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1 ontaneous and chronic serum sickness-induced proliferative glomerulonephritis.
2 fuse (53%), focal (28%), and mesangial (13%) proliferative glomerulonephritis.
3 ated with recurrent bacterial infections and proliferative glomerulonephritis.
4 lupus erythematosus with antinuclear Abs and proliferative glomerulonephritis.
5 y revealed enlarged glomeruli with mesangial-proliferative glomerulonephritis.
6 o hypercellularity in human and experimental proliferative glomerulonephritis.
7 ing could be of pathological significance in proliferative glomerulonephritis.
8 ere found in Munich Wistar Fromter rats with proliferative glomerulonephritis.
9 smaller quantities in patients with non-IgA proliferative glomerulonephritis and in healthy controls
10 ria at flare and was higher in patients with proliferative glomerulonephritis and in patients with im
11 kidney function in different mouse models of proliferative glomerulonephritis and lupus nephritis by
13 gration in the anti-Thy 1 model of mesangial proliferative glomerulonephritis and provide evidence fo
14 strate the major role played by PI3Kalpha in proliferative glomerulonephritis and show that in this c
16 lomerulonephritis, and diffuse endocapillary proliferative glomerulonephritis associated with systemi
18 the crucial role played by this pathway for proliferative glomerulonephritis development by promotin
19 gic diagnoses on recurrence included diffuse proliferative glomerulonephritis, focal proliferative gl
22 anded (ss) DNA (11F8) induces severe diffuse proliferative glomerulonephritis in nonautoimmune mice w
26 black 76%, other 36%; P < 0.05) and diffuse proliferative glomerulonephritis +/- membranous glomerul
27 fuse proliferative glomerulonephritis, focal proliferative glomerulonephritis, membranous glomerulone
28 1) normal by light microscopy, (2) mesangial proliferative glomerulonephritis, or (3) focal segmental
29 develop antiphospholipid syndrome (APS) and proliferative glomerulonephritis that is markedly accele
30 with the reference group of individuals with proliferative glomerulonephritis, the risk of death or i
32 enterocolitis with adherent bacterial rods, proliferative glomerulonephritis, tubular necrosis, and
34 teria for acute transplant glomerulopathy or proliferative glomerulonephritis were not satisfied.
35 autoantibody levels and developed mesangial proliferative glomerulonephritis, which resembled system
36 (hu)Tg/CFH(-/-) mice spontaneously developed proliferative glomerulonephritis, which was accelerated
37 triggered severe nephritis, characterized by proliferative glomerulonephritis with crescent formation
38 Renal biopsy demonstrated a florid, diffuse, proliferative glomerulonephritis with glomerular immune
39 e cohort included the following 26 patients: proliferative glomerulonephritis with MIg deposits (PGNM
42 trong evidence against monoclonality in most proliferative glomerulonephritis with monoclonal Ig depo
45 frequency of myoglobin cast nephropathy and proliferative glomerulonephritis with monoclonal IgG dep
48 Testing of ten cases of the IgG variant of proliferative glomerulonephritis with monoclonal immunog
49 Anti-PR3 treated mice had mild pauci-immune proliferative glomerulonephritis, with infiltration of h