranous nephropathy.
20 n and therapeutic targeting in patients with membranous nephropathy.
21 romote immune dysregulation and, ultimately, membranous nephropathy.
22 uniquely present within the biopsy tissue in membranous nephropathy.
23 (PLA2R1) is the major autoantigen in primary membranous nephropathy.
24 ainst PLA2R in drug development programs for membranous nephropathy.
25 for serologic evaluation of NELL1-associated membranous nephropathy.
26 itope spreading" determines the prognosis of membranous nephropathy.
27 een made in the discovery of autoantigens in membranous nephropathy.
28 ew window onto the humoral aspect of primary membranous nephropathy.
29 cyclophosphamide regimen in the treatment of membranous nephropathy.
30 that underlie the pathophysiology of primary membranous nephropathy.
31 ed with malignancy than other known types of membranous nephropathy.
32 thway and induced podocyte injury in primary membranous nephropathy.
33 ng, immunologic, THSD7A-associated, model of membranous nephropathy.
34 s nephritis and within rare cases of primary membranous nephropathy.
35 peutic intervention in patients with primary membranous nephropathy.
36 A2R1) is the major autoantigen in idiopathic membranous nephropathy.
37 toantigen in 70% of patients with idiopathic membranous nephropathy.
38 y showed phospholipase A 2 receptor-negative membranous nephropathy.
39 S variants, in minimal change disease, or in membranous nephropathy.
40 he UPS depended on oxidative modification in membranous nephropathy.
41 imal-change disease and a low correlation in membranous nephropathy.
42 d human glomerular diseases, particularly in membranous nephropathy.
43 rtant advances regarding the pathogenesis of membranous nephropathy.
44 R) is the major target antigen in idiopathic membranous nephropathy.
45 R) are sensitive and specific for idiopathic membranous nephropathy.
46 dict response to treatment with rituximab in membranous nephropathy.
47 l segmental glomerulosclerosis (2/4), and/or membranous nephropathy (1/4) but no definitive features
48 Here, we describe a patient with recurrent membranous nephropathy 13 days after kidney transplantat
51 e and 252 presumed patients with FSGS [40%], membranous nephropathy [40%], and minimal change disease
53 n the prominent expression of FHR-5 in human membranous nephropathy, a disease in which complement ac
54 (18-75 years) with biopsy-proven idiopathic membranous nephropathy, a plasma creatinine concentratio
55 n and cancer and is the major autoantigen in membranous nephropathy, a rare but severe autoimmune kid
56 g a large cohort of patients with idiopathic membranous nephropathy according to a restrictive treatm
57 steroid-sensitive nephrotic syndrome or with membranous nephropathy after transplantation had low lev
60 For the subset of patients with idiopathic membranous nephropathy and deteriorating excretory renal
63 and HLA-D loci in 248 patients with primary membranous nephropathy and identified two independent si
65 rt of 117 Caucasian patients with idiopathic membranous nephropathy and nephrotic-range proteinuria u
69 in membrane nephropathy, lupus nephritis and membranous nephropathy, and correlated with estimated gl
71 (PLA(2)R1) are found in 80% of patients with membranous nephropathy, and previous studies described t
72 most prevalent circulating autoantibodies in membranous nephropathy are against phospholipase A2 rece
73 he two antigens associated with drug-induced membranous nephropathy are neural epidermal growth facto
74 nical syndromes associated with drug-induced membranous nephropathy are similar in that proteinuria r
75 e glomerulonephritis and another patient had membranous nephropathy as the cause of end-stage renal d
76 and podocyte MC5R appears to protect against membranous nephropathy, as demonstrated by its necessity
77 been made in our understanding of idiopathic membranous nephropathy, as well as treatment of this dis
78 t research investigations into mechanisms of membranous nephropathy associated with gold salts, penic
79 e 1 (NELL1) is the second leading antigen in membranous nephropathy, associated with malignancy, cert
81 (St-Cp) therapy for patients with idiopathic membranous nephropathy at high risk of progression to ES
83 autoimmune kidney disease; however, primary membranous nephropathy autoantigens remained elusive unt
84 is a resurgence of interest in drug-induced membranous nephropathy because of the widespread availab
86 - was induced in minimal change disease and membranous nephropathy, but not focal segmental glomerul
87 om such deposits in patients with idiopathic membranous nephropathy, but not in those with lupus memb
89 A2R is the target of the autoimmune disease, membranous nephropathy, characterised by production of a
91 given sheep anti-Fx1A to induce experimental membranous nephropathy; control rats received normal she
92 gmental glomerulosclerosis, minimal changes, membranous nephropathy, diffuse mesangial sclerosis and
94 r antigen discovery in malignancy-associated membranous nephropathy examining immune complexes eluted
95 rmal growth factor-like 1 (NELL1)-associated membranous nephropathy following lipoic acid supplementa
96 ndings have transformed our understanding of membranous nephropathy from that of an idiopathic diseas
97 r cohort, 15 of 154 patients with idiopathic membranous nephropathy had circulating autoantibodies to
103 rulosclerosis (HR, 0.80; 95% CI, 0.77-0.82), membranous nephropathy (HR, 0.88; 95% CI, 0.83-0.93), me
104 nephropathy (HRa, 0.74; 95% CI, 0.59-0.92), membranous nephropathy (HRa, 0.47; 95% CI, 0.29-0.75), a
105 disease, focal segmental glomerulosclerosis, membranous nephropathy, IgA nephropathy, antineutrophil
106 ase were primary FSGS, diabetic nephropathy, membranous nephropathy, immunoglobulin A nephropathy, an
112 phritis is an experimental model that mimics membranous nephropathy in humans, wherein the glomerular
113 in seven patients, diabetic nephropathy and membranous nephropathy in one patient, and death due to
116 peutic advances for patients with idiopathic membranous nephropathy, including antibody inhibition th
117 ed podocyte foot-process architecture in rat membranous nephropathy, indicating disease-modifying eff
118 immune deposits in patients with idiopathic membranous nephropathy, indicating that PLA(2)R is a maj
136 d decline in renal function in patients with membranous nephropathy may be due to renal vein thrombos
137 actors, compared with IgAN (referent), FSGS, membranous nephropathy, membranoproliferative GN, lupus
138 ed as a surrogate for long-term prognosis in membranous nephropathy (MGN), variability in proteinuria
139 plasm-associated glomerulopathy, autoimmune (membranous nephropathy, minimal change disease) and para
140 D7A) is a target antigen identified in adult membranous nephropathy (MN) along with the major antigen
143 ultiple autoantigens have been identified in membranous nephropathy (MN) by tissue-based proteomics.
144 Absent a remission of proteinuria, primary membranous nephropathy (MN) can lead to ESRD over many y
147 he Heymann nephritis (HN) rat model of human membranous nephropathy (MN) have shown that IgG antibodi
148 fies a new antigen responsible for secondary membranous nephropathy (MN) in a patient with mucopolysa
155 Phospholipase A2 receptor (PLA2R)-associated membranous nephropathy (MN) is a leading cause of nephro
173 Drugs are an important secondary cause of membranous nephropathy (MN) with the most common drugs a
174 As recently as 2002, most cases of primary membranous nephropathy (MN), a relatively common cause o
175 A) are the two major autoantigens in primary membranous nephropathy (MN), and define two molecular su
176 ssion in two-thirds of patients with primary membranous nephropathy (MN), even after other treatments
177 xceptionally strong genetic risk factors for membranous nephropathy (MN), leading, through an unknown
178 is (FSGS), minimal change disease (MCD), and membranous nephropathy (MN), may respond well to cyclosp
187 erosis [FSGS], minimal-change disease [MCD], membranous nephropathy [MNP], lupus nephritis [LN], and
188 ncluding IgA nephropathy and IgA vasculitis, membranous nephropathy, nephrotic syndrome, minimal chan
190 vs IgAN, ranged from 0.49 for DN to 0.92 for membranous nephropathy or ADPKD) than by lower rates of
191 and nephrotic syndrome caused by idiopathic membranous nephropathy or focal segmental glomeruloscler
192 s from patients with idiopathic or secondary membranous nephropathy or other proteinuric or autoimmun
194 glomerulonephritis, minimal change disease, membranous nephropathy, or FSGS to 3%-5% in IgA nephropa
197 ive glomerulonephritis, IgA nephropathy, and membranous nephropathy), patients with systemic lupus er
198 serum samples from patients with idiopathic membranous nephropathy, patients with other glomerular d
202 critical role in the pathogenesis of primary membranous nephropathy (PMN), an autoimmune kidney disea
204 correlate with the immunological activity of membranous nephropathy, potentially exhibiting a more ra
209 cohort with anti-PLA2R1-negative idiopathic membranous nephropathy recognized a glomerular protein t
215 y, serum from patients with NCAM1-associated membranous nephropathy showed reactivity to NCAM1 recomb
216 ents (70%) with idiopathic but not secondary membranous nephropathy specifically identified a 185-kD
217 g that it can release the ectodomains of the membranous nephropathy target antigens phospholipase A2
218 D risk was significantly higher for FSGS and membranous nephropathy than for presumed minimal change
219 shown in phospholipase A2 receptor positive membranous nephropathy that known antibodies can be dete
220 lomerulopathies minimal-change nephrosis and membranous nephropathy, there is an increase in Shp2 pho
221 red with PLA2R- and THSD7A-positive cases of membranous nephropathy, there was a greater proportion o
222 e graft contributes to recurrence of primary membranous nephropathy through the disease susceptibilit
223 use of immunosuppressive drugs in idiopathic membranous nephropathy to patients at the highest risk o
224 of immune deposit formation in experimental membranous nephropathy to the role of a microRNA in FSGS
226 eterologous mouse model of THSD7A-associated membranous nephropathy, various melanocortin agents, inc
227 The mean age of patients with NELL1-positive membranous nephropathy was 66.8 years, with a slight mal
228 n groups into five subgroups, interestingly, membranous nephropathy was the most common pathologic ty
230 nts with newly diagnosed PLA(2)R1-associated membranous nephropathy, we investigated the clinical rol
231 with a nephrotic syndrome and biopsy-proven membranous nephropathy were administered a 3 to 6-month
232 while taking an NSAID and if other causes of membranous nephropathy were excluded and a rapid remissi
233 tibodies in serum samples from patients with membranous nephropathy were mainly IgG4, the predominant
235 were serially evaluated in 15 patients with membranous nephropathy who exhibited relapsing nephrosis
237 samples from the 74 patients with idiopathic membranous nephropathy who were seropositive for anti-PL
238 pholipase A(2) receptor-associated recurrent membranous nephropathy with circulating anti-Phospholipa
239 s renal function in patients with idiopathic membranous nephropathy with declining renal function.
240 a kidney transplant and developed recurrent membranous nephropathy with fine granular co-localizatio
241 y-based minimal change nephropathy, FSGS, or membranous nephropathy, with 94% sensitivity and 92% PPV
242 y in this cohort of patients with idiopathic membranous nephropathy yielded favorable outcomes while