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1 revealed endocapillary proliferative (35%), membranoproliferative (29%) and membranous (29%) pattern
3 noninvolved portion of the kidney revealed a membranoproliferative glomerular lesion, a lesion usuall
5 athological diagnoses on renal biopsies were membranoproliferative glomerulonephritis (23%) followed
6 ciated with hemolytic uremic syndrome (HUS), membranoproliferative glomerulonephritis (dense deposit
7 (FSGS), 57; immunoglobulin A nephritis, 22; membranoproliferative glomerulonephritis (GN), 18; and m
8 C3 glomerulopathy (C3G) and immune-complex membranoproliferative glomerulonephritis (IC-MPGN) are r
13 opathies, such as IgA nephropathy (IgAN) and membranoproliferative glomerulonephritis (MPGN) remains
16 , a model of cryoglobulinemia and associated membranoproliferative glomerulonephritis (MPGN), in whic
19 as been associated with de novo or recurrent membranoproliferative glomerulonephritis and acute trans
20 d-stage renal disease in 12; one patient had membranoproliferative glomerulonephritis and another pat
21 een reported to be typically associated with membranoproliferative glomerulonephritis and less freque
23 nty-one patients with biopsy-proven, diffuse membranoproliferative glomerulonephritis and significant
24 By 6 months of age, ABCA1-/- animals develop membranoproliferative glomerulonephritis due to depositi
25 malities in factor H have been implicated in membranoproliferative glomerulonephritis in both humans
26 ch was before the development of spontaneous membranoproliferative glomerulonephritis in some Cfh(-/-
27 in a mouse model of cryoglobulin-associated membranoproliferative glomerulonephritis induced by over
29 ients had immune-complex glomerulonephritis: membranoproliferative glomerulonephritis type 1 (n = 12)
30 The predominant renal biopsy findings were membranoproliferative glomerulonephritis type 1 or type
31 ceased donor transplants were not present in membranoproliferative glomerulonephritis type I (adjuste
33 reviously published studies of patients with membranoproliferative glomerulonephritis type I are smal
34 allograft for end-stage renal disease due to membranoproliferative glomerulonephritis type I is prese
37 ypical hemolytic uremic syndrome (aHUS), and membranoproliferative glomerulonephritis type II (MPGN2)
38 Dense deposit disease (DDD; also known as membranoproliferative glomerulonephritis type II) is a p
39 eration, atypical hemolytic uremic syndrome, membranoproliferative glomerulonephritis type II, and pa
42 plant FSGS was 2.25 (1.6-3.1), P<0.0001, for membranoproliferative glomerulonephritis was 2.37 (1.3-4
43 Renal involvement usually manifests as a membranoproliferative glomerulonephritis with marked mon
44 enal (membranous glomerulonephritis [GN] and membranoproliferative glomerulonephritis); hematologic (
45 nephritis, specifically cryoglobulinemic and membranoproliferative glomerulonephritis, and has also b
46 al was seen with recurrent and de novo FSGS, membranoproliferative glomerulonephritis, and HUS/TTP.
47 hey developed splenomegaly, lymphadenopathy, membranoproliferative glomerulonephritis, and lymphocyti
48 nephritides (e.g. Alport's Syndrome, type II membranoproliferative glomerulonephritis, and membranous
49 vere kidney disorders including mesangial or membranoproliferative glomerulonephritis, and/or Henoch
50 gy, whereas overexpression of TSLP induced a membranoproliferative glomerulonephritis, as previously
51 ulting from other glomerular diseases (FSGS, membranoproliferative glomerulonephritis, IgA nephropath
52 riably demonstrating severe neonatal anemia, membranoproliferative glomerulonephritis, liver fibrosis
53 tic nephropathy, membranous lupus nephritis, membranoproliferative glomerulonephritis, postinfectious
54 3 glomerulopathies/immune complex-associated membranoproliferative glomerulonephritis, serum-induced
55 on with hepatitis C virus (HCV) infection is membranoproliferative glomerulonephritis, with or withou
61 s nephropathy (HR, 0.88; 95% CI, 0.83-0.93), membranoproliferative GN (HR, 0.84; 95% CI, 0.76-0.92),
63 t of 141 patients with C3G and Ig-associated membranoproliferative GN (Ig-MPGN) for anti-FB and anti-
65 hropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative GN (MPGN) (n=19-23 for each diseas
70 sis of HLA serotypes in 338 individuals with membranoproliferative GN and 15,614 individuals with non
71 ent gene mutations typically causing primary membranoproliferative GN and implicate an underlying aut
72 immune complex GNs such as membranous GN and membranoproliferative GN are particularly common renal m
73 whole-genome sequence data from 165 primary membranoproliferative GN cases and 10,250 individuals wi
76 +/-eGFR was 39.5+/-20.4 ml/min per 1.73 m(2) Membranoproliferative GN was the predominant histologic
77 iated crescentic GN, lupus nephritis, type I membranoproliferative GN), and nephrotic syndrome (minim
80 AN (referent), FSGS, membranous nephropathy, membranoproliferative GN, lupus nephritis, and vasculiti
81 A nephropathy and one specimen of sclerosing membranoproliferative GN, showed bright (2-3+) C4d stain
86 ntified DGKE gene variants as the cause of a membranoproliferative-like glomerular microangiopathy.
89 way and frequently deviates from the classic membranoproliferative pattern of injury on light microsc