ライフサイエンスコーパス: nephritis

1 phritis and 1412 patients with lupus without nephritis).

2 a murine model of crescentic GN (nephrotoxic nephritis).

3 loid cells was sufficient to protect against nephritis.

4 nephritis, viral nephritis, and interstitial nephritis.

5 en thought to promote inflammation and lupus nephritis.

6 ficiency, two with pneumonitis, and one with nephritis.

7 nd anti-glomerular basement membrane-induced nephritis.

8 injury in experimental, crescentic anti-GBM nephritis.

9 etention of neutrophils in antibody-mediated nephritis.

10 ular parietal epithelial cells in crescentic nephritis.

11 immune-mediated nephropathies like in lupus nephritis.

12 etermine common pathways in murine and human nephritis.

13 sangial compartment in mesangioproliferative nephritis.

14 hritis and in a mouse chronic model of lupus nephritis.

15 B cell expansion, BAFF secretion, and lupus nephritis.

16 nmet need for successful management of lupus nephritis.

17 te underlying pathogenic mechanisms in lupus nephritis.

18 the kidney by accelerated serum nephrotoxic nephritis.

19 s associates with viral infections and lupus nephritis.

20 of age and steadily increases prior to lupus nephritis.

21 s-like autoimmune disease with strong kidney nephritis.

22 e with the occurrence of proliferative lupus nephritis.

23 veloped to explain the pathogenesis of lupus nephritis.

24 sary to identify targets that do not promote nephritis.

25 pathway may serve as early markers in lupus nephritis.

26 d Stat3 has been reported in lupus and lupus nephritis.

27 ysfunction that suggested acute interstitial nephritis.

28 involved in tissue injury relating to lupus nephritis.

29 ion and targeted therapies for patients with nephritis.

30 (TLR7) is sufficient for the development of nephritis.

31 tified as playing an important role in lupus nephritis.

32 till being used in refractory cases of lupus nephritis.

33 hogenesis, diagnosis, and treatment of lupus nephritis.

34 es, but also in the inflamed kidney in lupus nephritis.

35 or to pregnancy in patients with quiet lupus nephritis.

36 tment in a murine model of antibody-mediated nephritis.

37 rtments in both human and experimental lupus nephritis.

38 or the NLRP3 inflammasome in mediating lupus nephritis.

39 roteinuria, and histologic features of lupus nephritis.

40 classes that mediate posttransplant anti-GBM nephritis.

41 uent production of autoantibodies and severe nephritis.

42 promote renal disease in patients with lupus nephritis.

43 in both the murine and human forms of lupus nephritis.

44 translate these observations to human lupus nephritis.

45 ve renal biomarker of kidney injury in lupus nephritis.

46 e accelerated and deteriorated type of lupus nephritis.

47 ng, can attenuate granulomatous interstitial nephritis.

48 th subacute bacterial endocarditis and shunt nephritis.

49 ified in urine, correlates with active lupus nephritis.

50 tibody-induced inflammation, including lupus nephritis.

51 eactivity in the murine model of nephrotoxic nephritis.

52 nostic factors: young age-of-onset and lupus nephritis.

53 osuppressive medications in women with lupus nephritis.

54 ages and autoantibodies are central to lupus nephritis.

55 etic nephropathy, IgA nephropathy, and lupus nephritis.

56 n aid for immunosuppressive therapy in lupus nephritis.

57 ic UA crystal nephropathy with granulomatous nephritis.

58 S and PTPRZ receptors in patients with lupus nephritis.

59 mice develop systemic autoimmunity and lupus-nephritis.

60 l therapeutic target for patients with lupus nephritis.

61 for the histological classification of lupus nephritis.

62 tility of these biomarkers in tracking lupus nephritis.

63 reas of individuals with proliferative lupus nephritis.

64 w that BAFF promotes events leading to lupus nephritis.

65 osed with crescentic transformation of lupus nephritis, 1 was diagnosed with anti-GBM nephritis, and

66 (96%)], with interstitial lymphoplasmacytic nephritis [23 of 25 (92%)], and glomerular and interstit

67 tion to be excellent for understanding lupus nephritis (49% versus 33%), risk factors (43% versus 27%

68 nsic IL-6R signaling, we induced nephrotoxic nephritis, a mouse model for crescentic GN, in mice lack

69 have been identified as biomarkers for lupus nephritis, a serious complication of systemic lupus eryt

70 y biomarker that varies over time with lupus nephritis activity and treatment.

71 logy of the leading cause of pediatric acute nephritis, acute postinfectious GN, including mechanisms

72 antinuclear Abs and immune complex-mediated nephritis along with other manifestations of SLE-like di

73 an descent with SLE (588 patients with lupus nephritis and 1412 patients with lupus without nephritis

74 bone marrow cells severely aggravated lupus nephritis and accelerated death.

75 gene are associated with the risk for lupus nephritis and could be mechanistically involved in disea

76 hil transcripts during progression to active nephritis and distinct signatures in response to treatme

77 rome type 1 who developed tubulointerstitial nephritis and ESRD in association with autoantibodies ag

78 fibrotic markers in animal models with lupus nephritis and folic acid nephropathy.

79 hropathy characterized by tubulointerstitial nephritis and formation of enlarged nuclei in the kidney

80 yzed kidney samples from patients with lupus nephritis and from healthy control subjects using single

81 g cases of systemic lupus erythematosus with nephritis and healthy controls revealed a stronger assoc

82 we know about processes that may cause lupus nephritis and how such basic processes may be affected i

83 in kidney biopsies from patients with lupus nephritis and identified miR-150 as the most differentia

84 dy further reveals a role for FcgammaRIIA in nephritis and in platelet activation in SLE.

85 63 reflects histologic inflammation in lupus nephritis and is a promising activity biomarker that var

86 reversed established severe proteinuria and nephritis and largely restored normal glomerular and tub

87 hingolipid metabolism in patients with lupus nephritis and MRL/lpr lupus mice.

88 upregulation in experimental rat anti-Thy1.1 nephritis and murine mesangioproliferative nephritis mod

89 f drugs to prevent, and perhaps treat, lupus nephritis and other autoinflammatory diseases caused by

90 s of human lupus inform the requirements for nephritis and provide targets for intervention.

91 the pathogenic mechanisms that lead to lupus nephritis and provide the rationale for the latest and n

92 idneys of lupus mice and patients with lupus nephritis and suggest that molecules in this pathway may

93 In knockout mice lacking IL-34, nephritis and systemic illness are suppressed.

94 s promote lupus nephritis, we compared lupus nephritis and systemic illness in MRL-Fas(lpr) mice expr

95 ages with adenosine attenuated granulomatous nephritis and the progressive decline in GFR.

96 Tubulointerstitial nephritis and uveitis (TINU) syndrome is characterized b

97 Tubulointerstitial nephritis and uveitis syndrome is under-recognized in th

98 Tubulointerstitial nephritis and uveitis syndrome should be considered in t

99 ere diagnosed with uveitis before nephritis; nephritis and uveitis were diagnosed within 1 week from

100 vent during deferred treatment (interstitial nephritis) and one during the placebo phase of deferred

101 pus nephritis, 1 was diagnosed with anti-GBM nephritis, and 4 were diagnosed with isolated acute tubu

102 yndrome, production of anti-dsDNA Abs, lupus nephritis, and accumulation of CD3(+)B220(+)CD4(-)CD8(-)

103 ase entities, such as IgA nephropathy, lupus nephritis, and ANCA GN; and additional features as detai

104 the pathogenesis of immune complex-mediated nephritis, and BTK inhibition as a promising therapeutic

105 urvival in patients with proliferative lupus nephritis, and combined administration of these agents b

106 erulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropathy.

107 interconnection between lupus nephritis, IgA nephritis, and diabetic nephropathy.

108 a broad range of symptoms, such as diarrhea, nephritis, and encephalitis.

109 rinary tract infection/pyelonephritis, viral nephritis, and interstitial nephritis.

110 plement activation in dermatomyositis, lupus nephritis, and necrotic muscle fibres in Duchenne dystro

111 erfusion injury, allergic asthma, autoimmune nephritis, and rheumatoid arthritis.

112 nephropathy, membranoproliferative GN, lupus nephritis, and vasculitis associated with HRs (95% confi

113 Peripheral neuropathy, interstitial nephritis, and vasculitis were more common in those with

114 res in 23 necropsies: dermatitis, severe pan-nephritis, and/or severe systemic multiorgan necrotizing

115 y of the secreted protein Tubulointerstitial nephritis antigen-like 1 (Tinagl1) suppresses TNBC progr

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

117 ion, as current therapeutics targeting lupus nephritis are limited and, thus, in great demand.

118 We used nephrotoxic serum nephritis as a model of immune-mediated nephropathy.

119 istory of glomerulonephritis or interstitial nephritis, as cause of renal failure, represented the on

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

121 factors underlying the pathogenesis of lupus nephritis associated with systemic lupus erythematosus a

122 e 1 activity early during the progression of nephritis (before significant elevation of GlcCer and La

123 uss current therapeutic strategies for lupus nephritis, briefly review recent advances in understandi

124 ss of IL-17 in Roquin(san/san) mice improved nephritis by downregulating immunoglobulin (Ig)G, IgG1,

125 vated autoantibody levels and promoted lupus nephritis by inducing BAFF production in the kidneys, an

126 ays a previously unappreciated role in lupus nephritis by inducing renal TLSs and regulating the posi

127 ence of ERalpha on molecular pathways during nephritis by microarray analysis of glomerular extract g

128 the potential for renal protection in lupus nephritis by targeting this pathway, we introduced the F

129 In lupus nephritis, C5-b9 deposits co-localized with IgG, IgM, C1

130 he presence of proteinuria, the pathology of nephritis can fall into one of five classes defined by d

131 tly receiving a potential tubulointerstitial nephritis-causing medication.

132 osis, whereas concomitant tubulointerstitial nephritis-causing medications and treatment with steroid

133 In human lupus nephritis, CDM confirmed that myeloid DCs present antige

134 common renal lesion is chronic interstitial nephritis (CIN).

135 phics, treatment, disease activity (DA), and nephritis class, we confirmed a prevalent IFN signature

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

137 reased in SLE patients especially with lupus nephritis, compared to healthy controls.

138 temic lupus erythematosus and class IV lupus nephritis confirmed with biopsy and treated with mycophe

139 urrent approaches to the management of lupus nephritis continue to rely on high-dose corticosteroids

140 es in renal iron homeostasis occurs in lupus nephritis, contributing to the development of kidney inj

141 ed by rapidly progressive tubulointerstitial nephritis culminating in end-stage renal failure and uro

142 ious study of anti-C1q in experimental lupus nephritis demonstrated an important role for FcgammaRs i

143 Lupus nephritis demonstrates familial aggregation and accounts

144 tion in dendritic cells (DCs) did not affect nephritis, despite the importance of DCs in renal inflam

145 ERalpha protects female mice from developing nephritis, despite the presence of immune complexes and

146 Our findings suggest that tubulointerstitial nephritis developed in these patients as a result of an

147 different disease models (nephrotoxic serum nephritis, diabetes, doxorubicin toxicity, and CD2AP def

148 mRNA than did those from patients with lupus nephritis, diabetic nephropathy, or nephrotic syndrome.

149 Immune complex tubulointerstitial nephritis due to antibodies to brush border antigens of

150 staining was detected in pure class 5 lupus nephritis (eight of 18 patients) and in presumed primary

151 We measured urine CD163 at lupus nephritis flares in patients from a Mexican cohort and c

152 e predisposed to autoantibody production and nephritis following exposure to the TLR3 ligand poly(I:C

153 serum levels of autoantibodies and developed nephritis following treatment with poly(I:C) to mimic mi

154 ors (PPI) use and risk of acute interstitial nephritis has been described.

155 dney biopsy samples from patients with lupus nephritis has begun to define the phenotypes of both inf

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

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

158 vo prevented the formation of TLSs and lupus nephritis; however, it did not reduce immune cell infilt

159 tive GN (HR, 0.84; 95% CI, 0.76-0.92), lupus nephritis (HR, 0.69; 95% CI, 0.66-0.71), vasculitis (HR,

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

161 N) in adults, while Henoch-Schonlein purpura nephritis (HSPN) in children.

162 ropathy with features of tubulo-interstitial nephritis, hypertension and tendency for hyperkalemia, t

163 , with closest interconnection between lupus nephritis, IgA nephritis, and diabetic nephropathy.

164 lls induced remission of anti-RNP-associated nephritis in >/= 80% of treated mice, even with donor/re

165 ement membrane reactive serum-induced immune nephritis in A2AR-deficient mice.

166 ey), including viruses associated with acute nephritis in chickens.

167 lls and consequently developed reduced lupus nephritis in comparison with wild-type mice.

168 ge and succumb to a disease resembling lupus nephritis in humans.

169 ressive GN similar to class III and IV lupus nephritis in humans.

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

171 agen-induced arthritis and spontaneous lupus nephritis in MRL/lpr mice.

172 nd humoral autoimmune responses during lupus nephritis in NZB/W F1 mice and emphasize the potential c

173 ice may be protective against development of nephritis in part through downregulation of CXCR3, reduc

174 ity and predicts the onset and recurrence of nephritis in patients with systemic lupus erythematosus

175 d to controls, despite evidence of increased nephritis in Psgl-1(-/-) mice.

176 utoantigen gp70 overproduction that promotes nephritis in susceptible mice and that SNERV encodes for

177 filtration process during the progression of nephritis in the lupus-prone New Zealand Black/New Zeala

178 ting an autoimmune response to SmD and lupus nephritis in the NZM2328 background.

179 eron responses, autoantibody production, and nephritis in the pristane model of lupus.

180 actor (BAFF)) for use in patients with lupus nephritis in the USA and in difficult-to-treat patients

181 duction of anti-glomerular basement membrane nephritis in young mice, iPLA2gamma KO mice exhibited si

182 strongest evidence of association with lupus nephritis independent of HLA-DR2 and HLA-DR3 (P=8.5x10(-

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

184 The pathogenesis of lupus nephritis involves a variety of pathogenic mechanisms.

185 In a chronic model of proliferative nephritis, IRF1 and renal-expressed TNFR2 were essential

186 Tubulointerstitial nephritis is a common cause of kidney failure and may ha

187 Lupus nephritis is a manifestation of SLE resulting from glome

188 Lupus nephritis is a potentially devastating complication of s

189 Lupus nephritis is a potentially fatal autoimmune disease for

190 Lupus nephritis is an immune complex GN that develops as a fre

191 Although nephritis is diagnosed by the presence of proteinuria, t

192 upus is prevented by Psgl-1 deficiency while nephritis is exacerbated.

193 mes, the pathogenic role of T cells in lupus nephritis is not clear.

194 This form of nephritis is sometimes associated with autoimmune diseas

195 Lupus nephritis is the most common target-organ manifestation

196 ), an autosomal-recessive tubulointerstitial nephritis, is the most common cause of hereditary end-st

197 ions predispose to karyomegalic interstitial nephritis (KIN) and cancer rather than to FA.

198 Karyomegalic interstitial nephritis (KIN) is a chronic interstitial nephropathy ch

199 Karyomegalic interstitial nephritis (KIN) is a rare renal interstitial disease ent

200 in humans leads to karyomegalic interstitial nephritis (KIN), a rare hereditary kidney disease charac

201 n human Fan1 cause karyomegalic interstitial nephritis (KIN), but it is unclear whether defective ICL

202 urred in two patients patients (both grade 3 nephritis leading to treatment discontinuation).

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

204 nfiltrate the kidneys of patients with lupus nephritis (LN) and are critical for the pathogenesis of

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

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

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

208 Management of patient with Lupus Nephritis (LN) continues to remain a challenge for the t

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

210 Lupus nephritis (LN) is a common manifestation of systemic lup

211 Lupus nephritis (LN) is a complication of the autoimmune disea

212 Lupus nephritis (LN) is a form of glomerulonephritis that cons

213 Lupus nephritis (LN) is a major contributor to morbidity and m

214 Lupus nephritis (LN) is a potentially dangerous end organ path

215 Lupus nephritis (LN) is an autoimmune disease that occurs when

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

217 Treatment of lupus nephritis (LN) remains challenging.

218 ranous nephropathy (MN) and eight with lupus nephritis (LN) served as controls.

219 and systemic lupus erythematosus (SLE)/lupus nephritis (LN) shared many loci based on GWAS on Chinese

220 Lupus nephritis (LN) was the most common secondary glomerulone

221 ved cells is a key pathogenic event in lupus nephritis (LN), but the process is poorly understood.

222 associated with faster progression to lupus nephritis (LN)-associated end-stage renal disease (LN-ES

223 e potential targets of autoimmunity in lupus nephritis (LN).

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

225 with systemic lupus erythematosus and lupus nephritis (LN).

226 time in discriminating LN patients from non-nephritis lupus patients (SLE) and further to get new in

227 The nephrotoxic nephritis model of GN was studied in AREG(-/-) mice afte

228 mproves renal disease in a spontaneous lupus nephritis model through prevention of the direct injurio

229 d renal disease in a mouse nephrotoxic serum nephritis model was inhibited by amino acid metabolism a

230 1 nephritis and murine mesangioproliferative nephritis models.

231 ining of infected kidney showed interstitial nephritis, mononuclear cell infiltrates, and reduced siz

232 ntrolled trial (RCT), adult women with lupus nephritis, mostly from racial/ethnic minority background

233 ondrocalcinosis, synovitis, and interstitial nephritis (n=1 each).

234 ignificant enrichment in patients with lupus nephritis (n=32) compared with controls (n=15).

235 new perspectives for studies on drug-induced nephritis, nanocrystals, and local lipid or carbohydrate

236 patients were diagnosed with uveitis before nephritis; nephritis and uveitis were diagnosed within 1

237 aths due to heart disease, cancer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower re

238 monocyte subset behavior during nephrotoxic nephritis (NTN) in a novel WKY-hCD68-GFP monocyte/macrop

239 n, we studied these cells in the nephrotoxic nephritis (NTN) model of acute crescentic GN.

240 ve been observed for IL-6 in the nephrotoxic nephritis (NTN) model of acute crescentic GN.

241 e function of these cells in the nephrotoxic nephritis (NTN) model of cGN.

242 ed the function of Treg17 in the nephrotoxic nephritis (NTN) model of crescentic GN.

243 l-mediated murine model of nephrotoxic serum nephritis (NTS).

244 RV) envelope glycoprotein gp70 and resultant nephritis occur in lupus-prone mice, but whether NEERV m

245 Tlr9 overexpression resulted in ameliorated nephritis, opposite of the effect of deleting Tlr9.

246 glomerular podocytes of patients with lupus nephritis or focal segmental GN but not in normal kidney

247 mpared with samples from patients with lupus nephritis or healthy black controls, AASK-N samples had

248 d nephritis than patients with lupus without nephritis or healthy controls.

249 stals and tubular injury, acute interstitial nephritis, or mitochondrial toxicity.

250 o nephronophthisis, chronic GN, interstitial nephritis, or unknown etiology.

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

252 t decade, an improved understanding of lupus nephritis pathogenesis fueled several clinical trials of

253 s have all been recently implicated in lupus nephritis pathogenesis.

254 alivary glands or kidney biopsies from lupus nephritis patients.

255 ntal membranous nephropathy (passive Heymann nephritis (PHN)), complement C5b-9-induced proteinuria w

256 the kidney has the capacity to dampen lupus nephritis, possibly by modulating inflammation and oxida

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

258 at patients with APTN, but not those without nephritis, produce two kinds of alloantibodies against a

259 ced Fli-1 expression have significantly less nephritis, prolonged survival, and decreased infiltratin

260 ough IL-6 is proinflammatory in murine lupus nephritis, protective effects have been observed for IL-

261 rge-scale genome-wide investigation of lupus nephritis provide evidence of multiple biologically rele

262 with nephrotoxic serum to induce crescentic nephritis (rapidly progressive GN), this genetic inactiv

263 of miR-193a in a mouse model of nephrotoxic nephritis resulted in reduced crescent formation and dec

264 alysis of glomeruli during nephrotoxic serum nephritis revealed significant upregulation of genes rel

265 were associated with renal disease in lupus nephritis samples.

266 atures in response to treatment in different nephritis subclasses.

267 n pelagic animals to have Salmonella-induced nephritis suggesting that Salmonella may have been a con

268 e for FcgammaRs in the pathogenesis of lupus nephritis, suggesting a direct effect on phagocytes.

269 ence of multiple biologically relevant lupus nephritis susceptibility loci.

270 icantly higher in patients with active lupus nephritis than in patients with active extrarenal SLE, i

271 urine and kidneys of patients with lupus and nephritis than patients with lupus without nephritis or

272 e response, with an aggravated course of the nephritis that was reversible on anti-IFNgamma treatment

273 d a novel therapeutic approach in crescentic nephritis, that of glucocorticoid antagonism, which was

274 During nephritis, the altered activity of metabolic pathways, s

275 e are different pathogenic pathways in lupus nephritis, the emerging pathogenic mechanism(s) may be e

276 d is not labeled for patients suffering from nephritis, the leading cause of patient mortality.

277 fer of biTregs suppressed the development of nephritis to an extent similar to that observed with tra

278 or Gcn2 converted Ab-induced, self-limiting nephritis to fatal end-stage renal disease.

279 ival improved, the goals for advancing lupus nephritis treatment shifted to identifying therapies tha

280 e to improve upon the standard-of-care lupus nephritis treatments.

281 ility to detect therapeutic benefit in lupus nephritis trials.

282 Treatment of lupus nephritis urine samples with 0.5% acetic acid produced t

283 Nephrotoxic serum nephritis was induced in wild-type (WT) and ubiquitin-bi

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

285 Tubulointerstitial nephritis was the dominant lesion in 93% of the 60 patie

286 se model of acute crescentic GN (nephrotoxic nephritis), we identified CD4(+) T cells and gammadelta

287 arenal and systemic mechanisms promote lupus nephritis, we compared lupus nephritis and systemic illn

288 e distinct functions of Axl and Mer in lupus nephritis, we compared the severity of nephrotoxic serum

289 By using the murine model of nephrotoxic nephritis, we investigated the role of S100A8/A9 [myeloi

290 In vivo, rats with Thy1 nephritis were treated with TH1177 or vehicle.

291 ications of SS (ie, vasculitis, interstitial nephritis) were also more common in men (64% vs 40%, P =

292 n the first week of experimental nephrotoxic nephritis, whereas reduction in glomerular numbers occur

293 ency in B cells was sufficient to exacerbate nephritis while extinguishing anti-nucleosome antibodies

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

295 ar translatable to human patients with lupus nephritis, whose expression of IL-34, cFMS, and PTPRZ is

296 In nephrotoxic nephritis, wild-type (WT) mice with glomerulonephritis h

297 (-/-)MRL.lpr mice displayed attenuated lupus nephritis with a striking decrease in the accumulation o

298 Treatment of Thy1 nephritis with TH1177 significantly reduced glomerular i

299 us uveitis (6/52, 11.5%), tubulointerstitial nephritis with uveitis (6/52, 11.5%), and juvenile idiop

300 miR-155-deficient mice developed less severe nephritis, with reduced histologic and functional injury