ライフサイエンスコーパス: glomerulonephritis

1 een documented in glomeruli of patients with glomerulonephritis.

2 re needed to induce a necrotizing/crescentic glomerulonephritis.

3 nds, and it can reduce renal inflammation in glomerulonephritis.

4 glomerulonephritis or necrotizing/crescentic glomerulonephritis.

5 y and thereby promotes renal inflammation in glomerulonephritis.

6 ponses are critical for the phenotype of the glomerulonephritis.

7 op high titers of antinuclear Abs and severe glomerulonephritis.

8 renal function in a rat model of crescentic glomerulonephritis.

9 r the development of immune complex-mediated glomerulonephritis.

10 s including anti-DNA antibody production and glomerulonephritis.

11 from development of lupus autoantibodies and glomerulonephritis.

12 which deposit in their kidneys, resulting in glomerulonephritis.

13 deposition, and tissue inflammation such as glomerulonephritis.

14 f HIV nephropathy and in collapsing forms of glomerulonephritis.

15 evidenced by anti-nuclear Ab deposition and glomerulonephritis.

16 unich Wistar Fromter rats with proliferative glomerulonephritis.

17 utoimmune nature of this most common primary glomerulonephritis.

18 scentic lesions in a patient with crescentic glomerulonephritis.

19 immune complex deposition leading to chronic glomerulonephritis.

20 ia in an FcR-dependent, Ab-mediated model of glomerulonephritis.

21 itional level of protection from Ab-mediated glomerulonephritis.

22 ases such as antibody-mediated rejection and glomerulonephritis.

23 e, including acute rheumatic fever and acute glomerulonephritis.

24 be a therapeutic target in human Ab-mediated glomerulonephritis.

25 els of hypertension-induced renal damage and glomerulonephritis.

26 re mediated by PR3 or elastase during active glomerulonephritis.

27 al hemolytic uremic syndrome and symptoms of glomerulonephritis.

28 neutralization abrogated the development of glomerulonephritis.

29 ship between anti-LAMP-2 antibodies and ANCA glomerulonephritis.

30 d were largely protected from development of glomerulonephritis.

31 with anti-LAMP-2 antibodies did not develop glomerulonephritis.

32 merular endothelial cell (GEC) injury during glomerulonephritis.

33 e, including vasculitic lesion formation and glomerulonephritis.

34 Rs) are potential serine protease targets in glomerulonephritis.

35 eys, where they cause necrotizing crescentic glomerulonephritis.

36 e of his renal failure was poststreptococcal glomerulonephritis.

37 and proinflammatory cytokine production, and glomerulonephritis.

38 cytoplasmic antibodies-related pauci-immune glomerulonephritis.

39 n in post-infectious and rapidly progressive glomerulonephritis.

40 inding clues to the pathogenesis of anti-GBM glomerulonephritis.

41 ingle most predictive marker of histological glomerulonephritis.

42 e mouse GBM in vivo nor induced experimental glomerulonephritis.

43 iveness to MPO and a tendency to more severe glomerulonephritis.

44 biopsy of at least one individual showed C3 glomerulonephritis.

45 chronic serum sickness-induced proliferative glomerulonephritis.

46 eptible to experimentally induced crescentic glomerulonephritis.

47 cal (28%), and mesangial (13%) proliferative glomerulonephritis.

48 ermines glomerular damage in immune-mediated glomerulonephritis.

49 alloantibodies mediating rapidly progressive glomerulonephritis.

50 clonal gammopathy that mimics immune-complex glomerulonephritis.

51 One patient experienced posttransplant C3 glomerulonephritis.

52 P-1 is indeed activated during the course of glomerulonephritis.

53 vestigating pathogenetic mechanisms of lupus glomerulonephritis.

54 l to the origins of this very common form of glomerulonephritis.

55 delays the appearance of autoantibodies and glomerulonephritis.

56 lomerulosclerosis in experimental crescentic glomerulonephritis.

57 repression in the rat strain susceptible to glomerulonephritis.

58 pment and function and succumb to autoimmune glomerulonephritis.

59 PARP-1 can be a novel therapeutic target in glomerulonephritis.

60 , organ transplantation, and immune-mediated glomerulonephritis.

61 en monocytes and neutrophils in induction of glomerulonephritis.

62 therapeutic strategy in rapidly progressive glomerulonephritis.

63 hil cytoplasmatic antibody (ANCA)-associated glomerulonephritis.

64 n a model of in situ immune complex-mediated glomerulonephritis.

65 e-emptive treatment in abrogating crescentic glomerulonephritis.

66 ate injury in complement-dependent models of glomerulonephritis.

67 ctional role in the normal glomerulus and in glomerulonephritis.

68 lin-3a ameliorated all aspects of crescentic glomerulonephritis.

69 and attenuated renal tissue damage in acute glomerulonephritis.

70 e with elevated autoantibody levels and mild glomerulonephritis.

71 Transgenic ApoA-I also improved SLE-mediated glomerulonephritis.

72 otein (MRP) 8/14, calprotectin] in promoting glomerulonephritis.

73 blockade may be a new therapeutic target in glomerulonephritis.

74 a naturally occurring model of VL-associated glomerulonephritis.

75 on renal biopsies were membranoproliferative glomerulonephritis (23%) followed by IgA nephropathy (19

76 opathy (52%), arthralgia or arthritis (44%), glomerulonephritis (35%), cutaneous ulcers (16%), and cu

77 omoted influx of DC precursors in crescentic glomerulonephritis, a DC-dependent aggressive type of ne

78 Mouse experimental autoimmune glomerulonephritis, a model of human antiglomerular base

79 tineutrophil cytoplasmic antibody-associated glomerulonephritis (AAGN) patients are still limited.

80 L-10(-/-) CD4(+) T cells develop more severe glomerulonephritis after induction of anti-glomerular ba

81 IL-10-deficient mice exhibit exacerbation of glomerulonephritis after induction with anti-glomerular

82 ations and the most frequent form of primary glomerulonephritis among Europeans.

83 one, and this was associated with autoimmune glomerulonephritis and a range of malignancies in aged m

84 Glomerulonephritis and acute tubular necrosis were prese

85 ng from cutaneous and visceral vasculitis to glomerulonephritis and B-cell non-Hodgkin lymphoma.

86 position, also remained free of histological glomerulonephritis and clinical disease.

87 raft survival" was assessed in patients with glomerulonephritis and compared with those with autosoma

88 ntargeted formulations, with protection from glomerulonephritis and decreases in IFN-gamma-positive C

89 allograft survival in patients with primary glomerulonephritis and determined if the risk of graft l

90 rs of autoantibodies, delayed progression of glomerulonephritis and diminished renal-infiltrating Tfh

91 igh-fat diet, Sle16.Ldlr(-/-) mice developed glomerulonephritis and displayed enhanced glomerular C3

92 a lupus-like disease with autoantibodies and glomerulonephritis and early death.

93 th anti-glomerular basement membrane-induced glomerulonephritis and experimental encephalomyelitis ar

94 e most potent n-3 fatty acid that suppresses glomerulonephritis and extends life span of systemic lup

95 lexes of other cause, particularly recurrent glomerulonephritis and hepatitis C.

96 7 cells in a mouse model of acute crescentic glomerulonephritis and in a mouse chronic model of lupus

97 plasticity in acute and chronic experimental glomerulonephritis and introduce anti-CD3 treatment as a

98 rescue organ function in rapidly progressive glomerulonephritis and lung haemorrhage; other indicatio

99 kg of myeloperoxidase resulted in crescentic glomerulonephritis and lung hemorrhage in all animals.

100 00 microg/kg induced pauci-immune crescentic glomerulonephritis and lung hemorrhage in all immunized

101 that all animals reliably develop crescentic glomerulonephritis and lung hemorrhage.

102 Kidneys develop glomerulonephritis and proteinuria, reflecting tissue in

103 This included membranoproliferative glomerulonephritis and relapses in IgA nephropathy.

104 hat often manifests as focal and necrotizing glomerulonephritis and renal failure.

105 s derived from an experimental rat system of glomerulonephritis and used ABBA to identify >1000 disea

106 55 years; 30 with and 30 without SLE-related glomerulonephritis) and 60 age- and sex-matched healthy

107 moter by JunD (an established determinant of glomerulonephritis), and a consistent change in Ifitm3 e

108 infiltrating granulocytes, much more severe glomerulonephritis, and a reduced lifespan.

109 of switched autoantibodies, the incidence of glomerulonephritis, and early lethality.

110 cluding minimal change nephrosis, membranous glomerulonephritis, and IgA nephropathy.

111 t includes arthralgia, purpura, skin ulcers, glomerulonephritis, and peripheral neuropathy.

112 aematuria, recurrent macroscopic haematuria, glomerulonephritis, and progressive renal failure.

113 Lbw2, a locus previously linked to survival, glomerulonephritis, and splenomegaly, to investigate its

114 obulinemia, autoantibodies, lymphadenopathy, glomerulonephritis, and vasculitis.

115 c lupus erythematosus (SLE), with or without glomerulonephritis; and to correlate ocular findings wit

116 perimental anti-glomerular basement membrane glomerulonephritis (anti-GBM-GN), using two leading mous

117 With the emergence of necrotizing/crescentic glomerulonephritis, approximately 0.15% of renal CD4(+)

118 Many types of glomerulonephritis are initiated by the deposition of im

119 the progression from benign autoimmunity to glomerulonephritis are largely unknown.

120 It confirmed that PEDs associated with C3 glomerulonephritis are not vascularized, but rather of s

121 es and their relationship to disease in ANCA glomerulonephritis are not well described.

122 pathogenic Th17 cells in the development of glomerulonephritis are still not fully understood.

123 ctivating FcgammaRs in promoting features of glomerulonephritis as seen in other model systems.

124 of heparanase in two models of experimental glomerulonephritis, being anti-glomerular basement membr

125 nly 1 active copy of Tlr7 develop late-onset glomerulonephritis but not APS.

126 28.DR3(+)AE(0) mice developed anti-dsDNA and glomerulonephritis, but anti-dsDNA titers were higher in

127 4) has been suggested in previous studies of glomerulonephritis, but the complex integration of these

128 ole during the initiation and progression of glomerulonephritis, but the exact mechanisms are not cle

129 proteinuria and renal damage in experimental glomerulonephritis by decreasing glomerular HS expressio

130 te that TLR4 stimulation triggers crescentic glomerulonephritis by effects on both the adaptive and i

131 nhibition potently limits the development of glomerulonephritis by impacting both cell- and effector

132 f SPARC in mediating experimental crescentic glomerulonephritis by inducing passive nephrotoxic nephr

133 hesized that the MDM2 would drive crescentic glomerulonephritis by NF-kappaB-dependent glomerular inf

134 Dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) are widely recognized subtypes

135 C3 glomerulonephritis (C3GN) results from abnormalities in

136 including dense deposit disease (DDD) and C3 glomerulonephritis (C3GN).

137 Dense deposit disease is a rare glomerulonephritis caused by uncontrolled stimulation of

138 elucidate its role in mesangioproliferative glomerulonephritis, CCN3 systemically was overexpressed

139 duced functional and histological indices of glomerulonephritis, CD74(+) and CXCR4(+) leukocyte recru

140 use chromosome 1 are associated with chronic glomerulonephritis (cGN) and acute GN (aGN).

141 sangium and induce the mesangioproliferative glomerulonephritis characteristic of IgAN.

142 tory disorders, with proposed involvement in glomerulonephritis, chronic lung disease, sepsis, and va

143 hibited significantly enhanced postchallenge glomerulonephritis compared to the placebo group (P = 0.

144 gG Abs and developed immune complex-mediated glomerulonephritis, compared with Blk(+/+) mice.

145 Crescentic glomerulonephritis (Crgn) is a complex disease where the

146 Crescentic glomerulonephritis (Crgn) is a complex disorder where ma

147 m patients with dense deposit disease and C3 glomerulonephritis demonstrated that C3b:protein complex

148 protocol, no animals developed hematuria or glomerulonephritis, despite having identical levels of a

149 sed systemic inflammation and immune complex glomerulonephritis, despite intact TLR signaling within

150 he importance of IL-10 as protection against glomerulonephritis development.

151 ts with IgA nephropathy selected from the UK Glomerulonephritis DNA Bank.

152 In experimental autoimmune glomerulonephritis (EAG), a model of Goodpasture's disea

153 Experimental autoimmune glomerulonephritis (EAG), an animal model of Goodpasture

154 t little is known about their roles in viral glomerulonephritis (eg, HIV nephropathy).

155 rent diseases, such as rheumatoid arthritis, glomerulonephritis, etc.

156 nd is protective against autoimmune-mediated glomerulonephritis, even in the face of high titer autoa

157 that S100A8/A9 plays a critical role during glomerulonephritis, exerting and amplifying autocrine an

158 ated interferon and ribavirin; patients with glomerulonephritis experienced improvement in renal func

159 but not CR2-Crry, also significantly reduced glomerulonephritis, expression of serum anti-double-stra

160 e: production of anti-Sm/RNP autoantibodies, glomerulonephritis, generation of Ly6C(hi) monocytes, an

161 In lupus glomerulonephritis, glomerular immune complexes were bel

162 M) lupus-prone mice with spontaneous chronic glomerulonephritis (GN) and anti-glomerular basement mem

163 collected from rodent models of inflammatory glomerulonephritis (GN) as well as from patients with cr

164 t on autoantibody production and spontaneous glomerulonephritis (GN) in a mouse model of SLE.

165 Crescentic glomerulonephritis (GN) is a devastating disease with ra

166 Recurrent glomerulonephritis (GN) remains an important cause of ki

167 ether kidney transplantation rates differ by glomerulonephritis (GN) subtype remains largely unknown.

168 e in systemic lupus erythematosus (SLE) with glomerulonephritis (GN) vary widely, likely because they

169 betes mellitus (DM), hypertension (HTN), and glomerulonephritis (GN) were analyzed, and then compared

170 dent anti-glomerular basement membrane (GBM) glomerulonephritis (GN), in alpha7nAChR-deficient (alpha

171 ks, DKO mice developed mesangioproliferative glomerulonephritis (GN), leading to severe proteinuria.

172 arly one half of patients with lupus develop glomerulonephritis (GN), which often leads to renal fail

173 e (GBM), usually causing rapidly progressive glomerulonephritis (GN).

174 ce exhibit increased mortality attributed to glomerulonephritis (GN).

175 ortant differential diagnoses, such as acute glomerulonephritis (GN).

176 of T cells in the inflammatory renal disease glomerulonephritis (GN).

177 tion and is activated in glomerular cells in glomerulonephritis (GN).

178 second most common reason was recurrence of glomerulonephritis (GN; 35.3%, 6/17).

179 S lesions, including necrotizing vasculitis, glomerulonephritis, granulomatous lymphadenitis, and bro

180 ft loss varied with donor source within each glomerulonephritis group.

181 g and deceased donor transplants within each glomerulonephritis group.

182 less of renal involvement, but patients with glomerulonephritis had more DLDs per eye, larger deposit

183 susceptibility to end-organ damage in lupus glomerulonephritis have been discovered.

184 hrotoxic nephritis, wild-type (WT) mice with glomerulonephritis have elevated serum levels of S100A8/

185 ly younger, male, with lower BMI, history of glomerulonephritis, higher serum level of uric acid, and

186 ly younger, male, with lower BMI, history of glomerulonephritis, higher serum level of uric acid, and

187 ding pauci-immune necrotizing and crescentic glomerulonephritis, IgG4 immunohistochemistry had a sens

188 Moreover, in patients with crescentic glomerulonephritis, IL-26 is expressed by renal arterial

189 nephropathy (IgAN), the most common form of glomerulonephritis, implicating independent defects in a

190 tion on spontaneous recovery from autoimmune glomerulonephritis in a rat model.

191 use overexpressing PP2Ac in T cells develops glomerulonephritis in an IL-17-dependent manner.

192 ization with mouse alpha3IV-NC1 caused fatal glomerulonephritis in DBA/1 mice.

193 the mouse GBM in vivo, eliciting crescentic glomerulonephritis in Fcgr2b(-/-) mice susceptible to Ab

194 itopes in vivo influences the development of glomerulonephritis in mice passively immunized with huma

195 gen-induced arthritis in mice and crescentic glomerulonephritis in rats, in part by decreasing macrop

196 heightened susceptibility to immune-mediated glomerulonephritis in the absence of other immune defect

197 susceptibility locus that has been linked to glomerulonephritis in the NZM2410 mouse.

198 lting from experimentally induced crescentic glomerulonephritis in these rats.

199 e compared the severity of nephrotoxic serum glomerulonephritis in wild-type (WT), Axl-knockout (KO),

200 esidual genetic susceptibility to crescentic glomerulonephritis in WKY.LCrgn1,2 rats associated with

201 ment membrane and lipopolysaccharide-induced glomerulonephritis, in wild-type and heparanase-deficien

202 from kidney inflammation in T-cell-mediated glomerulonephritis, indicating therapeutic potential of

203 to track intestinal T cell mobilization upon glomerulonephritis induction, and we found that Th17 cel

204 nt findings show that transformation of mild glomerulonephritis into end-stage disease coincides with

205 Glomerulonephritis is a common and debilitating feature

206 Glomerulonephritis is a common cause of end-stage renal

207 Glomerulonephritis is a major cause of morbidity in pati

208 Glomerulonephritis is a major cause of morbidity in pati

209 Lupus glomerulonephritis is a prototype of immune complex dise

210 Mesangioproliferative glomerulonephritis is associated with overactive PDGF re

211 Rapidly progressive glomerulonephritis is characterized by glomerular necroi

212 Glomerulonephritis is one of the most serious manifestat

213 Glomerulonephritis is one of the most severe manifestati

214 lpr) mice, the progression of immune complex glomerulonephritis is only modestly diminished and the p

215 nephropathy (IgAN), the most common primary glomerulonephritis, is characterized by renal immunodepo

216 a dominant role in the progression of lupus glomerulonephritis leading to renal failure.

217 Induction of experimental glomerulonephritis led to an increased heparanase expres

218 ite the high incidence of infection-mediated glomerulonephritis, little is known about pathogenesis o

219 evere neonatal anemia, membranoproliferative glomerulonephritis, liver fibrosis, deforming arthropath

220 reas WT mice rapidly developed proliferative glomerulonephritis, marked proteinuria, and increased mo

221 Drusen-like deposits in the absence of glomerulonephritis may support the recent proposal that

222 liest manifestations of recurrent membranous glomerulonephritis (MGN) in renal allografts.

223 In an in vivo glomerulonephritis model, roscovitine treatment decrease

224 avir, lupus-prone (NZBxNZW) F(1) mice die of glomerulonephritis more than a month earlier than untrea

225 evaluated the risk of membranoproliferative glomerulonephritis (MPGN) and cryoglobulinemia in chroni

226 Membranoproliferative glomerulonephritis (MPGN) recently was reclassified to r

227 velop cryoglobulinemic membranoproliferative glomerulonephritis (MPGN).

228 onephritis (n=329); those with ANCA-negative glomerulonephritis (n=104); those with fimbriated, gram-

229 wo academic centers) from patients with ANCA glomerulonephritis (n=329); those with ANCA-negative glo

230 rence of the primary disease (n=11), de novo glomerulonephritis (n=7), T-cell-mediated rejection (n=4

231 asis, n = 2; Graves disease, n 1; membranous glomerulonephritis, n = 2; rheumatoid arthritis, n = 1;

232 at MPO-ANCA cause necrotizing and crescentic glomerulonephritis (NCGN) and vasculitis.

233 ciated vasculitis and necrotizing crescentic glomerulonephritis (NCGN).

234 oster, and poliomyelitis), and inflammatory (glomerulonephritis, nephrotic syndrome, and osteoarthrit

235 in this model of acute, neutrophil-dependent glomerulonephritis, NETs are generated in the glomerular

236 lung basement membranes, neither crescentic glomerulonephritis nor alveolitis ensued, likely because

237 e (GBM) disease is a rare form of autoimmune glomerulonephritis often accompanied by lung haemorrhage

238 d C57BL/6 x SJL mice developed hematuria and glomerulonephritis on the MR and standard diets but not

239 Prior history of glomerulonephritis or interstitial nephritis, as cause o

240 to clinical signs of experimental autoimmune glomerulonephritis or necrotizing/crescentic glomerulone

241 level off when only CKD patients affected by glomerulonephritis or systemic diseases ("progressive CK

242 splants compared to those with inflammation: glomerulonephritis (P = 0.009), viral nephropathies (P =

243 posit disease and, to a lesser extent, in C3 glomerulonephritis patients, but not in healthy controls

244 neutrophil cytoplasmic antibodies-associated glomerulonephritis, penacillamine-associated renal disea

245 Postinfectious glomerulonephritis (PIGN) is primarily a childhood disea

246 have the opposite effects on autoimmunity or glomerulonephritis, possibly as the result of compensato

247 ide potential markers for diagnosis of lupus glomerulonephritis progression and flares.

248 of T helper cells, a function important for glomerulonephritis progression.

249 though there was no significant reduction in glomerulonephritis, proteinuria, or mortality.

250 with LN (>/=2 visits with an ICD-9 code for glomerulonephritis, proteinuria, or renal failure) were

251 identified from >/=2 ICD-9 billing codes for glomerulonephritis, proteinuria, or renal failure, each

252 rain, we have identified multiple crescentic glomerulonephritis QTL (Crgn) and positionally cloned ge

253 Membranoproliferative glomerulonephritis recurred in eight patients (19%) at a

254 d increased life span, suppressed crescentic glomerulonephritis, reduced spleen size, and diminished

255 enic strain by introgressing these loci from glomerulonephritis-resistant Lewis rats onto the WKY gen

256 AV) is a common cause of rapidly progressive glomerulonephritis resulting in end-stage renal disease

257 Numerous studies indicated that glomerulonephritis results from a systemic break in B ce

258 Crescentic rapidly progressive glomerulonephritis (RPGN) represents the most aggressive

259 severe diffuse lupus nephritis by 12 weeks (glomerulonephritis scores of 2.6 +/- 0.4 versus 0.4 +/-

260 HEV-associated glomerulonephritis seems to be an HEV-related extrahepat

261 une complex-associated membranoproliferative glomerulonephritis, serum-induced endothelial C5b-9 depo

262 mor, sclerosing mesenteritis, and membranous glomerulonephritis should all be added to the list of di

263 with MPO(409-428) induced focal necrotizing glomerulonephritis similar to that seen after whole MPO

264 s, we developed a murine model of thrombotic glomerulonephritis (TGN), a known cause of acute renal f

265 hospholipid syndrome (APS) and proliferative glomerulonephritis that is markedly accelerated by the Y

266 CX3CR1 as a potential therapeutic target in glomerulonephritis that may involve fewer adverse side e

267 evelop a generalized autoimmune disease with glomerulonephritis that resembles SLE.

268 diverse clinical manifestations ranging from glomerulonephritis to neurological dysfunction.

269 ts were not present in membranoproliferative glomerulonephritis type I (adjusted hazard ratios [HRa],

270 Membranoproliferative glomerulonephritis type I [24 of 25 (96%)], with interst

271 udies of patients with membranoproliferative glomerulonephritis type I are small or have short follow

272 95% CI, 1.56-2.78) for membranoproliferative glomerulonephritis type II.

273 a new role for Ifitm3 in the pathogenesis of glomerulonephritis via a mechanism involving promoter hy

274 Proliferative glomerulonephritis was associated with infiltrating kidn

275 Lupus-related glomerulonephritis was associated with more fundus abnor

276 Glomerulonephritis was characterized by features that su

277 acrophage A2AR in progressive kidney injury, glomerulonephritis was induced in CD11b-DTR transgenic m

278 On the basis of temporal VL staging, glomerulonephritis was initiated by IgG and complement d

279 ause IL-17 is important in the expression of glomerulonephritis, we studied the mechanism through whi

280 the stability of the Th17 phenotype in acute glomerulonephritis, we subjected nephritic mice to CD3-s

281 rapeutic intervention in rapidly progressive glomerulonephritis, we treated mice with established glo

282 mmune complex deposition in the kidneys, and glomerulonephritis were examined.

283 t, no significant differences in severity of glomerulonephritis were observed between groups.

284 Younger age, living donor graft, and chronic glomerulonephritis were significantly associated with re

285 basement membrane-induced (anti-GBM-induced) glomerulonephritis when expressed on murine neutrophils.

286 to Rag1(-/-) mice induced focal necrotizing glomerulonephritis when glomerular MPO deposition was in

287 levels and developed mesangial proliferative glomerulonephritis, which resembled systemic lupus eryth

288 ) mice spontaneously developed proliferative glomerulonephritis, which was accelerated in a chronic s

289 eficient mice in both models of experimental glomerulonephritis, which was accompanied by a better re

290 Patients with glomerulonephritis who achieved SVR12 experienced an imp

291 Lyn(+/-) mice develop IgG autoantibodies and glomerulonephritis with age.

292 op anti-GBM antibodies and focal necrotizing glomerulonephritis with crescent formation.

293 Alport syndrome, hereditary glomerulonephritis with hearing loss, results from mutat

294 We conclude that proliferative glomerulonephritis with monoclonal IgG deposits does not

295 e report the largest series of proliferative glomerulonephritis with monoclonal IgG deposits, a form

296 onephritis, we treated mice with established glomerulonephritis with nutlin-3a.

297 dentify a dual role for CCN3 in experimental glomerulonephritis with pro-angiogenic and antimesangiop

298 nephropathy (IgAN), the most common form of glomerulonephritis, with discovery and follow-up in 20,6

299 ted mice had mild pauci-immune proliferative glomerulonephritis, with infiltration of human and mouse

300 Mer-KO mice developed severe glomerulonephritis, with significantly decreased surviva