ライフサイエンスコーパス: focal segmental glomerulosclerosis

1 s needed (for example, APOL1 kidney disease, focal segmental glomerulosclerosis).

2 ic domain showed histology characteristic of focal segmental glomerulosclerosis.

3 resulting in progressive kidney failure and focal segmental glomerulosclerosis.

4 odocyte numbers decrease in association with focal segmental glomerulosclerosis.

5 13.1, a region with genes linked to familial focal segmental glomerulosclerosis.

6 od pressure did correlate with the degree of focal segmental glomerulosclerosis.

7 ents with renal failure caused by idiopathic focal segmental glomerulosclerosis.

8 5% higher odds of CKD and 84% higher odds of focal segmental glomerulosclerosis.

9 uric patients with reduced renal function or focal segmental glomerulosclerosis.

10 raemic syndrome, diabetic kidney disease and focal segmental glomerulosclerosis.

11 in participants with two APOL1 variants and focal segmental glomerulosclerosis.

12 lic and biallelic APOL1 variants with CKD or focal segmental glomerulosclerosis.

13 racterized by skeletal changes, glaucoma and focal segmental glomerulosclerosis.

14 icularly in podocytes, in human kidneys with focal segmental glomerulosclerosis.

15 damage, but chronic overactivation leads to focal segmental glomerulosclerosis.

16 -function mutations cause autosomal dominant focal segmental glomerulosclerosis.

17 th HIV-associated nephropathy and idiopathic focal segmental glomerulosclerosis.

18 teinuric kidney disease that resembles human focal segmental glomerulosclerosis.

19 disease and membranous nephropathy, but not focal segmental glomerulosclerosis.

20 progressed to renal failure associated with focal segmental glomerulosclerosis.

21 he underlying disease mechanism in inherited focal segmental glomerulosclerosis.

22 risk for hypertension-attributable ESRD and focal segmental glomerulosclerosis.

23 njury in sclerosing glomerulopathies such as focal segmental glomerulosclerosis.

24 thelial cells in diabetic nephropathy and in focal segmental glomerulosclerosis.

25 in assembly assay identified alpha-actinin-4/focal segmental glomerulosclerosis 1 (FSGS1) as an essen

26 followed by a family history of CKD (23.4%), focal segmental glomerulosclerosis (18.0%), cystic kidne

27 athy (4/4), transplant glomerulopathy (3/4), focal segmental glomerulosclerosis (2/4), and/or membran

28 a cross-linking approach, we have identified focal segmental glomerulosclerosis 3/CD2-associated prot

29 There was a surprisingly high prevalence of focal segmental glomerulosclerosis (50%) and global glom

30 identified in human patients with inherited focal segmental glomerulosclerosis, a condition that can

31 utations in INF2 are linked to two diseases: focal segmental glomerulosclerosis, a kidney disease, an

32 e with early-onset proteinuria and global or focal segmental glomerulosclerosis, accompanied by an al

33 CI, 1.04 to 1.33), as well as higher odds of focal segmental glomerulosclerosis (adjusted odds ratio,

34 I], 1.11 to 1.40), as well as higher odds of focal segmental glomerulosclerosis (adjusted odds ratio,

35 e models of both obstructive nephropathy and focal segmental glomerulosclerosis (adriamycin nephropat

36 The 33 patients with recurrent focal segmental glomerulosclerosis after transplantation

37 ses in patient biopsies and a mouse model of focal segmental glomerulosclerosis allowed for accurate

38 -associated nephropathy with collapsing-type focal segmental glomerulosclerosis and characteristic tu

39 inhibited by CAP-KAc-actin, suggesting that focal segmental glomerulosclerosis and Charcot-Marie-Too

40 ssion of RARRES1 in mice in the experimental focal segmental glomerulosclerosis and diabetic kidney d

41 ed normal at birth but developed progressive focal segmental glomerulosclerosis and died in terminal

42 tients with congenital (onset 0 to 3 months) focal segmental glomerulosclerosis and five patients wit

43 ium channel TRPC6 lead to autosomal dominant focal segmental glomerulosclerosis and podocyte expressi

44 iologies, including diabetic kidney disease, focal segmental glomerulosclerosis and polycystic kidney

45 r receptor (suPAR) have been associated with focal segmental glomerulosclerosis and poor clinical out

46 kidney abnormalities, including albuminuria, focal segmental glomerulosclerosis and progressive kidne

47 L1 nephropathy - that typically manifests as focal segmental glomerulosclerosis and the clinical synd

48 duction, we briefly review new insights into focal segmental glomerulosclerosis and the role of podoc

49 table syndrome in evaluation of females with focal segmental glomerulosclerosis and to consider their

50 omavirus hominis type I), recurrent disease (focal segmental glomerulosclerosis), and posttransplant

51 d nephropathy, which is a collapsing form of focal segmental glomerulosclerosis, and an increased inc

52 otein deposits in the glomeruli, progressive focal segmental glomerulosclerosis, and effacement of vi

53 al change disease, 7 of 74 (9%) with primary focal segmental glomerulosclerosis, and only in rare cas

54 ts who had two APOL1 variants, biopsy-proven focal segmental glomerulosclerosis, and proteinuria (uri

55 sses the spectrum of minimal change disease, focal segmental glomerulosclerosis, and related disorder

56 Glomerulomegaly and focal segmental glomerulosclerosis are histopathological

57 s of nephrosis and why some patients develop focal segmental glomerulosclerosis are less striking, bu

58 females with normal genital development and focal segmental glomerulosclerosis associated with a WT1

59 These Tg mice develop a collapsing focal segmental glomerulosclerosis associated with micro

60 s an early pathomechanism in mice developing focal-segmental glomerulosclerosis associated with funct

61 8% higher odds of CKD and 61% higher odds of focal segmental glomerulosclerosis; biallelic APOL1 vari

62 human TRPC6 channel cause autosomal-dominant focal segmental glomerulosclerosis, but the molecular co

63 e associated with kidney diseases, including focal segmental glomerulosclerosis, characterized by pro

64 Obesity has been associated with a secondary focal segmental glomerulosclerosis coined obesity-relate

65 Focal segmental glomerulosclerosis correlated with prote

66 tage kidney disease (ESKD), early-onset CKD, focal segmental glomerulosclerosis, cystic kidney diseas

67 and lies near the K255E mutation that causes focal segmental glomerulosclerosis) demonstrated increas

68 pregulated in the glomeruli of patients with focal segmental glomerulosclerosis, diabetic nephropathy

69 Patients with focal segmental glomerulosclerosis exhibited specific TM

70 rophy in nephronopenia to the development of focal segmental glomerulosclerosis (FGS) in humans.

71 polycystic kidney disease (ADPKD), familial focal segmental glomerulosclerosis (FSG), hypomagnesemia

72 esent report describes five patients who had focal segmental glomerulosclerosis (FSGS) (four with rec

73 A) administration to patients with recurrent focal segmental glomerulosclerosis (FSGS) after transpla

74 e observational cohort studies (135/153 with focal segmental glomerulosclerosis (FSGS) and 119/113 wi

75 the development of extracapillary lesions in focal segmental glomerulosclerosis (FSGS) and crescentic

76 Here, we show that, in African Americans, focal segmental glomerulosclerosis (FSGS) and hypertensi

77 ned kidney biopsy specimens of patients with focal segmental glomerulosclerosis (FSGS) and minimal ch

78 ngenital nephrotic syndrome characterized by focal segmental glomerulosclerosis (FSGS) and proteinuri

79 We identified an association of focal segmental glomerulosclerosis (FSGS) and proteinuri

80 Mutations in INF2 lead to the kidney disease focal segmental glomerulosclerosis (FSGS) and the neurol

81 enteenfold higher odds (95% CI 11 to 26) for focal segmental glomerulosclerosis (FSGS) and twenty-nin

82 Idiopathic forms of Focal Segmental Glomerulosclerosis (FSGS) are caused by

83 Primary and secondary forms of focal segmental glomerulosclerosis (FSGS) are characteri

84 Primary and secondary forms of focal segmental glomerulosclerosis (FSGS) are common cau

85 Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are glomerulop

86 Hypertensive nephropathy (HN) and focal segmental glomerulosclerosis (FSGS) are significan

87 se plasminogen activator receptor (suPAR) in focal segmental glomerulosclerosis (FSGS) as the circula

88 articular, genetic testing reclassified some focal segmental glomerulosclerosis (FSGS) cases into col

89 The histopathologic diagnosis of primary focal segmental glomerulosclerosis (FSGS) has come to in

90 Familial forms of focal segmental glomerulosclerosis (FSGS) have been link

91 (ACTN4) cause an autosomal dominant form of focal segmental glomerulosclerosis (FSGS) in affected hu

92 ulin M nephropathy (IgM) in 14 patients, and focal segmental glomerulosclerosis (FSGS) in five patien

93 lop glomerular lesions that mimic collapsing focal segmental glomerulosclerosis (FSGS) in humans with

94 both familial and sporadic steroid-resistant focal segmental glomerulosclerosis (FSGS) in the pediatr

95 Focal segmental glomerulosclerosis (FSGS) is a cause of

96 Focal segmental glomerulosclerosis (FSGS) is a common ca

97 Focal segmental glomerulosclerosis (FSGS) is a common ca

98 Focal segmental glomerulosclerosis (FSGS) is a common fo

99 Collapsing focal segmental glomerulosclerosis (FSGS) is a distinct

100 Focal segmental glomerulosclerosis (FSGS) is a leading c

101 Focal segmental glomerulosclerosis (FSGS) is a pathologi

102 Focal segmental glomerulosclerosis (FSGS) is a pattern o

103 Focal segmental glomerulosclerosis (FSGS) is a podocytop

104 Focal segmental glomerulosclerosis (FSGS) is a relativel

105 Focal segmental glomerulosclerosis (FSGS) is a syndrome

106 Recurrent focal segmental glomerulosclerosis (FSGS) is heralded by

107 Focal segmental glomerulosclerosis (FSGS) is not a speci

108 Focal segmental glomerulosclerosis (FSGS) is one of the

109 Apolipoprotein L1 (APOL1)-associated focal segmental glomerulosclerosis (FSGS) is the dominan

110 Focal segmental glomerulosclerosis (FSGS) is the main pa

111 Focal segmental glomerulosclerosis (FSGS) is the most co

112 Focal segmental glomerulosclerosis (FSGS) lesions have b

113 merular tuft participate in the formation of focal segmental glomerulosclerosis (FSGS) lesions.

114 D-1 antibody to young mice with experimental focal segmental glomerulosclerosis (FSGS) lowered protei

115 In collapsing focal segmental glomerulosclerosis (FSGS) of HIV-associa

116 Primary focal segmental glomerulosclerosis (FSGS) often causes n

117 ses to immunosuppressive therapy, those with focal segmental glomerulosclerosis (FSGS) often exhibit

118 We tested three strategies to identify focal segmental glomerulosclerosis (FSGS) or minimal cha

119 ents, who displayed elevated TNF levels, and focal segmental glomerulosclerosis (FSGS) patients, whos

120 lar plasmin (ogen) was found in PAN rats and focal segmental glomerulosclerosis (FSGS) patients.

121 nt of kidney transplantation recipients with focal segmental glomerulosclerosis (FSGS) recurrence.

122 Focal segmental glomerulosclerosis (FSGS) recurs after k

123 and podocyte loss during the pathogenesis of focal segmental glomerulosclerosis (FSGS) remains undefi

124 y potential markers of steroid-resistance in focal segmental glomerulosclerosis (FSGS) we evaluated i

125 or inverted formin-2 (INF2) mutations causes focal segmental glomerulosclerosis (FSGS) with or withou

126 nary cells from 15 (41%) of 36 patients with focal segmental glomerulosclerosis (FSGS), 2 (10%) of 20

127 Common forms of glomerulonephritis seen were focal segmental glomerulosclerosis (FSGS), 57; immunoglo

128 tein, alpha-actinin 4 (ACTN4), are linked to focal segmental glomerulosclerosis (FSGS), a chronic kid

129 alpha-actinin-4 have been linked to familial focal segmental glomerulosclerosis (FSGS), a common rena

130 Dominant INF2 mutations cause focal segmental glomerulosclerosis (FSGS), a kidney dise

131 in 4 (ACTN4) are linked to familial forms of focal segmental glomerulosclerosis (FSGS), a kidney dise

132 Collapsing focal segmental glomerulosclerosis (FSGS), also known as

133 d primary nephrotic syndrome (NS), including focal segmental glomerulosclerosis (FSGS), as a primary

134 n (CELL), seen in some patients with primary focal segmental glomerulosclerosis (FSGS), comprises pro

135 ble for a dominantly inherited form of human focal segmental glomerulosclerosis (FSGS), evidence supp

136 ssociates with increased risk for idiopathic focal segmental glomerulosclerosis (FSGS), HIV-1-associa

137 ociate with the nondiabetic kidney diseases, focal segmental glomerulosclerosis (FSGS), HIV-associate

138 MYH9 as a susceptibility gene for idiopathic focal segmental glomerulosclerosis (FSGS), HIV-associate

139 In collapsing forms of focal segmental glomerulosclerosis (FSGS), including idi

140 otic syndrome, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), infection-rel

141 frequencies of minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), LN and hepati

142 of idiopathic nephrotic syndrome, including focal segmental glomerulosclerosis (FSGS), minimal chang

143 Histologically, 60% exhibited focal segmental glomerulosclerosis (FSGS), often collaps

144 a subset of adults and children with primary focal segmental glomerulosclerosis (FSGS), proteinuria a

145 Specific diagnoses included were focal segmental glomerulosclerosis (FSGS), rapidly progr

146 This approach was applied to study focal segmental glomerulosclerosis (FSGS), the leading c

147 Focal segmental glomerulosclerosis (FSGS), the second le

148 disposing to idiopathic and HIV-1-associated focal segmental glomerulosclerosis (FSGS), we carried ou

149 e-specific genes are associated with genetic focal segmental glomerulosclerosis (FSGS), yet the poten

150 (ACTN4) cause an autosomal dominant form of focal segmental glomerulosclerosis (FSGS).

151 ding c-Src phosphorylation, proteinuria, and focal segmental glomerulosclerosis (FSGS).

152 minimal-change nephrotic syndrome (MCNS) and focal segmental glomerulosclerosis (FSGS).

153 the phenotype from CNF to one of congenital focal segmental glomerulosclerosis (FSGS).

154 ting causative factor has been postulated in focal segmental glomerulosclerosis (FSGS).

155 no generally accepted treatment for primary focal segmental glomerulosclerosis (FSGS).

156 with either minimal change disease (MCD) or focal segmental glomerulosclerosis (FSGS).

157 mplicated in chronic kidney disease, such as focal segmental glomerulosclerosis (FSGS).

158 n several forms of kidney disease, including focal segmental glomerulosclerosis (FSGS).

159 in glomeruli of patients with biopsy-proven focal segmental glomerulosclerosis (FSGS).

160 tibodies in minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS).

161 , the target cells in the kidney, leading to focal segmental glomerulosclerosis (FSGS).

162 kidney's filtration unit, a condition called focal segmental glomerulosclerosis (FSGS).

163 ion of chronic kidney disease (CKD), such as focal segmental glomerulosclerosis (FSGS).

164 a rare cause of autosomal dominant familial focal segmental glomerulosclerosis (FSGS).

165 e strain to adriamycin-induced (ADR-induced) focal segmental glomerulosclerosis (FSGS).

166 aminonucleoside (PAN) and from patients with focal segmental glomerulosclerosis (FSGS).

167 eceptor (suPAR) was associated recently with focal segmental glomerulosclerosis (FSGS).

168 roposed as a cause of two thirds of cases of focal segmental glomerulosclerosis (FSGS).

169 RPC6) gene are a cause of autosomal dominant focal segmental glomerulosclerosis (FSGS).

170 oss, and a prototypic injury response called focal segmental glomerulosclerosis (FSGS).

171 esponsible for familial forms of adult onset focal segmental glomerulosclerosis (FSGS).

172 docytes in all examined glomerular diseases (focal segmental glomerulosclerosis [FSGS], minimal-chang

173 children (mean age, 6.9 years; 136 boys; 57% focal segmental glomerulosclerosis, FSGS) were followed

174 lear RNA-seq data showed similarity to human focal segmental glomerulosclerosis glomerular RNA-seq da

175 Two human patients with focal segmental glomerulosclerosis had a mutation predic

176 To determine whether patients with focal segmental glomerulosclerosis have a circulating fa

177 se individuals without such variants to have focal segmental glomerulosclerosis, HIV-associated nephr

178 ) (referent) and lower for all other groups: focal segmental glomerulosclerosis (HR, 0.80; 95% CI, 0.

179 hropathy (HRa, 0.47; 95% CI, 0.29-0.75), and focal segmental glomerulosclerosis (HRa, 0.69; 95% CI, 0

180 arteriosclerosis in idiopathic and secondary focal segmental glomerulosclerosis, hypertensive nephros

181 Minimal change disease and primary focal segmental glomerulosclerosis in adults, along with

182 tified five families with autosomal dominant focal segmental glomerulosclerosis in which disease segr

183 ion of podocytes associated with progressive focal-segmental glomerulosclerosis in CD2AP-/- mice.

184 Using a model of focal segmental glomerulosclerosis, increased filtration

185 Focal segmental glomerulosclerosis is a nonspecific rena

186 rculating factor found in some patients with focal segmental glomerulosclerosis is associated with re

187 Focal segmental glomerulosclerosis is the leading cause

188 responsive nephrotic syndrome, in particular focal segmental glomerulosclerosis, its pathogenesis and

189 upports the clinical value of subclassifying focal segmental glomerulosclerosis lesions (S1).

190 for primary podocytopathies manifesting with focal segmental glomerulosclerosis lesions includes gluc

191 kidney biopsy are minimal change lesions and focal segmental glomerulosclerosis lesions.

192 icient to induce spontaneous proteinuria and focal segmental glomerulosclerosis-like glomerular damag

193 We found that focal segmental glomerulosclerosis-linked ACTN4 mutants

194 diseases, including minimal change disease, focal segmental glomerulosclerosis, membranous nephropat

195 en healthy control samples and patients with focal-segmental glomerulosclerosis, membranous glomerulo

196 l expansion, capsular adhesions (synechiae), focal segmental glomerulosclerosis, mild persistent prot

197 obtained from patients with IgA nephropathy, focal segmental glomerulosclerosis, minimal change disea

198 eristic histological patterns, most commonly focal segmental glomerulosclerosis, minimal changes, mem

199 rtensive nephrosclerosis (n = 7), idiopathic focal segmental glomerulosclerosis (n = 11), focal scler

200 People With a Type of Kidney Disease Called Focal Segmental Glomerulosclerosis, NCT05213624.

201 athy, diffuse proliferative lupus nephritis, focal segmental glomerulosclerosis (not collapsing glome

202 pathologic entity that includes proteinuria, focal segmental glomerulosclerosis often of the collapsi

203 Podocytes in glomeruli from humans with focal segmental glomerulosclerosis or diabetic nephropat

204 tochemistry of tissues from individuals with focal segmental glomerulosclerosis or nonalcoholic steat

205 Primary focal segmental glomerulosclerosis (pFSGS) is an acquire

206 s a major challenge in patients with primary focal segmental glomerulosclerosis (pFSGS).

207 le to the biopsies from patients with AS and focal segmental glomerulosclerosis, possibly indicating

208 ht recent progress in the physiopathology of focal segmental glomerulosclerosis recurrence after tran

209 the kidneys examined histologically with the focal segmental glomerulosclerosis score computed from p

210 ) and a form of autosomal recessive familial focal segmental glomerulosclerosis (SRN1), respectively.

211 1 was increased in human kidneys manifesting focal segmental glomerulosclerosis suggesting a correlat

212 d on top of ARHGAP24, a gene associated with focal segmental glomerulosclerosis, suggesting this gene

213 eveloping chronic kidney disease, especially focal segmental glomerulosclerosis -, than European Amer

214 basement membrane glomerulonephritis, and a focal segmental glomerulosclerosis that is characteristi

215 were associated with morphologic changes of focal segmental glomerulosclerosis together with interst

216 ey diseases such as diabetic nephropathy and focal segmental glomerulosclerosis, we observed upregula

217 used by idiopathic membranous nephropathy or focal segmental glomerulosclerosis were confirmed by gen

218 sis in the 5/6 nephrectomy (Nx) rat model of focal segmental glomerulosclerosis were investigated.

219 ial proliferative glomerulonephritis, or (3) focal segmental glomerulosclerosis were studied.

220 Focal segmental glomerulosclerosis, which is a common gl

221 ry mutations in actin-binding proteins cause focal segmental glomerulosclerosis, while other organs r

222 ophy and a renal biopsy specimen that showed focal segmental glomerulosclerosis with abnormal podocyt

223 (HIVAN), is an aggressive form of collapsing focal segmental glomerulosclerosis with accompanying tub

224 rapeutic strategy for glomerulonephritis and focal segmental glomerulosclerosis with parietal epithel

225 Histologically, HIVAN is a collapsing focal segmental glomerulosclerosis with prominent tubula

226 This review discusses the development of focal segmental glomerulosclerosis, with particular atte