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 he age of 29 weeks (after the development of lupus nephritis).

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

4 titative renal biomarker of kidney injury in lupus nephritis.

5 the aspects of disease progression in human lupus nephritis.

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

7 ers of specific histologic manifestations of lupus nephritis.

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

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

10 urther examine the potential of abatacept in lupus nephritis.

11 r conducting further studies of abatacept in lupus nephritis.

12 IgM in these mice confer protection against lupus nephritis.

13 nti-glomerular basement membrane disease and lupus nephritis.

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

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

16 as combined membranous and focal or diffuse lupus nephritis.

17 oduction and significantly delays death from lupus nephritis.

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

19 ing their recruitment into the kidney during lupus nephritis.

20 prevent relapse after the initial control of lupus nephritis.

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

22 d with increased disease activity and active lupus nephritis.

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

24 therapy of both proliferative and membranous lupus nephritis.

25 hages in aggressive proliferative lesions of lupus nephritis.

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

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

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

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

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

31 hosphamide for the induction of remission in lupus nephritis.

32 ronic transplant rejection and recurrence of lupus nephritis.

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

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

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

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

37 was independently associated with recurrent lupus nephritis.

38 ission induction and maintenance therapy for lupus nephritis.

39 ive to cyclophosphamide for the treatment of lupus nephritis.

40 ed with the histopathology activity index of lupus nephritis.

41 SF-1-dependent systemic mechanism central to lupus nephritis.

42 anifestations in patients with biopsy-proven lupus nephritis.

43 ted by renal biopsy and 26 with a history of lupus nephritis.

44 een shown to be effective in treating murine lupus nephritis.

45 ity and therapeutic targets in proliferative lupus nephritis.

46 re found in kidney biopsies of patients with lupus nephritis.

47 weeks, most (NZB x NZW)F1 mice had developed lupus nephritis.

48 renal disease and treats established murine lupus nephritis.

49 infiltrating in the kidneys of patients with lupus nephritis.

50 ay have potential diagnostic significance in lupus nephritis.

51 d that certain PON1 SNPs are associated with lupus nephritis.

52 the onset of proteinuria and worsened SNF(1) lupus nephritis.

53 n no previous studies of the epidemiology of lupus nephritis.

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

55 glomerulonephritis closely resembling human lupus nephritis.

56 eatment, and outcome of patients with severe lupus nephritis.

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

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

59 ajor unmet need for successful management of lupus nephritis.

60 acerbate underlying pathogenic mechanisms in lupus nephritis.

61 l cells associates with viral infections and lupus nephritis.

62 10 wk of age and steadily increases prior to lupus nephritis.

63 ong been thought to promote inflammation and lupus nephritis.

64 rrelate with the occurrence of proliferative lupus nephritis.

65 een developed to explain the pathogenesis of lupus nephritis.

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

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

68 cesses involved in tissue injury relating to lupus nephritis.

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

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

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

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

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

74 compartments in both human and experimental lupus nephritis.

75 role for the NLRP3 inflammasome in mediating lupus nephritis.

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

77 idney promote renal disease in patients with lupus nephritis.

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

79 We identified 208 cases of biopsy-proven lupus nephritis (176 women, 32 men): the overall prevale

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

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 Recurrent lupus nephritis and chronic rejection of the kidney tran

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

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

86 at EBV-immortalized cells from patients with lupus nephritis and healthy individuals did not produce

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

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

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

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

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

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

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

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

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

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

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

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

99 nee arthritis in a patient with class III-IV lupus nephritis and speculate on the association between

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

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

102 hesis that the PD-1/PD-L1 pathway suppresses lupus nephritis and the systemic illness in MRL-Fas(lpr)

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

104 23R-mediated signaling in the development of lupus nephritis and urge the consideration of proper bio

105 re pronounced association with proliferative lupus nephritis and with longitudinal response to lupus

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 y on autoantibody production, development of lupus nephritis, and mortality were determined.

116 iated with disease activity, damage accrual, lupus nephritis, and mortality.

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

118 among men, African Americans, patients with lupus nephritis, and patients with anti-double-stranded

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

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

121 yzed in relation to PON1 activity, SLE risk, lupus nephritis, antiphospholipid antibody (aPL) positiv

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 latory T cells that delay the development of lupus nephritis by suppressing hypergammaglobulinemia an

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

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

145 pidemiology, genetics, cardiovascular risks, lupus nephritis, CNS disease, the antiphospholipid syndr

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

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

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

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

150 also elevated in the urine of patients with lupus nephritis, correlating well with urine protein lev

151 rstanding of the immunology and phenotype of lupus nephritis current therapies have insufficient effi

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

153 Lupus nephritis demonstrates familial aggregation and ac

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

155 ween serum NOx levels and markers of SLE and lupus nephritis disease activity.

156 The SLE group included 23 patients with lupus nephritis documented by renal biopsy and 26 with a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 ide or tripdiolide significantly ameliorated lupus nephritis in (NZB x NZW)F1 mice, reduced cytokine

179 of triptolide and tripdiolide on established lupus nephritis in (NZB x NZW)F1 mice.

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

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

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

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

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

185 s no hypoalbuminemia or apparent evidence of lupus nephritis in mice treated with either of the 2 dit

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

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

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

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

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

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

192 he prevalence and incidence of biopsy-proven lupus nephritis in the northwest of England in 2001 and

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

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

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

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

197 tant in the pathogenesis of murine and human lupus nephritis; in murine models, we had found that a s

198 of several strains of mice with spontaneous lupus nephritis, including the MRL/lpr, NZM2410, and B6.

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

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

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

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

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

204 Lupus nephritis is a manifestation of SLE resulting from

205 Lupus nephritis is a potentially devastating complicatio

206 Lupus nephritis is an immune complex GN that develops as

207 Recurrent lupus nephritis is infrequent and relatively benign, wit

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

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

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

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

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

213 vels were significantly higher in those with lupus nephritis (LN) (median 17.1 ng/mg creatinine, inte

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

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

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

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

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

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

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

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

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

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

224 Treatment of lupus nephritis (LN) remains challenging.

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

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

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

228 1q) are potential targets of autoimmunity in lupus nephritis (LN).

229 al electrophoresis in 32 patients with FSGS, lupus nephritis, membranous nephropathy, or diabetic nep

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

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

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

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

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

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

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

237 on levels distinguished active from inactive lupus nephritis (P = 0.02) and were positively associate

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

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

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

241 Lupus nephritis patient medical records from 125 pairs o

242 Compared with patients without nephritis, lupus nephritis patients had higher IFN scores (overall

243 Subset analysis revealed that only in lupus nephritis patients were increasing CVs for SPS (P

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

245 human systemic lupus erythematosus (SLE) and lupus nephritis patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

265 nephritis and with longitudinal response to lupus nephritis therapy provides a rationale for the stu

266 Y6E levels, may be useful as a biomarker for lupus nephritis therapy.

267 en analyzing the subset of 143 subjects with lupus nephritis, there was also no evidence of associati

268 Among patients with lupus nephritis, those with proliferative lesions had hi

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

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

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

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

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

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

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

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

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

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

279 n effort to identify potential biomarkers in lupus nephritis, urine from mice with spontaneous lupus

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 nephritis, urine from mice with spontaneous lupus nephritis was screened for the presence of VCAM-1,

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

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

288 ney in response to TWEAK are instrumental in Lupus nephritis; we therefore hypothesized that TWEAK/Fn

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 (age 18 years and older) with biopsy-proven lupus nephritis were identified from 5 sources: renal bi

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

294 rom the medical records of 215 patients with lupus nephritis were sent to 8 nephrologists and 29 rheu

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

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