ライフサイエンスコーパス: glomerulonephritis

1 hil cytoplasmatic antibody (ANCA)-associated glomerulonephritis.

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

3 e-emptive treatment in abrogating crescentic glomerulonephritis.

4 ate injury in complement-dependent models of glomerulonephritis.

5 ctional role in the normal glomerulus and in glomerulonephritis.

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

7 and attenuated renal tissue damage in acute glomerulonephritis.

8 e with elevated autoantibody levels and mild glomerulonephritis.

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

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

11 blockade may be a new therapeutic target in glomerulonephritis.

12 a naturally occurring model of VL-associated glomerulonephritis.

13 re needed to induce a necrotizing/crescentic glomerulonephritis.

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

15 glomerulonephritis or necrotizing/crescentic glomerulonephritis.

16 imilar, or increased, risk of infections and glomerulonephritis.

17 y and thereby promotes renal inflammation in glomerulonephritis.

18 ponses are critical for the phenotype of the glomerulonephritis.

19 op high titers of antinuclear Abs and severe glomerulonephritis.

20 renal function in a rat model of crescentic glomerulonephritis.

21 r the development of immune complex-mediated glomerulonephritis.

22 s including anti-DNA antibody production and glomerulonephritis.

23 rrent bacterial infections and proliferative glomerulonephritis.

24 from development of lupus autoantibodies and glomerulonephritis.

25 which deposit in their kidneys, resulting in glomerulonephritis.

26 deposition, and tissue inflammation such as glomerulonephritis.

27 f HIV nephropathy and in collapsing forms of glomerulonephritis.

28 evidenced by anti-nuclear Ab deposition and glomerulonephritis.

29 unich Wistar Fromter rats with proliferative glomerulonephritis.

30 utoimmune nature of this most common primary glomerulonephritis.

31 scentic lesions in a patient with crescentic glomerulonephritis.

32 immune complex deposition leading to chronic glomerulonephritis.

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

34 itional level of protection from Ab-mediated glomerulonephritis.

35 ases such as antibody-mediated rejection and glomerulonephritis.

36 e, including acute rheumatic fever and acute glomerulonephritis.

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

38 els of hypertension-induced renal damage and glomerulonephritis.

39 re mediated by PR3 or elastase during active glomerulonephritis.

40 al hemolytic uremic syndrome and symptoms of glomerulonephritis.

41 neutralization abrogated the development of glomerulonephritis.

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

43 d were largely protected from development of glomerulonephritis.

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

45 merular endothelial cell (GEC) injury during glomerulonephritis.

46 e, including vasculitic lesion formation and glomerulonephritis.

47 Rs) are potential serine protease targets in glomerulonephritis.

48 e of his renal failure was poststreptococcal glomerulonephritis.

49 95% CI: 0.40, 0.68; P < .001) in identifying glomerulonephritis.

50 and proinflammatory cytokine production, and glomerulonephritis.

51 cytoplasmic antibodies-related pauci-immune glomerulonephritis.

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

53 ingle most predictive marker of histological glomerulonephritis.

54 e mouse GBM in vivo nor induced experimental glomerulonephritis.

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

56 biopsy of at least one individual showed C3 glomerulonephritis.

57 chronic serum sickness-induced proliferative glomerulonephritis.

58 eptible to experimentally induced crescentic glomerulonephritis.

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

60 ermines glomerular damage in immune-mediated glomerulonephritis.

61 alloantibodies mediating rapidly progressive glomerulonephritis.

62 eresis, and 2 of these grafts were lost from glomerulonephritis.

63 d vasculitis (AAV), with rapidly progressive glomerulonephritis.

64 onic elastography for the early detection of glomerulonephritis.

65 een documented in glomeruli of patients with glomerulonephritis.

66 eased the IFN signature, pDC activation, and glomerulonephritis.

67 eys, where they cause necrotizing crescentic glomerulonephritis.

68 n in post-infectious and rapidly progressive glomerulonephritis.

69 One patient experienced posttransplant C3 glomerulonephritis.

70 repression in the rat strain susceptible to glomerulonephritis.

71 en monocytes and neutrophils in induction of glomerulonephritis.

72 therapeutic strategy in rapidly progressive glomerulonephritis.

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

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

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

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

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

78 mation in the kidneys as well as scoring for glomerulonephritis activity.

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

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

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

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

83 Glomerulonephritis and acute tubular necrosis were prese

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

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

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

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

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

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

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

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

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

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

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

95 7 cells in a mouse model of acute crescentic glomerulonephritis and in a mouse chronic model of lupus

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

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

98 Kidneys develop glomerulonephritis and proteinuria, reflecting tissue in

99 This included membranoproliferative glomerulonephritis and relapses in IgA nephropathy.

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

101 al cortex SWS was lower in participants with glomerulonephritis and stage 1 CKD (preserved renal func

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

103 55 years; 30 with and 30 without SLE-related glomerulonephritis) and 60 age- and sex-matched healthy

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

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

106 disorders, chronic kidney disease and acute glomerulonephritis, and diabetes have been increasing.

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

108 , recurrent bacterial infections, crescentic glomerulonephritis, and end-stage renal failure.

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

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

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

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

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

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

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

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

117 or over a century, acute 'post-streptococcal glomerulonephritis' (APSGN) was the prototypical form of

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

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

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

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

122 We report that proliferative glomerulonephritis arose only in the presence of all thr

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

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

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

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

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

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

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

130 lopathy - dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) - have overlapping clinical an

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

132 C3 glomerulonephritis (C3GN) results from abnormalities in

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

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

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

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

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

138 tal glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CGN) remain poorly understood.

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

140 otic syndrome diagnosis codes exceed that of glomerulonephritis codes identified children with nephro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 li is suspected to promote tissue injury and glomerulonephritis (GN).

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

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

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

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

174 g and deceased donor transplants within each glomerulonephritis group.

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

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

177 erosis (FSGS), LN and hepatitis B associated glomerulonephritis (HBV-GN) significantly decreased betw

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

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

180 sing an Institute of Cancer Research-derived glomerulonephritis (ICGN) mouse model of nephrosis, we e

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

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

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

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

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

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

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

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

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

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

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

192 lting from experimentally induced crescentic glomerulonephritis in these rats.

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

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

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

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

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

198 Glomerulonephritis is a common and debilitating feature

199 Glomerulonephritis is a common cause of end-stage renal

200 Glomerulonephritis is a major cause of morbidity in pati

201 Glomerulonephritis is a major cause of morbidity in pati

202 Rapidly progressive glomerulonephritis is characterized by glomerular necroi

203 Glomerulonephritis is one of the most serious manifestat

204 Glomerulonephritis is one of the most severe manifestati

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

206 Induction of experimental glomerulonephritis led to an increased heparanase expres

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

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

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

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

211 Results Fifty-three participants with glomerulonephritis (mean age +/- standard deviation, 49

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

213 gonism protects mice from a T-cell-dependent glomerulonephritis model by inhibition of T-cell prolife

214 In an in vivo glomerulonephritis model, roscovitine treatment decrease

215 lomerular basement membrane antibody-induced glomerulonephritis model.

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

217 Membranoproliferative glomerulonephritis (MPGN) recently was reclassified to r

218 me trend appeared with membranoproliferative glomerulonephritis (MPGN), diabetic nephropathy (DN) and

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

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

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

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

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

224 ciated vasculitis and necrotizing crescentic glomerulonephritis (NCGN).

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

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

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

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

229 act (ten out of 55 individuals), and chronic glomerulonephritis (one out of seven individuals).

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

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

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

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

234 tography depicts abnormal renal stiffness in glomerulonephritis, particularly among patients with ear

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

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

237 (IgAN, 24.09%) were the most common primary glomerulonephritis (PGN).

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

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

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

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

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

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

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

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

246 Background Glomerulonephritis refers to renal diseases characterize

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

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

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

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

251 Staphylococcus infection-associated glomerulonephritis (SAGN) and primary IgA nephropathy (I

252 umber of Staphylococcus infection-associated glomerulonephritis (SAGN) cases increased owing to a sur

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

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

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

256 nephritis (LN) was the most common secondary glomerulonephritis (SGN) in adults, while Henoch-Schonle

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

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

259 ted renal SWS was lower in participants with glomerulonephritis than in healthy volunteers in the par

260 Lupus nephritis (LN) is a form of glomerulonephritis that constitutes one of the most seve

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

262 ulin deposits (PGNMID) is a distinct form of glomerulonephritis that often recurs after kidney transp

263 diverse clinical manifestations ranging from glomerulonephritis to neurological dysfunction.

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

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

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

267 lytic uremic syndrome, membranoproliferative glomerulonephritis type II, and paroxysmal nocturnal hem

268 95% CI, 1.56-2.78) for membranoproliferative glomerulonephritis type II.

269 pical form of bacterial infection-associated glomerulonephritis, typically occurring after resolution

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

271 Lupus-related glomerulonephritis was associated with more fundus abnor

272 Glomerulonephritis was characterized by features that su

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

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

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

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

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

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

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

280 2017, study participants with biopsy-proven glomerulonephritis were prospectively examined with US t

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

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

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

284 a plasmid expressing 6PGD(391-410), develop glomerulonephritis when MPO is deposited in glomeruli.

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

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

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

288 Patients with glomerulonephritis who achieved SVR12 experienced an imp

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

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

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

292 ded the following 26 patients: proliferative glomerulonephritis with MIg deposits (PGNMID) (n = 13),

293 e cohort included 26 patients: proliferative glomerulonephritis with MIg deposits (PGNMID) (n=13), AL

294 Proliferative glomerulonephritis with monoclonal immunoglobulin deposi

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

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

297 teinuria, and their renal pathology revealed glomerulonephritis with typical abnormalities, such as m

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