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

4 sary to identify targets that do not promote nephritis.

5 pathway may serve as early markers in lupus nephritis.

6 en thought to promote inflammation and lupus nephritis.

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

8 ysfunction that suggested acute interstitial nephritis.

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

10 involved in tissue injury relating to lupus nephritis.

11 ion and targeted therapies for patients with nephritis.

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

13 tified as playing an important role in lupus nephritis.

14 till being used in refractory cases of lupus nephritis.

15 hogenesis, diagnosis, and treatment of lupus nephritis.

16 nd anti-glomerular basement membrane-induced nephritis.

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

18 or to pregnancy in patients with quiet lupus nephritis.

19 injury in experimental, crescentic anti-GBM nephritis.

20 rtments in both human and experimental lupus nephritis.

21 or the NLRP3 inflammasome in mediating lupus nephritis.

22 roteinuria, and histologic features of lupus nephritis.

23 classes that mediate posttransplant anti-GBM nephritis.

24 uent production of autoantibodies and severe nephritis.

25 promote renal disease in patients with lupus nephritis.

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

27 translate these observations to human lupus nephritis.

28 ve renal biomarker of kidney injury in lupus nephritis.

29 f cells of the immune system, dermatitis and nephritis.

30 spects of disease progression in human lupus nephritis.

31 nephritis, a DC-dependent aggressive type of nephritis.

32 ented the induction of experimental anti-GBM nephritis.

33 specific histologic manifestations of lupus nephritis.

34 AA to MRL-lpr mice also delayed the onset of nephritis.

35 erwent biopsy presented with subclinical BKV nephritis.

36 ts with class IV-S and those with IV-G lupus nephritis.

37 etention of neutrophils in antibody-mediated nephritis.

38 monitors those at higher risk of developing nephritis.

39 ular parietal epithelial cells in crescentic nephritis.

40 fer of CXCR6-competent NKT cells ameliorated nephritis.

41 tion, and thereby hastens the onset of lupus nephritis.

42 examine the potential of abatacept in lupus nephritis.

43 ucting further studies of abatacept in lupus nephritis.

44 isease progression following immune-mediated nephritis.

45 immune-mediated nephropathies like in lupus nephritis.

46 etermine common pathways in murine and human nephritis.

47 w that BAFF promotes events leading to lupus nephritis.

48 sangial compartment in mesangioproliferative nephritis.

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

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

51 nmet need for successful management of lupus nephritis.

52 te underlying pathogenic mechanisms in lupus nephritis.

53 the kidney by accelerated serum nephrotoxic nephritis.

54 s associates with viral infections and lupus nephritis.

55 of age and steadily increases prior to lupus nephritis.

56 s-like autoimmune disease with strong kidney nephritis.

57 e with the occurrence of proliferative lupus nephritis.

58 nephritis, viral nephritis, and interstitial nephritis.

59 veloped to explain the pathogenesis of lupus nephritis.

60 (96%)], with interstitial lymphoplasmacytic nephritis [23 of 25 (92%)], and glomerular and interstit

61 per year) and natural disease course of HSP nephritis (46% initial renal inflammation; 9% subsequent

62 of the Wistar-Kyoto (WKY) rat to nephrotoxic nephritis, a rat model of Crgn.

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

64 complement activation and the development of nephritis, accelerated atherosclerosis is, instead, rela

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

66 he endothelium - with implications for lupus nephritis and accelerated atherosclerosis.

67 g cases of systemic lupus erythematosus with nephritis and cases of systemic lupus erythematosus with

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

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

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

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

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

73 enal function and prevention of clinical BKV nephritis and graft loss.

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

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

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

77 nd FcgammaRIIIB on neutrophils induces lupus nephritis and in some cases arthritis only when the mice

78 TNFRII Ig treatment stabilized nephritis and markedly prolonged survival.

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

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

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

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

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

84 y an important role in protection from lupus nephritis and suggest that the NAA B cells may have an i

85 ouse model of interferon-alpha-induced lupus nephritis and treated mice with TNF receptor type II (TN

86 his was followed by progressive interstitial nephritis and tubulointerstitial renal fibrosis in 3-, 6

87 ation rate (GFR), chronic tubulointerstitial nephritis and ultrastructural changes in the proximal tu

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

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

90 t destruction in lupus-susceptible mice with nephritis and, paradoxically, Mo-dependent renal repair

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

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

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

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

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

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

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

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

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

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

101 ction in albuminuria, severity of crescentic nephritis, and number of glomerular macrophages compared

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

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

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

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

106 Alport post-transplant nephritis (APTN) is an aggressive form of anti-glomerula

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

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

109 or viruria, analysis of risk factors for BKV nephritis as an endpoint could lead to erroneous finding

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

111 vehicle-injected mice developed severe lupus nephritis, as evidenced by increased proteinuria (mean +

112 with SLE may reduce the occurrence of lupus nephritis, as well as diminish the risk of accelerated a

113 trial of mycophenolate mofetil, 3) the Lupus Nephritis Assessment with Rituximab (LUNAR) trial of rit

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

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

116 itis revealed strong associations with lupus nephritis at rs7708392 in European Americans and rs49588

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

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

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

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

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

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

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

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

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

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

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

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

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

130 In progressive nephritis (day 56), overexpression of CCN3 resulted in d

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

132 Lupus nephritis demonstrates familial aggregation and accounts

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

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

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

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

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

138 During experimental mesangioproliferative nephritis, expression of the glomerular CCN3 (nephroblas

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

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

141 ound acid hypersecretion, acute interstitial nephritis, gastric carcinoid tumor, cardiovascular risk

142 ficient Col4alpha3(-/-) mice with hereditary nephritis had significantly higher levels of total kidne

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

144 Recent clinical trials in lupus nephritis have all used different criteria to assess com

145 cyclitis, lymphadenopathy, neuropathies, and nephritis have also been reported with ipilimumab.

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

147 We used Heymann nephritis (HN), a rat model of human membranous nephriti

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

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

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

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

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

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

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

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

156 al Pathology Society classification of lupus nephritis in adult patients.

157 te renal failure, electrolyte imbalance, and nephritis in California, heat-related illness in Washing

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

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

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

161 activate neutrophils in vitro and to induce nephritis in mice.

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

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

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

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

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

167 nflammation, and, in turn, early-onset lupus nephritis in preclinical MRL/MpJ-Faslpr/Fas(lpr) mice (M

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

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

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

171 ich has the strongest association with lupus nephritis in the NZM2410 mouse model.

172 OR the patient must have biopsy-proven lupus nephritis in the presence of antinuclear antibodies or a

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

174 tes of the prevalence and incidence of lupus nephritis in the US to date.

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

176 her, MyD88 deficiency in B cells ameliorated nephritis, including antibody-independent interstitial T

177 valence and incidence rates of SLE and lupus nephritis increased with age, were higher in girls than

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

179 Early mesangial nephritis initiates a cascade of inflammatory signals th

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

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

182 The intrarenal etiology of lupus nephritis involves antibody binding to multiple intraren

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

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

185 Lupus nephritis is a manifestation of SLE resulting from glome

186 Lupus nephritis is a potentially devastating complication of s

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

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

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

190 Because the occurrence of BK virus (BKV) nephritis is far less frequent than BK viremia or viruri

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

192 This form of nephritis is sometimes associated with autoimmune diseas

193 es of diffuse proliferative (class IV) lupus nephritis is unknown.

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

195 of certain miRs has been described in lupus nephritis, it is unknown whether miRs contribute to fibr

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

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

198 FAN1 as a cause of karyomegalic interstitial nephritis (KIN), a disorder that serves as a model for r

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

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

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

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

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

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

205 Systemic lupus erythematosus (SLE) and lupus nephritis (LN) disproportionately affect individuals who

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

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

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

209 Lupus nephritis (LN) is a serious manifestation of systemic lu

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

211 Treatment of lupus nephritis (LN) remains challenging.

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

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

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

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

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

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

218 1 nephritis and murine mesangioproliferative nephritis models.

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

220 n an anti-glomerular basement membrane (GBM) nephritis mouse model.

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

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

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

224 r circulatory diseases; 2.77 (1.49-5.15) for nephritis, nephrotic syndrome, and nephrosis; 4.08 (1.38

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

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

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

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

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

230 sease following the induction of nephrotoxic nephritis (NTN).

231 nconsistent, and although acute interstitial nephritis, nutritional deficiencies (including B12 and h

232 t was more severe, similar to the aggravated nephritis observed in mice depleted of immature DCs.

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

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

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

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

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

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

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

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

241 alivary glands or kidney biopsies from lupus nephritis patients.

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

243 >/=50 years, diabetes, chronic interstitial nephritis, polycystic kidney disease, and 1-3 years of p

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

245 sms involved in human diseases presenting as nephritis (postinfectious GN, IgA nephropathy, antiglome

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

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

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

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

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

251 disappointing results of rituximab in lupus nephritis provided a clinical and mechanistic counterpoi

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

253 Nephritis, renal immune complex levels, and macrophage i

254 the children with SLE, 1,106 (37%) had lupus nephritis, representing a prevalence of 3.64 (95% CI 3.4

255 GC prodrugs by kidney cells would potentiate nephritis resolution, with a reduced risk of systemic to

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

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

258 ases of systemic lupus erythematosus without nephritis revealed strong associations with lupus nephri

259 atures in response to treatment in different nephritis subclasses.

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

261 gnate ligand CXCL16 early after induction of nephritis, suggesting that renal DC-derived CXCL16 might

262 istant to sheep anti-mouse GBM serum-induced nephritis, supporting the hypothesis that aGN is mediate

263 ence of multiple biologically relevant lupus nephritis susceptibility loci.

264 tosus (SLE) and a higher prevalence of lupus nephritis than do Caucasians.

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

266 ted less iNKT cell recruitment and developed nephritis that was more severe, similar to the aggravate

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

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

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

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

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

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

273 rge, multicenter trial of abatacept in lupus nephritis, to gain insight into which outcome measure, i

274 hritis (HN), a rat model of human membranous nephritis, to study the effects of TCV on autoimmune kid

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

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

277 plete response can determine whether a lupus nephritis trial is interpreted as a success or a failure

278 ility to detect therapeutic benefit in lupus nephritis trials.

279 asmic antibody-mediated crescentic GN, lupus nephritis, type I membranoproliferative GN), and nephrot

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

281 2 cases (95% CI 2.05-2.40) and that of lupus nephritis was 0.72 cases (95% CI 0.63-0.83) per 100,000

282 Lupus nephritis was identified from >/=2 ICD-9 billing codes f

283 Anti-GBM nephritis was induced in 129x1/svJ mice by anti-GBM seru

284 of miR-155 in T cell-mediated inflammation, nephritis was induced in miR-155(-/-) and wild-type mice

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

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

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

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

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

290 s (n = 144) with class III or class IV lupus nephritis were randomized 1:1 to receive rituximab (1,00

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

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

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

294 vels of proteinuria during nephrotoxic serum nephritis, whereas TRPC6 null mice exhibited reduced CaM

295 BK viremia can lead to nephritis, which can progress to irreversible kidney tra

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

300 ry protects against the development of lupus nephritis, with the aim of exploring the genetic and soc