ライフサイエンスコーパス: glomerular disease

1 the pathology of various diseases, including glomerular disease.

2 s; TRPC6 expression is increased in acquired glomerular disease.

3 e proteinuria in patients with B7-1-positive glomerular disease.

4 ationship between podocyte Sema3a excess and glomerular disease.

5 cells (MCs) is a key finding in progressive glomerular disease.

6 syndrome, is an antibody-mediated autoimmune glomerular disease.

7 y which it might discourage the evolution of glomerular disease.

8 atterning, contributes to the development of glomerular disease.

9 ating they were not a general consequence of glomerular disease.

10 ion strongly correlates with albuminuria and glomerular disease.

11 of urine protein charge forms identifies the glomerular disease.

12 utoantibodies or biopsy-proven recurrence of glomerular disease.

13 hannel 6), and the role of these proteins in glomerular disease.

14 ave significant roles in the pathobiology of glomerular disease.

15 not have a major influence on this aspect of glomerular disease.

16 podocyte genes may be a common etiology for glomerular disease.

17 ceptors in podocyte biology and non-diabetic glomerular disease.

18 d effective therapeutic stra-tegy for Alport glomerular disease.

19 lternative mechanism for the pathogenesis of glomerular disease.

20 ify novel signaling pathways contributing to glomerular disease.

21 rent efforts to implement clinical trials of glomerular disease.

22 nto potential pathogenic mechanisms of human glomerular disease.

23 implementing appropriately powered trials of glomerular disease.

24 plays a key role in glomerular function and glomerular disease.

25 as a determinant of human susceptibility to glomerular disease.

26 ta1 on mesangial cells, a TGF-beta target in glomerular disease.

27 abnormal capillary development might lead to glomerular disease.

28 y warrant evaluation in vivo in experimental glomerular disease.

29 rd (EHR) algorithm to identify children with glomerular disease.

30 ur investigation, may be responsible for the glomerular disease.

31 en causally implicated in the progression of glomerular disease.

32 (HCV) has been linked to the development of glomerular disease.

33 c antibodies, immunoglobulin deposition, and glomerular disease.

34 sion characteristic of most forms of chronic glomerular disease.

35 tubulointerstitial nephritis associated with glomerular disease.

36 hanism may underlie genetic Fn-deposit human glomerular disease.

37 reatment of a mouse model of immune-mediated glomerular disease.

38 tial RNA-based therapeutic strategy to treat glomerular disease.

39 us presenting a novel treatment strategy for glomerular disease.

40 e potential strategies to treat non-diabetic glomerular disease.

41 eased H3K27me3 levels and sensitized mice to glomerular disease.

42 s another potential therapeutic strategy for glomerular disease.

43 Fibrillary GN (FGN) is a rare primary glomerular disease.

44 keletal apparatus results in proteinuria and glomerular disease.

45 uld be a novel therapeutic avenue in chronic glomerular disease.

46 resents the most aggressive form of acquired glomerular disease.

47 TFEB activity may improve podocyte health in glomerular disease.

48 culation inflammation, and de novo/recurrent glomerular disease.

49 d its absolute requirement for prevention of glomerular disease.

50 miR-193a influences the behavior of PECs in glomerular disease.

51 tochondrial genes can result in experimental glomerular disease.

52 LF6 expression is reduced in mouse and human glomerular disease.

53 promotes podocyte injury and proteinuria in glomerular diseases.

54 lial cells (GECs) causes proteinuria in many glomerular diseases.

55 for the treatment of immune complex-mediated glomerular diseases.

56 macologic modulators to induce regression of glomerular diseases.

57 uring foot process effacement in a subset of glomerular diseases.

58 s of differentiation is the hallmark of many glomerular diseases.

59 cement observed in distinct subsets of human glomerular diseases.

60 ic nephropathy, as well as other nondiabetic glomerular diseases.

61 form a complex in normal podocytes, in human glomerular diseases.

62 h primary FSGS, but not in people with other glomerular diseases.

63 emolytic uremic syndrome (aHUS), and various glomerular diseases.

64 ion of angiotensin II to the pathogenesis of glomerular diseases.

65 cal tool for the diagnosis and monitoring of glomerular diseases.

66 for targeted drug therapy in lupus and other glomerular diseases.

67 , but is upregulated in both human and mouse glomerular diseases.

68 is likely to be a common mechanism promoting glomerular diseases.

69 in the kidney in diabetes and possibly other glomerular diseases.

70 ify candidate protein biomarkers to diagnose glomerular diseases.

71 progressive loss of renal function in human glomerular diseases.

72 R that are implicated in the pathogenesis of glomerular diseases.

73 ic effect in mesangial cells in inflammatory glomerular diseases.

74 e a useful therapeutic approach for treating glomerular diseases.

75 ntified as a component of immune deposits in glomerular diseases.

76 murine models of renal disease and in human glomerular diseases.

77 central manifestation of chronic progressive glomerular diseases.

78 merulus for investigation of and therapy for glomerular diseases.

79 t functions of leukocyte-associated genes in glomerular diseases.

80 ssion are characteristic features of several glomerular diseases.

81 o-interstitial fibrosis in chronic nephrotic glomerular diseases.

82 n of monocytes within the glomerulus seen in glomerular diseases.

83 to unravel the underlying pathophysiology of glomerular diseases.

84 including diabetic kidney disease and other glomerular diseases.

85 hannel activity of TRPC6 in association with glomerular diseases.

86 healthy glomeruli or in 19 types of non-FGN glomerular diseases.

87 tinely used to identify and classify various glomerular diseases.

88 e metabolizing role of APA in AngII-mediated glomerular diseases.

89 ts into the biology and (patho)physiology of glomerular diseases.

90 h is likely important for the development of glomerular diseases.

91 docyte function, is downregulated in various glomerular diseases.

92 festing as proteinuria, is the cause of many glomerular diseases.

93 n shown to cause proteinuria and progressive glomerular diseases.

94 arrier and are key targets of injury in many glomerular diseases.

95 that Gq-dependent TRPC6 activation underlies glomerular diseases.

96 ve therapeutic benefits for the treatment of glomerular diseases.

97 equencies in patients with FSGS (35%), other glomerular diseases (20%), and healthy volunteers (22%).

98 urvival and cope with stress during advanced glomerular disease, a new study shows.

99 In most forms of glomerular disease, abnormal filter barrier function res

100 epatic manifestations include immune complex glomerular disease, accelerated progression of CKD, incr

101 The algorithm identified 6657 children with glomerular disease across PEDSnet, >=50% of whom were se

102 After renal transplantation, persistent glomerular disease affecting the native kidneys typicall

103 ough case reports have described relapses of glomerular disease after COVID-19 vaccination, evidence

104 old (P<0.001) in patients with biopsy-proven glomerular disease and a 50% decrease in kidney function

105 s(lpr) mice revealed an overall reduction in glomerular disease and a significant reduction in vascul

106 ability of metformin to improve non-diabetic glomerular disease and chronic kidney disease (CKD) has

107 y vitamin D supplementation in patients with glomerular disease and chronic renal insufficiency, whic

108 to kidney podocytes often results in chronic glomerular disease and consecutive nephron malfunction.

109 acute interstitial nephritis (AIN), although glomerular disease and electrolyte disturbances have als

110 ietary interventions could prevent and treat glomerular disease and hypertension-induced nephropathy.

111 ied genes implicated as causal in hereditary glomerular disease and involved in molecular pathways of

112 Expert pathology reviews showed that glomerular disease and isolated immune complex depositio

113 d in injured podocytes in vitro and in human glomerular disease and participates in negative control

114 Light microscopic analysis shows extensive glomerular disease and proteinaceous casts.

115 role of oxidants in diabetic and nondiabetic glomerular disease and their role in tubulointerstitial

116 es is a new mechanism in the pathogenesis of glomerular disease and thus could represent a new therap

117 e interactions has been widely implicated in glomerular diseases and acute renal failure.

118 renal filtration draws from studies of human glomerular diseases and animal models of glomerular dysf

119 s sufficient for the development of numerous glomerular diseases and can be absolute (loss of podocyt

120 increased concentration of suPAR in various glomerular diseases and in other human pathologies with

121 inuria and glomerular injury in experimental glomerular diseases and induces remission of nephrotic s

122 odocyte depletion occurs in most progressive glomerular diseases and is thought to result from podocy

123 ad6 is upregulated in the mesangium in human glomerular diseases and may be involved in functions ind

124 feration is a characteristic feature of many glomerular diseases and often precedes extracellular mat

125 sis became widespread and before several new glomerular diseases and variants were described.

126 sk alleles have a greatly increased risk for glomerular disease, and APOL1-associated FSGS occurs ear

127 ate Alport syndrome, the commonest monogenic glomerular disease, and compared findings to other genet

128 argeted allele show progressive proteinuria, glomerular disease, and typically death by several month

129 (4712 with CKD stages 2 through 5, 866 with glomerular diseases, and 2777 with no kidney disease), t

130 tive extrarenal SLE, inactive SLE, and other glomerular diseases, and correlated with disease clinica

131 antibodies, from the 76 patients with other glomerular diseases, and from the 44 healthy controls re

132 membranous nephropathy, patients with other glomerular diseases, and healthy controls for antibodies

133 features of FGN overlap with those of other glomerular diseases, and no unique histologic biomarkers

134 glomerular abnormalities, 42% showed primary glomerular diseases, and only 16% had evidence of calcin

135 ved in patients with MCD in remission, other glomerular diseases, and systemic lupus erythematosus wi

136 hypertension, diabetes mellitus, and chronic glomerular disease are largely unknown.

137 h glucocorticoids ameliorate proteinuria and glomerular disease are not well understood.

138 Glomerular diseases are a major cause for chronic kidney

139 Glomerular diseases are classified using a descriptive t

140 The primary therapies for many glomerular diseases are glucocorticoids, which exert the

141 Glomerular diseases are not only a frequent cause of chr

142 he PLA2R and sPLA2 IB in the pathogenesis of glomerular diseases are unknown.

143 ive liver disease and increases the risks of glomerular disease as well as new onset diabetes after t

144 xin 43 in damaged glomeruli in patients with glomerular diseases as well as in mice after induction o

145 sed on a neutral isoelectric point) in other glomerular diseases as well.

146 le in a number of renal disorders, including glomerular diseases, ascribed to injury to the glomerulo

147 pha5(IV) and is characterized by progressive glomerular disease associated with a high-frequency sens

148 tunities for pharmacological intervention in glomerular diseases associated with ER stress.

149 ining its potential value as a biomarker for glomerular diseases associated with GBM alterations.

150 led the identification and classification of glomerular diseases based on two-dimensional information

151 profiling show great promise for identifying glomerular disease biomarkers.

152 In a glomerular disease biorepository cohort (n = 128), we me

153 nitiates an inflammatory cascade that causes glomerular disease but there are many modulating factors

154 of progressive renal failure associated with glomerular disease, but how this protein overload transl

155 development of several types of proteinuric glomerular disease, but the involvement of immunological

156 be used to identify the etiology in certain glomerular diseases, but in the future, LCM/MS can play

157 ates activation of NF-kappaB in a variety of glomerular diseases, but the mechanisms involved are unk

158 enetic reprogramming can improve outcomes in glomerular disease by repressing the reactivation of dev

159 obal glomerulosclerosis, and all progressive glomerular diseases can be considered superimposed accel

160 8 glomerular disease cases in the 100KG, unsolved via geno

161 ctional tetraspanin CD151 is associated with glomerular disease characterised by early onset proteinu

162 ogenitors for glomerular epithelial cells in glomerular disease characterized by podocyte depletion.

163 ogenitors for glomerular epithelial cells in glomerular disease characterized by podocyte depletion.

164 Podocyte damage is the basis of many glomerular diseases characterized by loss of interdigita

165 Nephrotic-range proteinuria is due to glomerular diseases characterized by podocyte injury.

166 omerulopathy, which represents a spectrum of glomerular diseases characterized on fluorescent microsc

167 Glomerular disease, characterized by podocyte injury and

168 ertebral fracture risk were increased in the glomerular disease cohort: adjusted IRR was 2.2 (95% CI,

169 In one of the largest glomerular disease cohorts to study plasminogen, we vali

170 e practice and university nephrologists (the Glomerular Disease Collaborative Network).

171 rotein is highly induced in individuals with glomerular diseases, connexin 43 may be a novel target f

172 Therefore, neutrophil participation in glomerular diseases deserves re-evaluation.

173 mouse Ig in this cryoglobulin; furthermore, glomerular disease develops when mice are injected with

174 with diabetic glomerulosclerosis as the only glomerular disease diagnosis (n=109).

175 Sle1.BAFF and B6.Nba2.BAFF mice, severity of glomerular disease did not obligately correlate with cir

176 odocyte mRNAs increased in all categories of glomerular disease evaluated, but levels ranged from hig

177 ice with Cfh(-/-) kidneys (n = 12) developed glomerular disease features, including increased albumin

178 is upregulated in podocytes in all examined glomerular diseases (focal segmental glomerulosclerosis

179 cation of cohorts of pediatric patients with glomerular disease for observational or prospective stud

180 nal biopsies from patients with a variety of glomerular diseases for expression of VPF/VEGF mRNA and

181 , and trial medicine related to podocyte and glomerular diseases for the benefit of patients, the Int

182 the design of new therapeutic strategies for glomerular diseases for which available therapies are no

183 with nephrotic syndrome resulting from other glomerular diseases (FSGS, membranoproliferative glomeru

184 and induce rhythmic expression of potential glomerular disease genes associated with nephrotic syndr

185 e not explained by mutations in known ECM or glomerular disease genes.

186 ican Americans, but whether APOL1-associated glomerular disease has a distinct clinical phenotype is

187 The association between malignancy and glomerular disease has been appreciated for over three d

188 by which alpha-actinin-4 deficiency leads to glomerular disease has not been defined.

189 to visceral epithelial cells in a variety of glomerular diseases has the potential for releasing rela

190 of in vivo alterations of physical forces in glomerular disease have been hampered by a lack of quant

191 Children and young adults with glomerular disease have significantly higher burden of s

192 Children with glomerular disease have unique risk factors for compromi

193 Patients with glomerular diseases have an injured renal filtration bar

194 logic features and outcome of HCV-associated glomerular disease (HCV-GD) in 14 patients with HIV coin

195 s RARRES1 expression is upregulated in human glomerular diseases, here we investigated the functional

196 onents have helped to build understanding of glomerular disease; however, the full composition and re

197 as detected in those patients with recurrent glomerular disease (HR 3.76, 95% CI 1.37-10.35, P=0.01),

198 the mAb rituximab may benefit the autoimmune glomerular disease idiopathic membranous nephropathy (IM

199 H3K27me3 content of podocytes and attenuated glomerular disease in adriamycin nephrotoxicity, SNx, an

200 Both mouse models showed more severe glomerular disease in APOL1-G1 compared with APOL1-G0 mi

201 pathic nephrotic syndrome is the most common glomerular disease in children.

202 revealed a membranoproliferative pattern of glomerular disease in five cases, and a membranous glome

203 ype, which contribute to the pathogenesis of glomerular disease in HIV-associated nephropathy (HIVAN)

204 n the development of immune complex-mediated glomerular disease in mice.

205 of the molecular and cellular mechanisms of glomerular disease in the intact living kidney.

206 ry in patients with LCCD and CN, and chronic glomerular disease in the other types, 35% of whom had s

207 egnancies, making it perhaps the most common glomerular disease in the world.

208 is causal for altered podocyte function and glomerular disease in vivo.

209 enrichment of genes implicated in monogenic glomerular diseases in podocytes.

210 t literature and elicited expert opinions on glomerular diseases in pregnancy with the aim to provide

211 ffacement is associated with proteinuria and glomerular disease, in three different mouse models, it

212 d with proteinuria and glomerulosclerosis in glomerular diseases including DN.

213 kappaB pathway in podocytes is implicated in glomerular diseases including proteinuria.

214 mice demonstrates changes characteristic of glomerular disease, including a thickened and disorganiz

215 the pathology traditionally associated with glomerular disease, including capillary wall injury.

216 is are common pathologic features of several glomerular diseases, including transplant rejection.

217 obiology and its role in the pathogenesis of glomerular disease increases, new targets for podocyte-s

218 -function in adult mice leads to proteinuric glomerular disease involving the three layers of the glo

219 l work in both basic and clinical studies of glomerular disease is needed to advance the field.

220 ation of podocyte gene expression in primary glomerular disease is poorly understood.

221 omeruli are highly sophisticated filters and glomerular disease is the leading cause of kidney failur

222 nical study of its antiproteinuric effect in glomerular disease is warranted.

223 ve indicated that heavy proteinuria in renal glomerular diseases is associated with the formation of

224 g pathways may act as factors in proteinuric glomerular diseases is poorly understood.

225 tive Heymann nephritis of rat, an autoimmune glomerular disease, is an immunohistological, ultrastruc

226 For the remaining glomerular diseases, LCM/MS has remained a research tool

227 In most forms of glomerular diseases, loss of size selectivity by the kid

228 The rarity of pediatric glomerular disease makes it difficult to identify suffic

229 an early step in the pathogenesis of various glomerular diseases, making these cells excellent target

230 subjects with FSGS, but not those with other glomerular diseases, manifested increased c-Src phosphor

231 therapies are beneficial in the treatment of glomerular diseases may be a reduction in injury to the

232 Among the primary glomerular diseases, MCD is usually sensitive to glucoco

233 sma albumin in the puromycin aminonucleoside glomerular disease model.

234 not typically classified as an inflammatory glomerular disease, mounting evidence supports the invol

235 ed findings to other genetic mouse models of glomerular disease (Myo1e-/-, Ptpro-/-).

236 In several glomerular diseases, nephrin expression decreases and po

237 Recurrence of glomerular disease occurred in two DSCI recipients, lead

238 ion of podocytes plays a central role in the glomerular disease of HIV-associated nephropathy (HIVAN)

239 Albuminuria is a hallmark of glomerular disease of various etiologies.

240 In glomerular diseases of diverse etiologies, dysfunction o

241 Glomerular disease often features altered histologic pat

242 The mechanism for delayed glomerular disease onset is unknown.

243 healthy volunteers (FSGS compared with other glomerular disease, P < 0.02; FSGS compared with healthy

244 of TRPC6 is increased in some acquired human glomerular diseases, particularly in membranous nephropa

245 ould evaluate the role of YAP in proteinuric glomerular disease pathogenesis and its potential utilit

246 o treatment, and provide novel insights into glomerular disease pathophysiology.

247 In glomerular disease, podocyte injury results in a dramati

248 Podocytopenia characterizes many forms of glomerular disease, preceding the development of glomeru

249 Glomerular disease presenting as proteinuria with or wit

250 d suffering, focusing on specific targets in glomerular disease, preserving meaning in life, and fost

251 rtensive change, but there are also specific glomerular disease processes present.

252 hat elevated gelatinase activity exacerbates glomerular disease progression in these mice.

253 While studying mechanisms of glomerular disease, rat ZHX3 was cloned from a down-regu

254 Children with glomerular disease received dialysis earlier and were le

255 Biopsy-proven glomerular disease recurrence was similar in patients in

256 The glomerular disease-related gene, CD2AP, exhibited an STR

257 Another glomerular disease-related gene, rabphilin 3A, exhibited

258 the regulation of these protein complexes in glomerular disease remains elusive.

259 ng loss-of-alpha-actinin-4 function in human glomerular diseases remains elusive.

260 n plasmin (ogen) uria and kidney function in glomerular diseases remains unclear.

261 Even in mice with severe glomerular disease, renal tubulointerstitial infiltrates

262 rticoids, which are frequently used to treat glomerular disease, reset the podocyte clock and induce

263 overwhelmed in podocytes during experimental glomerular disease, resulting in abnormal protein accumu

264 The most common form of glomerular disease seen in association with hepatitis C

265 In kidneys of young patients with underlying glomerular diseases similar pathologic events were ident

266 ding podocyte biology and its involvement in glomerular disease subjectively from my perspective.

267 isease among African-Americans, particularly glomerular diseases such as HIV nephropathy and idiopath

268 tients had a high proportion of albuminuria, glomerular diseases such as steroid-resistant nephrotic

269 hogenesis and treatment of rheumatologic and glomerular diseases such as systemic lupus erythematosus

270 e mechanism driving progression in all human glomerular diseases, suggest that urine pellet podocyte

271 For most glomerular diseases, targeted therapies are lacking.

272 Diagnosis of the type of glomerular disease that causes the nephrotic syndrome is

273 Alport syndrome is a hereditary glomerular disease that leads to kidney failure.

274 ldhood-onset lupus nephritis is an important glomerular disease that requires safe and effective trea

275 IgA nephropathy (IgAN) is a common chronic glomerular disease that, in most patients, slowly progre

276 nsin-aldosterone system (RAAS) inhibition in glomerular diseases, the events explaining this increase

277 ury to the podocyte may vary between various glomerular diseases, the inevitable consequence of podoc

278 r, no substantial advances have been made in glomerular disease therapies, and the standard of care f

279 enia or other psychotic disorder, those with glomerular disease, tubulo-interstitial disease, or chro

280 oteinuria and podocyturia varied markedly by glomerular disease type: a high correlation in minimal-c

281 ive study in 443 patients with biopsy-proven glomerular diseases undergoing kidney transplantation.

282 BLL and GFR was stronger among children with glomerular disease underlying CKD; in this group, each 1

283 FSGS is the most common primary glomerular disease underlying ESRD in the United States

284 In many glomerular diseases, VPF/VEGF-expressing cells were decr

285 it of patients, the International Society of Glomerular Disease was officially launched during the co

286 To elucidate its influence on glomerular disease, we have investigated TCF21 expressio

287 th humans and mice with "nonimmune" forms of glomerular disease, we hypothesized that natural IgM bin

288 ion with alemtuzumab increases recurrence of glomerular disease, we performed a retrospective study i

289 eting the computable phenotype definition of glomerular disease were defined as nonglomerular cases.

290 Glomerular diseases were observed in kidney biopsies obt

291 jor cause of chronic kidney disease (CKD) is glomerular disease, which can be attributed to a spectru

292 Podocyte injury is a hallmark of glomerular disease, which is generally displayed by the

293 n alpha1-null Alport mice exhibit attenuated glomerular disease with decreased matrix accumulation an

294 asize the need to treat every patient with a glomerular disease with either an angiotensin-converting

295 individual mice after chemical induction of glomerular disease (with Doxorubicin or LPS).

296 ephropathy (IgAN) is the most common primary glomerular disease worldwide and is a leading cause of r

297 ) nephropathy, the most common primary renal glomerular disease worldwide, is unknown.

298 IgA nephropathy is the most common glomerular disease worldwide.

299 y (IgAN) is the most prevalent among primary glomerular diseases worldwide.

300 zation of animal models of distinct forms of glomerular disease would likely facilitate the search fo