ライフサイエンスコーパス: IgA nephropathy

1 bowel disease affects development of ESKD in IgA nephropathy.

2 s, monitoring, and therapy for patients with IgA nephropathy.

3 from peripheral blood cells of patients with IgA nephropathy.

4 have implications for renal diseases such as IgA nephropathy.

5 ays an essential role in the pathogenesis of IgA nephropathy.

6 nt glycosylation of IgA1 in diseases such as IgA nephropathy.

7 isk of earlier inflammatory bowel disease in IgA nephropathy.

8 elevated serum IgA seen in liver disease and IgA nephropathy.

9 especially in the treatment of children with IgA nephropathy.

10 sylated IgA1-containing immune aggregates in IgA nephropathy.

11 for poststreptococcal glomerulonephritis or IgA nephropathy.

12 most all of the pathologic features of human IgA nephropathy.

13 enal progression for high-risk patients with IgA nephropathy.

14 and six vascular histopathologic features of IgA nephropathy.

15 (APRIL) is implicated in the pathogenesis of IgA nephropathy.

16 a disease-modifying effect in patients with IgA nephropathy.

17 romising avenue toward precision medicine in IgA nephropathy.

18 lated diseases, including IgA vasculitis and IgA nephropathy.

19 tein in clinical evaluation for treatment of IgA nephropathy.

20 APRIL) play key roles in the pathogenesis of IgA nephropathy.

21 elop glomerulonephritis that resembles human IgA nephropathy.

22 s well as suggesting therapeutic avenues for IgA nephropathy.

23 tion plays a key role in the pathogenesis of IgA nephropathy.

24 n implicated in autoimmune diseases, such as IgA nephropathy.

25 iac disease, inflammatory bowel disease, and IgA nephropathy.

26 ithout type 2 diabetes, including those with IgA nephropathy.

27 ia as compared with placebo in patients with IgA nephropathy.

28 ted elevated serum IgA as a causal factor in IgA nephropathy.

29 ith minimal fluid retention in patients with IgA nephropathy.

30 uria compared with irbesartan in adults with IgA nephropathy.

31 e for drusen in macular degeneration without IgA nephropathy.

32 al drusen have been described in people with IgA nephropathy.

33 lopathy is a very rare condition observed in IgA nephropathy.

34 d in an ongoing phase 3 trial in adults with IgA nephropathy.

35 in helping assess prognosis in patients with IgA nephropathy.

36 hway plays a key role in the pathogenesis of IgA nephropathy.

37 plays a central role in the pathogenesis of IgA nephropathy.

38 ad led to initial pretransplant diagnosis of IgA nephropathy.

39 nt evaluation as possible mediators of human IgA nephropathy.

40 ases such as systemic lupus erythematosus or IgA nephropathy.

41 nt C5 inhibitor, ravulizumab, in adults with IgA nephropathy.

42 ial therapeutic target in some patients with IgA nephropathy.

43 by 5-azacytidine ameliorated progression of IgA nephropathy.

44 odies assigned salient pathogenetic roles in IgA nephropathy.

45 ort a pivotal, phase 3 study of atacicept in IgA nephropathy.

46 enrolled 116 individuals with biopsy-proven IgA nephropathy.

47 ockade, reduced proteinuria in patients with IgA nephropathy.

48 3 NefIgArd trial of Nefecon in patients with IgA nephropathy.

49 ed with increased ESKD risk in patients with IgA nephropathy.

50 he drug to the distal ileum in patients with IgA nephropathy.

51 iology, diagnosis, and outcomes of recurrent IgA nephropathy.

52 ernative and lectin pathways are involved in IgA nephropathy.

53 the combined deletion of CFHR3 and CFHR1 in IgA nephropathy.

54 ephrosis, membranous glomerulonephritis, and IgA nephropathy.

55 est a role for miRNAs in the pathogenesis of IgA nephropathy.

56 is common and confers a protective effect in IgA nephropathy.

57 iferative glomerulonephritis and relapses in IgA nephropathy.

58 oviding a potential pharmacologic target for IgA nephropathy.

59 on in the hinge region of IgA1 characterizes IgA nephropathy.

60 GN could serve as an experimental model for IgA nephropathy.

61 g sporadic FSGS, minimal change disease, and IgA nephropathy.

62 alues 3 x 10(-2) to 5 x 10(-5)) but not with IgA nephropathy.

63 predictors of long-term clinical outcomes in IgA-nephropathy.

64 In patients with IgA nephropathy, 12 months of treatment with sibeprenlim

65 erative glomerulonephritis (23%) followed by IgA nephropathy (19%) and acute tubular injury (19%).

66 tested the efficacy of fish-oil treatment of IgA nephropathy, 2 reported beneficial effects on renal

67 Of 270 participants with IgA nephropathy (254 [94%] confirmed by previous biopsy)

68 geneous basement membrane abnormalities; one IgA nephropathy, 5 of 16 glomeruli globally sclerotic; o

69 tions for other Tn-related disorders such as IgA nephropathy, a condition that can result in renal fa

70 rried out a genome-wide association study of IgA nephropathy, a major cause of kidney failure worldwi

71 ed trial involving adults with biopsy-proven IgA nephropathy, a total urinary protein excretion of at

72 different targets in the pathophysiology of IgA nephropathy according to their relevance in the indi

73 acute poststreptococcal glomerulonephritis, IgA nephropathy, Alport's syndrome, and membranoprolifer

74 activation has a role in the pathogenesis of IgA nephropathy, an autoimmune disease mediated by patho

75 in tissues from patients with obstructive or IgA nephropathies and in mouse fibrotic kidneys.

76 -up of 12.6 years, 196 (4.95%) patients with IgA nephropathy and 330 (1.65%) matched controls develop

77 y, fall short at capturing the complexity of IgA nephropathy and can only crudely guide therapeutic d

78 s that have roles in human diseases, such as IgA nephropathy and cancer.

79 igen expression in human diseases, including IgA nephropathy and cancer.

80 Tg mice and kidney biopsies of patients with IgA nephropathy and CKD stages I to V, respectively.

81 We examined the frequency of drusen in IgA nephropathy and compared their location and composit

82 Rs) for future inflammatory bowel disease in IgA nephropathy and conditional logistic regression to a

83 istently, kidney biopsies from patients with IgA nephropathy and diabetic nephropathy exhibited subst

84 ate the association of genetic variants with IgA nephropathy and end-stage renal disease (ESRD, n = 1

85 IgA nephropathy and Henoch-Schonlein purpura nephritis a

86 Childhood IgA nephropathy and Henoch-Schonlein purpura nephritis h

87 man IgA1 and its role in the pathogenesis of IgA nephropathy and Henoch-Schonlein purpura nephritis h

88 use of immunosuppressive agents in pediatric IgA nephropathy and Henoch-Schonlein purpura nephritis,

89 IgA1 mesangial deposition is the hallmark of IgA nephropathy and Henoch-Schonlein purpura, the onset

90 diators of acute kidney injury and fibrosis, IgA nephropathy and idiopathic membranous nephropathy, a

91 ludes various glomerular diseases, including IgA nephropathy and IgA vasculitis, membranous nephropat

92 of these proteins in inflammatory injury in IgA nephropathy and IgA vasculitis.

93 cells are involved in the immunopathology of IgA nephropathy and in models of glomerulonephritis, isc

94 female, aged 40-80 years) with biopsy-proven IgA nephropathy and kidney failure were examined for the

95 In summary, lesions of TMA are frequent in IgA nephropathy and may occur in normotensive patients w

96 ibutes to the aberrant IgA1 glycosylation in IgA nephropathy and may represent a new therapeutic targ

97 t morbidity associated with diseases such as IgA nephropathy and membranoproliferative glomerulonephr

98 ion in human pIgR, A580V, is associated with IgA nephropathy and nasopharyngeal carcinoma.

99 complex-mediated GN, except two specimens of IgA nephropathy and one specimen of sclerosing membranop

100 inical intervention studies of patients with IgA nephropathy and other glomerular disorders.

101 d value in predicting risk of progression in IgA nephropathy and other kidney diseases.

102 least 18 years with biopsy-confirmed primary IgA nephropathy and persistent proteinuria despite optim

103 domized 34 adult patients with biopsy-proven IgA nephropathy and proteinuria >1 g/d, maintained on an

104 adults (aged >=18 years) with biopsy-proven IgA nephropathy and proteinuria of 1.0 g/day or higher d

105 18 years or older with biopsy-proven primary IgA nephropathy and proteinuria of at least 1.0 g per da

106 al, we enrolled adults with biopsy-confirmed IgA nephropathy and proteinuria with a 24-hour urinary p

107 Patients with IgA nephropathy and severe proteinuria have a high lifet

108 e received FDA approval for the treatment of IgA nephropathy and treatment-resistant hypertension, re

109 an essential role for UG in preventing mouse IgA nephropathy and warrant further studies to determine

110 athies (44 with FSGS, 21 with HIVAN, 32 with IgA nephropathy, and 74 healthy controls).

111 nic conditions (including diabetes mellitus, IgA nephropathy, and arterionephrosclerosis) as the prim

112 r use in atypical hemolytic uremic syndrome, IgA nephropathy, and C3 glomerulopathy.

113 glomerulonephritis, minimal change disease, IgA nephropathy, and diabetic nephropathy validates mult

114 copathologic diagnoses were lupus nephritis, IgA nephropathy, and diabetic nephropathy.

115 Williams syndrome, chronic fatigue syndrome, IgA nephropathy, and IgA deficiency.

116 rulopathies, including diabetic nephropathy, IgA nephropathy, and lupus nephritis.

117 S, membranoproliferative glomerulonephritis, IgA nephropathy, and membranous nephropathy), patients w

118 ated diseases, such as rheumatoid arthritis, IgA nephropathy, ankylosing spondylitis, and inflammator

119 presenting as nephritis (postinfectious GN, IgA nephropathy, antiglomerular basement membrane and an

120 glomerulosclerosis, membranous nephropathy, IgA nephropathy, antineutrophil cytoplasmic antibody-ass

121 tan in reducing proteinuria in patients with IgA nephropathy are incompletely understood.

122 ents with end-stage kidney disease caused by IgA nephropathy are transplanted every year, and each of

123 n added to supportive care, in patients with IgA nephropathy are uncertain.

124 ined a series of 128 patients diagnosed with IgA nephropathy between 2002 and 2008 who had a mean fol

125 Thrombotic microangiopathy (TMA) occurs in IgA nephropathy, but its clinical significance is not we

126 Hematuria is a cardinal symptom in IgA nephropathy, but its influence on the risk of diseas

127 genetic contribution to the pathogenesis of IgA nephropathy, but results from genetic association st

128 ot prove the efficacy of fish oil therapy in IgA nephropathy, but suggests that an additional placebo

129 in the IgA1 hinge region are associated with IgA nephropathy, but their contribution to its pathogene

130 oadly sensitized and had a high incidence of IgA nephropathy causing end-stage renal disease.

131 In addition, among patients with IgA nephropathy, comorbid inflammatory bowel disease ele

132 entially expressed in PBMCs of patients with IgA nephropathy compared with healthy persons.

133 51-year-old woman with a history of Berger's IgA nephropathy complained of visual impairment in both

134 Thus, in participants with IgA nephropathy, dapagliflozin reduced the risk of chron

135 r agonists, and targeted immunotherapies for IgA nephropathy demonstrate that sustained estimated glo

136 ease also was more common before a confirmed IgA nephropathy diagnosis.

137 e supportive care in patients with high-risk IgA nephropathy did not significantly improve the outcom

138 y not requiring electron microscopy included IgA nephropathy, diffuse proliferative lupus nephritis,

139 dult patients (aged >=18 years) with primary IgA nephropathy, estimated glomerular filtration rate (e

140 Retinal drusen are uncommon in IgA nephropathy, even with kidney failure.

141 Testing of 12 cases of monotypic IgA nephropathy excluded monoclonal deposits in six by r

142 Patients with IgA nephropathy exhibited lower C1GALT1 expression, whic

143 ns and specimens obtained from patients with IgA nephropathy, focal segmental glomerulosclerosis, min

144 We followed a cohort of 112 patients with IgA nephropathy for a mean+/-SEM period of 14+/-10.2 yea

145 3 has been a continued focus of the study of IgA nephropathy (formerly Berger disease) and IgA vascul

146 IgA nephropathy frequently leads to progressive CKD.

147 anous glomerulonephritis, diabetes mellitus, IgA nephropathy, Goodpasture's syndrome, and Alport synd

148 ey biopsy and the reported family history of IgA nephropathy had led to initial pretransplant diagnos

149 IgA nephropathy has an impact on renal health care costs

150 Patients with IgA nephropathy have an increased risk of inflammatory b

151 interactions involved in the pathogenesis of IgA nephropathy have revealed the autoimmune nature of t

152 eserving renal function in immunoglobulin A (IgA) nephropathy have yielded conflicting results.

153 ic crescentic glomerulonephritis (RPGN/ICG), IgA nephropathy (IgA), mesangioproliferative glomerulone

154 nd immune response pathways were enriched in IgA nephropathy/IgA vasculitis with nephropathy compared

155 en comparing adults with children within the IgA nephropathy/IgA vasculitis with nephropathy group, 5

156 In IgA nephropathy, IgA1 contains O-glycans that are galact

157 In IgA nephropathy, IgA1 molecules with incompletely galact

158 nsplant rates were highest for patients with IgA nephropathy (IgAN) (referent) and lower for all othe

159 IgA nephropathy (IgAN) and IgA vasculitis with nephritis

160 efficacy in other glomerulopathies, such as IgA nephropathy (IgAN) and membranoproliferative glomeru

161 Population-based incidence data for IgA nephropathy (IgAN) are available for some countries

162 ciated glomerulonephritis (SAGN) and primary IgA nephropathy (IgAN) are separate disease entities req

163 Evidence from the Oxford IgA nephropathy (IgAN) cohort supports the clinical valu

164 Patients diagnosed with IgA nephropathy (IgAN) commonly experience a substantial

165 s (CICs) isolated from sera of patients with IgA nephropathy (IgAN) consist of undergalactosylated, m

166 Some patients diagnosed with benign IgA nephropathy (IgAN) develop a progressive clinical co

167 Primary IgA nephropathy (IgAN) diagnosis is based on IgA-dominan

168 ,131 patients with GN studied, patients with IgA nephropathy (IgAN) had the lowest mortality rates an

169 rm follow-up after renal transplantation for IgA nephropathy (IgAN) have suggested an incidence of re

170 Although IgA nephropathy (IgAN) is a common cause of glomerulonep

171 IgA nephropathy (IgAN) is a common cause of renal failur

172 IgA nephropathy (IgAN) is a common chronic glomerular di

173 IgA nephropathy (IgAN) is a common form of primary glome

174 IgA nephropathy (IgAN) is a complex trait determined by

175 IgA nephropathy (IgAN) is a progressive form of kidney d

176 IgA nephropathy (IgAN) is associated with a risk for pos

177 IgA nephropathy (IgAN) is characterized by circulating i

178 IgA nephropathy (IgAN) is characterized by glomerular de

179 IgA nephropathy (IgAN) is characterized by mesangial cel

180 r long-term kidney survival in patients with IgA nephropathy (IgAN) is controversial.

181 The role of immunosuppression in IgA nephropathy (IgAN) is controversial.

182 IgA nephropathy (IgAN) is the leading primary GN worldwi

183 IgA nephropathy (IgAN) is the most common form of glomer

184 IgA nephropathy (IgAN) is the most common form of primar

185 Berger's IgA nephropathy (IgAN) is the most common primary glomer

186 IgA nephropathy (IgAN) is the most common primary glomer

187 IgA nephropathy (IgAN) is the most common type of glomer

188 IgA nephropathy (IgAN) is the most prevalent among prima

189 IgA nephropathy (IgAN) often follows infections and feat

190 The pediatric International IgA Nephropathy (IgAN) Prediction Tool comprises two mod

191 The International IgA Nephropathy (IgAN) Prediction Tool is the preferred

192 IgA nephropathy (IgAN) represents the leading cause of k

193 The clinical course of IgA nephropathy (IgAN) varies from asymptomatic nonprogr

194 al budesonide (Nefecon) for the treatment of IgA nephropathy (IgAN) was first demonstrated by the pha

195 ggest treatment with corticosteroids (CS) in IgA nephropathy (IgAN) when proteinuria is persistently

196 tion have been linked to the pathogenesis of IgA nephropathy (IgAN), a kidney disease characterized b

197 IgA nephropathy (IgAN), characterized by mesangial IgA1

198 In IgA nephropathy (IgAN), IgA immune complexes are deposit

199 tients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative GN (MPGN)

200 In IgA nephropathy (IgAN), serum IgA1 with abnormal O-glyco

201 In IgA nephropathy (IgAN), serum IgA1 with abnormal O-glyco

202 in about 6-8% of the disease heritability of IgA nephropathy (IgAN), suggesting that there are still

203 A deposition is the pathognomonic feature of IgA nephropathy (IgAN), the extent of mesangial IgA accu

204 The hallmark of IgA nephropathy (IgAN), the most common form of glomerul

205 ed a genome-wide association study (GWAS) of IgA nephropathy (IgAN), the most common form of glomerul

206 IgA nephropathy (IgAN), the most common primary glomerul

207 IgA nephropathy (IgAN), the most prevalent primary glome

208 IgA nephropathy (IgAN), the world's most common primary

209 1 may contribute to pathogenic mechanisms in IgA nephropathy (IgAN).

210 dney plays a key role in the pathogenesis of IgA nephropathy (IgAN).

211 ntibody under investigation for treatment of IgA nephropathy (IgAN).

212 ions are risk factors for the progression of IgA Nephropathy (IgAN).

213 athway has a key role in the pathogenesis of IgA nephropathy (IgAN).

214 /HORMAD2/LIF/OSM locus to be associated with IgA nephropathy (IgAN).

215 racellular matrix lead to the progression of IgA nephropathy (IgAN).

216 osylated hinge region O-glycans characterize IgA nephropathy (IgAN).

217 Membranous nephropathy (MN, 24.96%) and IgA nephropathy (IgAN, 24.09%) were the most common prim

218 A common renal disease, immunoglobulin A (IgA) nephropathy (IgAN), is associated with glomerular d

219 he underlying pathology of immunoglobulin A (IgA) nephropathy (IgAN), the most common glomerulonephri

220 Many of the alleles that protect against IgA nephropathy impart increased risk for other autoimmu

221 rogression of renal disease in patients with IgA nephropathy in a multicenter, placebo-controlled, ra

222 rving renal function in patients with severe IgA nephropathy in a randomized, open-label, parallel-gr

223 d their fragments may serve as biomarkers of IgA nephropathy in serum, urine, or renal tissue.

224 on susceptibility alleles that predispose to IgA nephropathy in the European population.

225 miR-148b function in PBMCs of patients with IgA nephropathy increased C1GALT1 mRNA and protein level

226 ed EBV-immortalized cells from patients with IgA nephropathy indicated a decrease in beta1,3-galactos

227 IgA nephropathy is a chronic immune-mediated kidney dise

228 IgA nephropathy is a chronic kidney disease defined by d

229 IgA nephropathy is an important global cause of kidney f

230 proteinuria in diabetes (types 1 and 2) and IgA nephropathy is related to the degree of podocyte dep

231 The pivotal event in the pathophysiology of IgA nephropathy is the binding of circulating IgA-contai

232 he paramount difficulty in the management of IgA nephropathy is the heterogeneity in its clinical pre

233 IgA nephropathy is the most common glomerular disease wo

234 IgA nephropathy is thought to be associated with mucosal

235 Immunoglobulin A (IgA) nephropathy is a common form of glomerulonephritis,

236 Immunoglobulin A (IgA) nephropathy is the most common form of primary glom

237 We now know that IgA nephropathy leads to progressive renal destruction i

238 sine modification ameliorated progression of IgA nephropathy-like kidney disease in mice.

239 gA levels and ameliorated progression of the IgA nephropathy-like kidney disease in miR-23b(-/-) and

240 f serum IgA levels and the development of an IgA nephropathy-like kidney disease in miR-23b(-/-) and

241 re/grade/class for disease entities, such as IgA nephropathy, lupus nephritis, and ANCA GN; and addit

242 luding infection-related glomerulonephritis, IgA nephropathy, lupus nephritis, and cryoglobulinaemic

243 ases affecting the glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropat

244 r understanding of the role of complement in IgA nephropathy may provide potential targets and ration

245 imab, at least at this stage and severity of IgA nephropathy, may reflect a failure of rituximab to r

246 patients with a single underlying diagnosis: IgA nephropathy (n = 5), diabetes (n = 7), or lupus neph

247 ferative glomerulonephritis type 1 (n = 12), IgA nephropathy (n = 7), and mesangial glomerulonephriti

248 ulizumab in Proliferative Lupus Nephritis or IgA Nephropathy (NCT04564339) was a randomized, double-b

249 ulizumab in Proliferative Lupus Nephritis or IgA Nephropathy, NCT04564339.

250 ntains genes that seem to influence familial IgA nephropathy, obesity, BP, insulin resistance, and ty

251 hat may be shared by other diseases, such as IgA nephropathy or age-related macular degeneration, and

252 rs characteristically occur in patients with IgA nephropathy or C3 glomerulopathy.

253 3 children with histopathologically verified IgA nephropathy or IgA vasculitis with nephropathy as we

254 from both adult and pediatric patients with IgA nephropathy or IgA vasculitis with nephropathy in re

255 membranous nephropathy, or FSGS to 3%-5% in IgA nephropathy or lupus nephritis.

256 Atacicept in Subjects with IgA Nephropathy (ORIGIN 3), NCT04716231.

257 a may have a significant favorable effect on IgA nephropathy outcomes.

258 acy and safety of atacicept in patients with IgA nephropathy over 96 weeks.

259 nal function loss in high-risk patients with IgA nephropathy, particularly those with moderately adva

260 production is believed to play a key role in IgA nephropathy pathogenesis; however, little is known a

261 Some 103 (2.53%) IgA nephropathy patients had an earlier inflammatory bow

262 nd IL-5 by peripheral blood lymphocytes from IgA nephropathy patients might result in the production

263 hort study, we compared 3963 biopsy-verified IgA nephropathy patients with 19,978 matched controls be

264 epigenetic regulatory mechanism, exaggerated IgA nephropathy phenotype in mice.

265 RNA modification resulted in an exaggerated IgA nephropathy phenotype.

266 Understanding why certain patients with IgA nephropathy progress to kidney failure while others

267 NAs specifically associated with the risk of IgA nephropathy progression.

268 nd displayed the best discrimination between IgA nephropathy progressors and non-progressors by recei

269 were found to be differentially expressed in IgA nephropathy progressors compared to non-progressors,

270 Adults with IgA nephropathy, proteinuria >=1 g/d, and eGFR >=30 ml/m

271 cludes poststreptococcal glomerulonephritis, IgA nephropathy, rapidly progressive glomerulonephritis

272 y, but not in those with lupus membranous or IgA nephropathy, recognized PLA(2)R.

273 Drusen in IgA nephropathy resemble drusen found in age-related mac

274 ximally titrated irbesartan in patients with IgA nephropathy resulted in significant reductions in pr

275 other autoimmune or infectious diseases, and IgA nephropathy risk allele frequencies closely parallel

276 derived from patients with sporadic forms of IgA nephropathy (see the related article beginning on pa

277 e-wide analysis in a cohort of patients with IgA nephropathy selected from the UK Glomerulonephritis

278 subtypes of segmental glomerulosclerosis in IgA nephropathy showing podocyte injury that also behave

279 ive Therapy for the Treatment of Progressive IgA Nephropathy (STOP-IgAN) Trial, 162 patients with IgA

280 nt models of mesangioproliferative GN and in IgA nephropathy, suggesting that GATA3 plays a critical

281 ould become the first specific treatment for IgA nephropathy targeting intestinal mucosal immunity up

282 ked to increased circulating IgA levels, and IgA nephropathy, the most common form of primary GN and

283 Immunoglobulin A (IgA) nephropathy, the most common form of glomerulonephr

284 molecular mechanism(s) of immunoglobulin A (IgA) nephropathy, the most common primary renal glomerul

285 s involving altered O-glycosylation, such as IgA nephropathy, Tn syndrome, Henoch-Schonlein purpura,

286 Among patients with IgA nephropathy, treatment with iptacopan resulted in a

287 Thus, NefIgArd is the first phase 3 IgA nephropathy trial to show clinically important impro

288 ion is a predictor of poor renal survival in IgA nephropathy.Trial registration TCTR, TCTR20140515001

289 enetic correlations of serum IgA levels with IgA nephropathy, type 2 diabetes, and body mass index, a

290 Disease manifestations and progression of IgA nephropathy vary widely between individuals, particu

291 splants) with end-stage renal disease due to IgA nephropathy were performed at the University of Cali

292 a studying APRIL inhibition, with a focus on IgA nephropathy where the clinical development of APRIL

293 ed 141 Caucasian patients with biopsy-proven IgA nephropathy who had minor abnormalities at presentat

294 g-term prognosis for Caucasian patients with IgA nephropathy who present with minor urinary abnormali

295 The long-term outcome of patients with IgA nephropathy who present with normal renal function,

296 Participants with IgA nephropathy who received atacicept (25, 75, or 150 m

297 tcome from a dataset of 148 individuals with IgA nephropathy who underwent renal biopsy at our instit

298 ndomly assigned adults with biopsy-confirmed IgA nephropathy who were at high risk for disease progre