ライフサイエンスコーパス: glomerular disease

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

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

3 atterning, contributes to the development of glomerular disease.

4 keletal apparatus results in proteinuria and glomerular disease.

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

6 ion strongly correlates with albuminuria and glomerular disease.

7 of urine protein charge forms identifies the glomerular disease.

8 utoantibodies or biopsy-proven recurrence of glomerular disease.

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

10 ave significant roles in the pathobiology of glomerular disease.

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

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

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

14 lternative mechanism for the pathogenesis of glomerular disease.

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

16 rent efforts to implement clinical trials of glomerular disease.

17 nto potential pathogenic mechanisms of human glomerular disease.

18 implementing appropriately powered trials of glomerular disease.

19 resents the most aggressive form of acquired glomerular disease.

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

21 as a determinant of human susceptibility to glomerular disease.

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

23 abnormal capillary development might lead to glomerular disease.

24 y warrant evaluation in vivo in experimental glomerular disease.

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

26 en causally implicated in the progression of glomerular disease.

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

28 c antibodies, immunoglobulin deposition, and glomerular disease.

29 sion characteristic of most forms of chronic glomerular disease.

30 tubulointerstitial nephritis associated with glomerular disease.

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

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

33 TFEB activity may improve podocyte health in glomerular disease.

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

35 d its absolute requirement for prevention of glomerular disease.

36 eased H3K27me3 levels and sensitized mice to glomerular disease.

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

38 tochondrial genes can result in experimental glomerular disease.

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

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

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

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

43 ationship between podocyte Sema3a excess and glomerular disease.

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

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

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

47 cement observed in distinct subsets of human glomerular diseases.

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

49 tinely used to identify and classify various glomerular diseases.

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

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

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

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

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

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

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

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

58 ify candidate protein biomarkers to diagnose glomerular diseases.

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

60 progressive loss of renal function in human glomerular diseases.

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

62 ic effect in mesangial cells in inflammatory glomerular diseases.

63 e a useful therapeutic approach for treating glomerular diseases.

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

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

66 central manifestation of chronic progressive glomerular diseases.

67 merulus for investigation of and therapy for glomerular diseases.

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

69 ssion are characteristic features of several glomerular diseases.

70 o-interstitial fibrosis in chronic nephrotic glomerular diseases.

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

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

73 docyte function, is downregulated in various glomerular diseases.

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

75 hannel activity of TRPC6 in association with glomerular diseases.

76 n shown to cause proteinuria and progressive glomerular diseases.

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

78 that Gq-dependent TRPC6 activation underlies glomerular diseases.

79 ve therapeutic benefits for the treatment of glomerular diseases.

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

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

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

83 macologic modulators to induce regression of glomerular diseases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 profiling show great promise for identifying glomerular disease biomarkers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Patients with glomerular diseases have an injured renal filtration bar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 In several glomerular diseases, nephrin expression decreases and po

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

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

188 In glomerular diseases of diverse etiologies, dysfunction o

189 Glomerular disease often features altered histologic pat

190 The mechanism for delayed glomerular disease onset is unknown.

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

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

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

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

195 In glomerular disease, podocyte injury results in a dramati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Glomerular diseases were observed in kidney biopsies obt

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

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

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

228 IgA nephropathy is the most common glomerular disease worldwide.

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

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