ライフサイエンスコーパス: lupus nephritis

1 odels of ATN and acute GN (NZM2410 mice with lupus nephritis).

2 n this pathway may serve as early markers in lupus nephritis.

3 at1 and Stat3 has been reported in lupus and lupus nephritis.

4 cesses involved in tissue injury relating to lupus nephritis.

5 n identified as playing an important role in lupus nephritis.

6 t is still being used in refractory cases of lupus nephritis.

7 he pathogenesis, diagnosis, and treatment of lupus nephritis.

8 ing the accelerated and deteriorated type of lupus nephritis.

9 tissues, but also in the inflamed kidney in lupus nephritis.

10 il prior to pregnancy in patients with quiet lupus nephritis.

11 compartments in both human and experimental lupus nephritis.

12 role for the NLRP3 inflammasome in mediating lupus nephritis.

13 els, proteinuria, and histologic features of lupus nephritis.

14 idney promote renal disease in patients with lupus nephritis.

15 isease in both the murine and human forms of lupus nephritis.

16 re, we translate these observations to human lupus nephritis.

17 titative renal biomarker of kidney injury in lupus nephritis.

18 the aspects of disease progression in human lupus nephritis.

19 ers of specific histologic manifestations of lupus nephritis.

20 quantified in urine, correlates with active lupus nephritis.

21 patients with class IV-S and those with IV-G lupus nephritis.

22 autoantibody-induced inflammation, including lupus nephritis.

23 flammation, and thereby hastens the onset of lupus nephritis.

24 urther examine the potential of abatacept in lupus nephritis.

25 r conducting further studies of abatacept in lupus nephritis.

26 IgM in these mice confer protection against lupus nephritis.

27 nti-glomerular basement membrane disease and lupus nephritis.

28 ne level, renal flare, or rescue therapy for lupus nephritis.

29 -dsDNA resulted in a dramatic improvement in lupus nephritis.

30 as combined membranous and focal or diffuse lupus nephritis.

31 oduction and significantly delays death from lupus nephritis.

32 ng the protection and treatment of mice with lupus nephritis.

33 r prognostic factors: young age-of-onset and lupus nephritis.

34 ing their recruitment into the kidney during lupus nephritis.

35 prevent relapse after the initial control of lupus nephritis.

36 phamide (IVC) for the induction treatment of lupus nephritis.

37 d with increased disease activity and active lupus nephritis.

38 orine, may be beneficial in the treatment of lupus nephritis.

39 therapy of both proliferative and membranous lupus nephritis.

40 hages in aggressive proliferative lesions of lupus nephritis.

41 icensed for use in induction of remission in lupus nephritis.

42 st a role for tacrolimus in the treatment of lupus nephritis.

43 m of immune complexes in the pathogenesis of lupus nephritis.

44 s well as in mice with spontaneously arising lupus nephritis.

45 immunosuppressive medications in women with lupus nephritis.

46 acrophages and autoantibodies are central to lupus nephritis.

47 rane [anti-GBM antibodies]), and spontaneous lupus nephritis.

48 hosphamide for the induction of remission in lupus nephritis.

49 ronic transplant rejection and recurrence of lupus nephritis.

50 g diabetic nephropathy, IgA nephropathy, and lupus nephritis.

51 to anti-GBM antibody-induced and spontaneous lupus nephritis.

52 CSF-1 is a potential therapeutic target for lupus nephritis.

53 s superior to IVC as induction treatment for lupus nephritis.

54 prominent in a mouse model (MRL-Fas(lpr)) of lupus nephritis.

55 was independently associated with recurrent lupus nephritis.

56 ission induction and maintenance therapy for lupus nephritis.

57 ive to cyclophosphamide for the treatment of lupus nephritis.

58 ed with the histopathology activity index of lupus nephritis.

59 ecision aid for immunosuppressive therapy in lupus nephritis.

60 he cFMS and PTPRZ receptors in patients with lupus nephritis.

61 the utility of these biomarkers in tracking lupus nephritis.

62 g novel therapeutic target for patients with lupus nephritis.

63 osals for the histological classification of lupus nephritis.

64 tial areas of individuals with proliferative lupus nephritis.

65 we show that BAFF promotes events leading to lupus nephritis.

66 ong been thought to promote inflammation and lupus nephritis.

67 ent of immune-mediated nephropathies like in lupus nephritis.

68 ulonephritis and in a mouse chronic model of lupus nephritis.

69 ficant B cell expansion, BAFF secretion, and lupus nephritis.

70 ajor unmet need for successful management of lupus nephritis.

71 acerbate underlying pathogenic mechanisms in lupus nephritis.

72 l cells associates with viral infections and lupus nephritis.

73 10 wk of age and steadily increases prior to lupus nephritis.

74 rrelate with the occurrence of proliferative lupus nephritis.

75 een developed to explain the pathogenesis of lupus nephritis.

76 cient mice develop systemic autoimmunity and lupus-nephritis.

77 diagnosed with crescentic transformation of lupus nephritis, 1 was diagnosed with anti-GBM nephritis

78 nformation to be excellent for understanding lupus nephritis (49% versus 33%), risk factors (43% vers

79 tasis have been identified as biomarkers for lupus nephritis, a serious complication of systemic lupu

80 ctivity biomarker that varies over time with lupus nephritis activity and treatment.

81 European descent with SLE (588 patients with lupus nephritis and 1412 patients with lupus without nep

82 ding the endothelium - with implications for lupus nephritis and accelerated atherosclerosis.

83 ion by bone marrow cells severely aggravated lupus nephritis and accelerated death.

84 Recurrent lupus nephritis and chronic rejection of the kidney tran

85 TNIP1 gene are associated with the risk for lupus nephritis and could be mechanistically involved in

86 of profibrotic markers in animal models with lupus nephritis and folic acid nephropathy.

87 e analyzed kidney samples from patients with lupus nephritis and from healthy control subjects using

88 XCR4/CXCL12 in lymphoproliferative lupus and lupus nephritis and highlight this axis as a promising t

89 what we know about processes that may cause lupus nephritis and how such basic processes may be affe

90 ession in kidney biopsies from patients with lupus nephritis and identified miR-150 as the most diffe

91 RIIA and FcgammaRIIIB on neutrophils induces lupus nephritis and in some cases arthritis only when th

92 ry CD163 reflects histologic inflammation in lupus nephritis and is a promising activity biomarker th

93 lycosphingolipid metabolism in patients with lupus nephritis and MRL/lpr lupus mice.

94 to the adoption of MMF for the treatment of lupus nephritis and nonrenal lupus.

95 ment of drugs to prevent, and perhaps treat, lupus nephritis and other autoinflammatory diseases caus

96 e type IV as a valuable treatment target for lupus nephritis and point out the importance of local ki

97 of MRL/lpr mice with dipyridamole alleviated lupus nephritis and prevented the appearance of skin ulc

98 te on the pathogenic mechanisms that lead to lupus nephritis and provide the rationale for the latest

99 e loss of CfH accelerates the development of lupus nephritis and recapitulates the functional and str

100 ere we report that clinical and pathological lupus nephritis and serum anti-nuclear Ab levels are gre

101 the kidneys of lupus mice and patients with lupus nephritis and suggest that molecules in this pathw

102 ls play an important role in protection from lupus nephritis and suggest that the NAA B cells may hav

103 hanisms promote lupus nephritis, we compared lupus nephritis and systemic illness in MRL-Fas(lpr) mic

104 NZW) mouse model of interferon-alpha-induced lupus nephritis and treated mice with TNF receptor type

105 23R-mediated signaling in the development of lupus nephritis and urge the consideration of proper bio

106 Five MRL/lpr mice (a model of lupus nephritis) and six C57BL/6 wild-type mice were ass

107 tive syndrome, production of anti-dsDNA Abs, lupus nephritis, and accumulation of CD3(+)B220(+)CD4(-)

108 r disease entities, such as IgA nephropathy, lupus nephritis, and ANCA GN; and additional features as

109 patients with refractory disease, including lupus nephritis, and antibody-mediated cytopenias, possi

110 oved survival in patients with proliferative lupus nephritis, and combined administration of these ag

111 e glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropathy.

112 he kidney, serum, and urine of patients with lupus nephritis, and eliminating CSF-1 suppresses lupus

113 T cells infiltrate kidneys of patients with lupus nephritis, and IL-23-treated lymph node cells from

114 mplify autoantibody production that leads to lupus nephritis, and in individuals with SLE IgE autoant

115 of complement activation in dermatomyositis, lupus nephritis, and necrotic muscle fibres in Duchenne

116 a, as well as disease susceptibility to HIV, lupus nephritis, and psoriasis among many other clinical

117 anous nephropathy, membranoproliferative GN, lupus nephritis, and vasculitis associated with HRs (95%

118 addition, clinical and pathology measures of lupus nephritis are abrogated.

119 Biologic agents for the treatment of lupus nephritis are being studied, including belimumab w

120 ploration, as current therapeutics targeting lupus nephritis are limited and, thus, in great demand.

121 , all vehicle-injected mice developed severe lupus nephritis, as evidenced by increased proteinuria (

122 tients with SLE may reduce the occurrence of lupus nephritis, as well as diminish the risk of acceler

123 Treatment of accelerated and severe lupus nephritis (ASLN) mice with Tris DBA resulted in im

124 ALMS) trial of mycophenolate mofetil, 3) the Lupus Nephritis Assessment with Rituximab (LUNAR) trial

125 Still, major limitations in the LUpus Nephritis Assessment with Rituximab (LUNAR) trial,

126 netic factors underlying the pathogenesis of lupus nephritis associated with systemic lupus erythemat

127 Children ages 5-18 years with new-onset lupus nephritis-associated ESRD were identified in the U

128 Among US children with lupus nephritis-associated ESRD, age, race, ethnicity, t

129 A total of 583 children had incident lupus nephritis-associated ESRD.

130 nephritis revealed strong associations with lupus nephritis at rs7708392 in European Americans and r

131 ate that in more than half of a cohort of 68 lupus nephritis biopsies, the tubulointerstitial infiltr

132 vivo, as evidenced by gene array analysis of lupus nephritis biopsies.

133 e discuss current therapeutic strategies for lupus nephritis, briefly review recent advances in under

134 emistry of renal biopsies from patients with lupus nephritis, but not anti-neutrophil cytoplasmic Ab-

135 cyclophosphamide (IVC) for the treatment of lupus nephritis, but these therapies have not been compa

136 icient MRL-lpr mice developed severe diffuse lupus nephritis by 12 weeks (glomerulonephritis scores o

137 ce elevated autoantibody levels and promoted lupus nephritis by inducing BAFF production in the kidne

138 AFF plays a previously unappreciated role in lupus nephritis by inducing renal TLSs and regulating th

139 ation profile contribute to tissue damage in lupus nephritis by mediating both local inflammation and

140 xplore the potential for renal protection in lupus nephritis by targeting this pathway, we introduced

141 In lupus nephritis, C5-b9 deposits co-localized with IgG, I

142 In human lupus nephritis, CDM confirmed that myeloid DCs present

143 New Zealand White) F1 (NZB/W) mouse model of lupus nephritis compared with healthy New Zealand White

144 ly decreased in SLE patients especially with lupus nephritis, compared to healthy controls.

145 ed systemic lupus erythematosus and class IV lupus nephritis confirmed with biopsy and treated with m

146 the current approaches to the management of lupus nephritis continue to rely on high-dose corticoste

147 The histopathologic classification of lupus nephritis continues to guide therapy, and treatmen

148 changes in renal iron homeostasis occurs in lupus nephritis, contributing to the development of kidn

149 A previous study of anti-C1q in experimental lupus nephritis demonstrated an important role for Fcgam

150 Lupus nephritis demonstrates familial aggregation and ac

151 CD163 mRNA than did those from patients with lupus nephritis, diabetic nephropathy, or nephrotic synd

152 1/EXT2 staining was detected in pure class 5 lupus nephritis (eight of 18 patients) and in presumed p

153 Patients with incident lupus nephritis ESRD (1995-2006) were identified in the

154 SIRs for lupus nephritis ESRD among those who were ages 5-39 year

155 te that the characteristics of patients with lupus nephritis ESRD and initial therapies have changed

156 s, treatments, and outcomes of patients with lupus nephritis ESRD.

157 We identified 12,344 incident cases of lupus nephritis ESRD.

158 ell depletion with rituximab in nonlupus and lupus nephritis (Explorer and Lunar, respectively) did n

159 We measured urine CD163 at lupus nephritis flares in patients from a Mexican cohort

160 has been the standard induction regimen for lupus nephritis, followed by a maintenance regimen of qu

161 reated mice were protected from the onset of lupus nephritis for 10 wk, with significantly improved s

162 d compared, 16 patients with newly diagnosed lupus nephritis from whom multiple samples were obtained

163 last year, complete and partial remission in lupus nephritis has been achieved in 60-89% of cases.

164 to kidney biopsy samples from patients with lupus nephritis has begun to define the phenotypes of bo

165 The treatment of lupus nephritis has changed significantly over the past

166 rapy, and treatment for all major classes of lupus nephritis has seen some shift in management during

167 chanism by which anti-DNA antibodies mediate lupus nephritis has yet to be conclusively determined.

168 Recent clinical trials in lupus nephritis have all used different criteria to asse

169 mmune mechanisms that cause tissue injury in lupus nephritis have been challenging to define.

170 Clinical trials of therapies for lupus nephritis have used many different primary outcome

171 d with a shorter time-to-event for recurrent lupus nephritis (hazard ratio [HR] 4.63, 95% confidence

172 in vivo prevented the formation of TLSs and lupus nephritis; however, it did not reduce immune cell

173 liferative GN (HR, 0.84; 95% CI, 0.76-0.92), lupus nephritis (HR, 0.69; 95% CI, 0.66-0.71), vasculiti

174 IgAN, for those with secondary GN subtypes: lupus nephritis [HR,0.91; 95% CI, 0.86-0.97], vasculitis

175 seases, with closest interconnection between lupus nephritis, IgA nephritis, and diabetic nephropathy

176 data set from a large trial of abatacept in lupus nephritis (IM101075).

177 MF and IVC as induction treatment for active lupus nephritis in a multinational, two-phase (induction

178 nd Renal Pathology Society classification of lupus nephritis in adult patients.

179 h17 cells and consequently developed reduced lupus nephritis in comparison with wild-type mice.

180 p progressive GN similar to class III and IV lupus nephritis in humans.

181 they age and succumb to a disease resembling lupus nephritis in humans.

182 mation, and triggers more severe early-onset lupus nephritis in MRL-Fas(lpr) mice.

183 reasing systemic CSF-1 hastened the onset of lupus nephritis in MRL-Fas(lpr) mice.

184 IL-34 and its two receptors increase during lupus nephritis in MRL-Fas(lpr) mice.

185 h collagen-induced arthritis and spontaneous lupus nephritis in MRL/lpr mice.

186 ular and humoral autoimmune responses during lupus nephritis in NZB/W F1 mice and emphasize the poten

187 polyinosinic: polycytidylic acid-accelerated lupus nephritis in NZB/W mice that is characterized by s

188 ving inflammation, and, in turn, early-onset lupus nephritis in preclinical MRL/MpJ-Faslpr/Fas(lpr) m

189 generating an autoimmune response to SmD and lupus nephritis in the NZM2328 background.

190 us, which has the strongest association with lupus nephritis in the NZM2410 mouse model.

191 erion OR the patient must have biopsy-proven lupus nephritis in the presence of antinuclear antibodie

192 estimates of the prevalence and incidence of lupus nephritis in the US to date.

193 ting factor (BAFF)) for use in patients with lupus nephritis in the USA and in difficult-to-treat pat

194 he prevalence and incidence rates of SLE and lupus nephritis increased with age, were higher in girls

195 d the strongest evidence of association with lupus nephritis independent of HLA-DR2 and HLA-DR3 (P=8.

196 Consistent with a functional role in lupus nephritis, intra-renal mRNA levels of PDGFRA and a

197 The pathogenesis of lupus nephritis involves a variety of pathogenic mechani

198 The intrarenal etiology of lupus nephritis involves antibody binding to multiple in

199 Lupus nephritis is a manifestation of SLE resulting from

200 Lupus nephritis is a potentially devastating complicatio

201 Lupus nephritis is a potentially fatal autoimmune diseas

202 Lupus nephritis is an immune complex GN that develops as

203 Recurrent lupus nephritis is infrequent and relatively benign, wit

204 ee themes, the pathogenic role of T cells in lupus nephritis is not clear.

205 Lupus nephritis is the most common target-organ manifest

206 bclasses of diffuse proliferative (class IV) lupus nephritis is unknown.

207 ession of certain miRs has been described in lupus nephritis, it is unknown whether miRs contribute t

208 f-reactive antibodies can target the kidney (lupus nephritis), leading to functional failure and poss

209 IgM anti-dsDNA protected MRL/lpr mice from lupus nephritis, likely by stopping the inflammatory cas

210 Juvenile-onset lupus nephritis (LN) affects up to 80% of juvenile-onset

211 ells infiltrate the kidneys of patients with lupus nephritis (LN) and are critical for the pathogenes

212 to renal damage and to the heterogeneity of lupus nephritis (LN) are not well understood.

213 Renal targets of autoimmunity in human lupus nephritis (LN) are unknown.

214 means to predict the onset and recurrence of lupus nephritis (LN) before overt renal injury is needed

215 Management of patient with Lupus Nephritis (LN) continues to remain a challenge for

216 Systemic lupus erythematosus (SLE) and lupus nephritis (LN) disproportionately affect individua

217 renal transplant outcomes in recipients with lupus nephritis (LN) has not been reported.

218 s with end-stage renal disease (ESRD) due to lupus nephritis (LN) have high rates of premature death.

219 Lupus nephritis (LN) is a common manifestation of system

220 Lupus nephritis (LN) is a complication of the autoimmune

221 Lupus nephritis (LN) is a form of glomerulonephritis tha

222 Lupus nephritis (LN) is a major contributor to morbidity

223 Lupus nephritis (LN) is a potentially dangerous end orga

224 Lupus nephritis (LN) is a serious manifestation of syste

225 Lupus nephritis (LN) is an autoimmune disease that occur

226 ced in the kidneys of both NZB/W F1 mice and lupus nephritis (LN) patients.

227 Treatment of lupus nephritis (LN) remains challenging.

228 y membranous nephropathy (MN) and eight with lupus nephritis (LN) served as controls.

229 IgAN and systemic lupus erythematosus (SLE)/lupus nephritis (LN) shared many loci based on GWAS on C

230 Lupus nephritis (LN) was the most common secondary glome

231 Biopsy samples (n = 14) from patients with lupus nephritis (LN) were immunostained with anti-CXCL12

232 d-derived cells is a key pathogenic event in lupus nephritis (LN), but the process is poorly understo

233 G2 are associated with faster progression to lupus nephritis (LN)-associated end-stage renal disease

234 rkers continue to show promise in evaluating lupus nephritis (LN).

235 1q) are potential targets of autoimmunity in lupus nephritis (LN).

236 tients with systemic lupus erythematosus and lupus nephritis (LN).

237 ntly improves renal disease in a spontaneous lupus nephritis model through prevention of the direct i

238 zed controlled trial (RCT), adult women with lupus nephritis, mostly from racial/ethnic minority back

239 gA nephropathy (n = 5), diabetes (n = 7), or lupus nephritis (n = 1).

240 owed significant enrichment in patients with lupus nephritis (n=32) compared with controls (n=15).

241 Despite several large clinical trials in lupus nephritis, no second line drug is licensed for use

242 in the glomerular podocytes of patients with lupus nephritis or focal segmental GN but not in normal

243 Compared with samples from patients with lupus nephritis or healthy black controls, AASK-N sample

244 end-stage renal disease (ESRD) secondary to lupus nephritis, or in the characteristics, treatments,

245 ty loci, showed evidence of association with lupus nephritis (P=0.06 and P=3.7x10(-5), respectively).

246 he past decade, an improved understanding of lupus nephritis pathogenesis fueled several clinical tri

247 factors have all been recently implicated in lupus nephritis pathogenesis.

248 In the lupus nephritis patients, anti-Apo A-I and anti-HDL leve

249 rmal salivary glands or kidney biopsies from lupus nephritis patients.

250 within the kidney has the capacity to dampen lupus nephritis, possibly by modulating inflammation and

251 -wide association studies of SLE to identify lupus nephritis-predisposing loci.

252 Although IL-6 is proinflammatory in murine lupus nephritis, protective effects have been observed f

253 his large-scale genome-wide investigation of lupus nephritis provide evidence of multiple biologicall

254 e, the disappointing results of rituximab in lupus nephritis provided a clinical and mechanistic coun

255 rarenal CSF-1, promotes macrophage-dependent lupus nephritis remain unclear.

256 Patients with active lupus nephritis (renal biopsy class III, IV, or V) were

257 r, of the children with SLE, 1,106 (37%) had lupus nephritis, representing a prevalence of 3.64 (95%

258 MRL/lpr or BWF1 mice with established SLE or lupus nephritis, respectively, were treated orally with

259 The frequency and outcome of recurrent lupus nephritis (RLN) among recipients of a kidney allog

260 oteins were associated with renal disease in lupus nephritis samples.

261 With advancing lupus nephritis, spCSF-1 was the predominant isoform res

262 nt role for FcgammaRs in the pathogenesis of lupus nephritis, suggesting a direct effect on phagocyte

263 ates systemic autoimmunity, but also impacts lupus nephritis, suggesting that IFN-I may be acting at

264 e evidence of multiple biologically relevant lupus nephritis susceptibility loci.

265 ythematosus (SLE) and a higher prevalence of lupus nephritis than do Caucasians.

266 significantly higher in patients with active lupus nephritis than in patients with active extrarenal

267 n increase in survival and an improvement in lupus nephritis that exceeded that of MRL/lpr mice lacki

268 t there are different pathogenic pathways in lupus nephritis, the emerging pathogenic mechanism(s) ma

269 In patients with recurrent lupus nephritis, the lesion in the engrafted kidney was

270 re increasing opportunities in patients with lupus nephritis to offer treatments tailored to the indi

271 gned 370 patients with classes III through V lupus nephritis to open-label MMF (target dosage 3 g/d)

272 m a large, multicenter trial of abatacept in lupus nephritis, to gain insight into which outcome meas

273 en to investigate whether recent advances in lupus nephritis treatment have led to changes in the inc

274 t survival improved, the goals for advancing lupus nephritis treatment shifted to identifying therapi

275 promise to improve upon the standard-of-care lupus nephritis treatments.

276 of complete response can determine whether a lupus nephritis trial is interpreted as a success or a f

277 the ability to detect therapeutic benefit in lupus nephritis trials.

278 cytoplasmic antibody-mediated crescentic GN, lupus nephritis, type I membranoproliferative GN), and n

279 Treatment of lupus nephritis urine samples with 0.5% acetic acid prod

280 as 2.22 cases (95% CI 2.05-2.40) and that of lupus nephritis was 0.72 cases (95% CI 0.63-0.83) per 10

281 M antibody-induced nephritis and spontaneous lupus nephritis was achieved by breeding mice with a gen

282 The presence of lupus nephritis was associated with the expression of CD

283 Lupus nephritis was identified from >/=2 ICD-9 billing c

284 Recurrent lupus nephritis was noted in 20 patients (11%), allograf

285 one of the 14 cases of mixed class 5 and 3/4 lupus nephritis was positive for EXT1/EXT2.

286 t intrarenal and systemic mechanisms promote lupus nephritis, we compared lupus nephritis and systemi

287 ate the distinct functions of Axl and Mer in lupus nephritis, we compared the severity of nephrotoxic

288 f immune complexes in the pathophysiology of lupus nephritis, we studied the role of CfH in the devel

289 The prevalence and incidence of SLE and lupus nephritis were calculated among Medicaid-enrolled

290 ivity Index (SLEDAI) scores, and presence of lupus nephritis were determined.

291 Finally, both human SLE and spontaneous lupus nephritis were found to be associated with kallikr

292 atients (n = 144) with class III or class IV lupus nephritis were randomized 1:1 to receive rituximab

293 t and in preventing relapse in patients with lupus nephritis who had a response to induction therapy.

294 Clinical distinction between patients with lupus nephritis who have active inflammation or chronic

295 s appear translatable to human patients with lupus nephritis, whose expression of IL-34, cFMS, and PT

296 IL-23R(-/-)MRL.lpr mice displayed attenuated lupus nephritis with a striking decrease in the accumula

297 consider the challenges in the management of lupus nephritis with respect to diagnosis and optimal th

298 literature on how to most effectively treat lupus nephritis with the least amount of toxicity.

299 as novel biomarkers of anti-GBM disease and lupus nephritis, with stronger correlation to renal dise

300 ancestry protects against the development of lupus nephritis, with the aim of exploring the genetic a