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

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

2 in sclerosing glomerulopathies such as focal segmental glomerulosclerosis.

3 l cells in diabetic nephropathy and in focal segmental glomerulosclerosis.

4 ain showed histology characteristic of focal segmental glomerulosclerosis.

5 ting in progressive kidney failure and focal segmental glomerulosclerosis.

6 e numbers decrease in association with focal segmental glomerulosclerosis.

7 a region with genes linked to familial focal segmental glomerulosclerosis.

8 ssure did correlate with the degree of focal segmental glomerulosclerosis.

9 ith renal failure caused by idiopathic focal segmental glomerulosclerosis.

10 y (CG) is an aggressive variant of focal and segmental glomerulosclerosis.

11 ith FSGS including podocyte loss, leading to segmental glomerulosclerosis.

12 e glomerular injury in the form of focal and segmental glomerulosclerosis.

13 her odds of CKD and 84% higher odds of focal segmental glomerulosclerosis.

14 syndrome, diabetic kidney disease and focal segmental glomerulosclerosis.

15 rticipants with two APOL1 variants and focal segmental glomerulosclerosis.

16 d biallelic APOL1 variants with CKD or focal segmental glomerulosclerosis.

17 ized by skeletal changes, glaucoma and focal segmental glomerulosclerosis.

18 atients with reduced renal function or focal segmental glomerulosclerosis.

19 ly in podocytes, in human kidneys with focal segmental glomerulosclerosis.

20 membrane splitting, and secondary focal and segmental glomerulosclerosis.

21 e, but chronic overactivation leads to focal segmental glomerulosclerosis.

22 ion mutations cause autosomal dominant focal segmental glomerulosclerosis.

23 -associated nephropathy and idiopathic focal segmental glomerulosclerosis.

24 ic kidney disease that resembles human focal segmental glomerulosclerosis.

25 se and membranous nephropathy, but not focal segmental glomerulosclerosis.

26 essed to renal failure associated with focal segmental glomerulosclerosis.

27 erlying disease mechanism in inherited focal segmental glomerulosclerosis.

28 for hypertension-attributable ESRD and focal segmental glomerulosclerosis.

29 s in INF2 cause the kidney disease focal and segmental glomerulosclerosis.

30 embly assay identified alpha-actinin-4/focal segmental glomerulosclerosis 1 (FSGS1) as an essential f

31 ed by a family history of CKD (23.4%), focal segmental glomerulosclerosis (18.0%), cystic kidney dise

32 4/4), transplant glomerulopathy (3/4), focal segmental glomerulosclerosis (2/4), and/or membranous ne

33 s-linking approach, we have identified focal segmental glomerulosclerosis 3/CD2-associated protein (F

34 was a surprisingly high prevalence of focal segmental glomerulosclerosis (50%) and global glomerulos

35 ified in human patients with inherited focal segmental glomerulosclerosis, a condition that can lead

36 ns in INF2 are linked to two diseases: focal segmental glomerulosclerosis, a kidney disease, and Char

37 es of fetal development results in focal and segmental glomerulosclerosis, a reduced number of nephro

38 early-onset proteinuria and global or focal segmental glomerulosclerosis, accompanied by an altered

39 04 to 1.33), as well as higher odds of focal segmental glomerulosclerosis (adjusted odds ratio, 1.61;

40 11 to 1.40), as well as higher odds of focal segmental glomerulosclerosis (adjusted odds ratio, 1.84;

41 ls of both obstructive nephropathy and focal segmental glomerulosclerosis (adriamycin nephropathy), w

42 The 33 patients with recurrent focal segmental glomerulosclerosis after transplantation had a

43 patient biopsies and a mouse model of focal segmental glomerulosclerosis allowed for accurate and co

44 iated nephropathy with collapsing-type focal segmental glomerulosclerosis and characteristic tubulocy

45 ited by CAP-KAc-actin, suggesting that focal segmental glomerulosclerosis and Charcot-Marie-Tooth dis

46 is mutated in two human diseases, focal and segmental glomerulosclerosis and Charcot-Marie-Tooth dis

47 of RARRES1 in mice in the experimental focal segmental glomerulosclerosis and diabetic kidney disease

48 mal at birth but developed progressive focal segmental glomerulosclerosis and died in terminal renal

49 Renal tissue showed focal and segmental glomerulosclerosis and extensive effacement an

50 with congenital (onset 0 to 3 months) focal segmental glomerulosclerosis and five patients with poss

51 sed histologically for evidence of focal and segmental glomerulosclerosis and hyalinosis (FSGS), and

52 annel TRPC6 lead to autosomal dominant focal segmental glomerulosclerosis and podocyte expression of

53 es, including diabetic kidney disease, focal segmental glomerulosclerosis and polycystic kidney disea

54 ptor (suPAR) have been associated with focal segmental glomerulosclerosis and poor clinical outcomes

55 abnormalities, including albuminuria, focal segmental glomerulosclerosis and progressive kidney dise

56 hropathy - that typically manifests as focal segmental glomerulosclerosis and the clinical syndrome o

57 n, we briefly review new insights into focal segmental glomerulosclerosis and the role of podocytes i

58 syndrome in evaluation of females with focal segmental glomerulosclerosis and to consider their risk

59 had significantly lower baseline eGFR, more segmental glomerulosclerosis and total glomerulosclerosi

60 imated glomerular filtration rate and higher segmental glomerulosclerosis and vascular arterial intim

61 us hominis type I), recurrent disease (focal segmental glomerulosclerosis), and posttransplant lympho

62 ropathy, which is a collapsing form of focal segmental glomerulosclerosis, and an increased incidence

63 deposits in the glomeruli, progressive focal segmental glomerulosclerosis, and effacement of visceral

64 iltration, glomerular hypertrophy, focal and segmental glomerulosclerosis, and intimal vascular hyper

65 nge disease, 7 of 74 (9%) with primary focal segmental glomerulosclerosis, and only in rare cases amo

66 had two APOL1 variants, biopsy-proven focal segmental glomerulosclerosis, and proteinuria (urinary p

67 he spectrum of minimal change disease, focal segmental glomerulosclerosis, and related disorders.

68 Glomerulomegaly and focal segmental glomerulosclerosis are histopathological hallm

69 ephrosis and why some patients develop focal segmental glomerulosclerosis are less striking, but rece

70 es with normal genital development and focal segmental glomerulosclerosis associated with a WT1 intro

71 arly pathomechanism in mice developing focal-segmental glomerulosclerosis associated with functional

72 These Tg mice develop a collapsing focal segmental glomerulosclerosis associated with microcystic

73 her odds of CKD and 61% higher odds of focal segmental glomerulosclerosis; biallelic APOL1 variants w

74 and active caspase-3 increased in focal and segmental glomerulosclerosis biopsies, and both proteins

75 TRPC6 channel cause autosomal-dominant focal segmental glomerulosclerosis, but the molecular componen

76 ciated with kidney diseases, including focal segmental glomerulosclerosis, characterized by proteinur

77 y has been associated with a secondary focal segmental glomerulosclerosis coined obesity-related glom

78 Focal segmental glomerulosclerosis correlated with proteinuria

79 idney disease (ESKD), early-onset CKD, focal segmental glomerulosclerosis, cystic kidney disease, alt

80 es near the K255E mutation that causes focal segmental glomerulosclerosis) demonstrated increased act

81 Our studies indicate that segmental glomerulosclerosis develops as a result of pod

82 ated in the glomeruli of patients with focal segmental glomerulosclerosis, diabetic nephropathy, fibr

83 Patients with focal segmental glomerulosclerosis exhibited specific TMEM63C

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

85 ystic kidney disease (ADPKD), familial focal segmental glomerulosclerosis (FSG), hypomagnesemia with

86 report describes five patients who had focal segmental glomerulosclerosis (FSGS) (four with recurrent

87 inistration to patients with recurrent focal segmental glomerulosclerosis (FSGS) after transplantatio

88 rvational cohort studies (135/153 with focal segmental glomerulosclerosis (FSGS) and 119/113 with min

89 velopment of extracapillary lesions in focal segmental glomerulosclerosis (FSGS) and crescentic glome

90 e, we show that, in African Americans, focal segmental glomerulosclerosis (FSGS) and hypertension-att

91 thy, minimal change disease (MCD), focal and segmental glomerulosclerosis (FSGS) and membranous nephr

92 dney biopsy specimens of patients with focal segmental glomerulosclerosis (FSGS) and minimal change d

93 We identified an association of focal segmental glomerulosclerosis (FSGS) and proteinuria in a

94 al nephrotic syndrome characterized by focal segmental glomerulosclerosis (FSGS) and proteinuria.

95 models of adriamycin (ADR)-induced focal and segmental glomerulosclerosis (FSGS) and streptozotocin (

96 ons in INF2 lead to the kidney disease focal segmental glomerulosclerosis (FSGS) and the neurological

97 fold higher odds (95% CI 11 to 26) for focal segmental glomerulosclerosis (FSGS) and twenty-nine-fold

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

99 Primary and secondary forms of focal segmental glomerulosclerosis (FSGS) are characterized by

100 Primary and secondary forms of focal segmental glomerulosclerosis (FSGS) are common causes of

101 Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are glomerulopathies

102 Hypertensive nephropathy (HN) and focal segmental glomerulosclerosis (FSGS) are significant caus

103 The development of focal and segmental glomerulosclerosis (FSGS) as a consequence of

104 sminogen activator receptor (suPAR) in focal segmental glomerulosclerosis (FSGS) as the circulating f

105 lar, genetic testing reclassified some focal segmental glomerulosclerosis (FSGS) cases into collagen

106 duals with the proteinuric disease focal and segmental glomerulosclerosis (FSGS) compared to control

107 e histopathologic diagnosis of primary focal segmental glomerulosclerosis (FSGS) has come to include

108 Familial forms of focal segmental glomerulosclerosis (FSGS) have been linked to

109 4) cause an autosomal dominant form of focal segmental glomerulosclerosis (FSGS) in affected humans.

110 nephropathy (IgM) in 14 patients, and focal segmental glomerulosclerosis (FSGS) in five patients.

111 omerular lesions that mimic collapsing focal segmental glomerulosclerosis (FSGS) in humans with colla

112 amilial and sporadic steroid-resistant focal segmental glomerulosclerosis (FSGS) in the pediatric pop

113 Focal segmental glomerulosclerosis (FSGS) is a cause of protei

114 Focal segmental glomerulosclerosis (FSGS) is a common cause of

115 Focal segmental glomerulosclerosis (FSGS) is a common cause of

116 Focal segmental glomerulosclerosis (FSGS) is a common form of

117 Focal and segmental glomerulosclerosis (FSGS) is a common, non-spe

118 Collapsing focal segmental glomerulosclerosis (FSGS) is a distinct clinic

119 Focal and segmental glomerulosclerosis (FSGS) is a histological pa

120 Focal and segmental glomerulosclerosis (FSGS) is a kidney disorder

121 Focal segmental glomerulosclerosis (FSGS) is a leading cause o

122 Focal segmental glomerulosclerosis (FSGS) is a pathological en

123 Focal segmental glomerulosclerosis (FSGS) is a pattern of kidn

124 Focal segmental glomerulosclerosis (FSGS) is a podocytopathy l

125 Focal segmental glomerulosclerosis (FSGS) is a relatively prev

126 Focal segmental glomerulosclerosis (FSGS) is a syndrome that i

127 Recurrent focal segmental glomerulosclerosis (FSGS) is heralded by prote

128 Focal segmental glomerulosclerosis (FSGS) is not a specific di

129 Focal segmental glomerulosclerosis (FSGS) is one of the leadin

130 Apolipoprotein L1 (APOL1)-associated focal segmental glomerulosclerosis (FSGS) is the dominant form

131 Focal segmental glomerulosclerosis (FSGS) is the main patholog

132 Focal segmental glomerulosclerosis (FSGS) is the most common p

133 Focal segmental glomerulosclerosis (FSGS) lesions have been li

134 r tuft participate in the formation of focal segmental glomerulosclerosis (FSGS) lesions.

135 tibody to young mice with experimental focal segmental glomerulosclerosis (FSGS) lowered proteinuria

136 In collapsing focal segmental glomerulosclerosis (FSGS) of HIV-associated ne

137 Primary focal segmental glomerulosclerosis (FSGS) often causes nephrot

138 immunosuppressive therapy, those with focal segmental glomerulosclerosis (FSGS) often exhibit poorer

139 We tested three strategies to identify focal segmental glomerulosclerosis (FSGS) or minimal change di

140 who displayed elevated TNF levels, and focal segmental glomerulosclerosis (FSGS) patients, whose TNF

141 asmin (ogen) was found in PAN rats and focal segmental glomerulosclerosis (FSGS) patients.

142 kidney transplantation recipients with focal segmental glomerulosclerosis (FSGS) recurrence.

143 Focal segmental glomerulosclerosis (FSGS) recurs after kidney

144 docyte loss during the pathogenesis of focal segmental glomerulosclerosis (FSGS) remains undefined.

145 ntial markers of steroid-resistance in focal segmental glomerulosclerosis (FSGS) we evaluated intra-g

146 erted formin-2 (INF2) mutations causes focal segmental glomerulosclerosis (FSGS) with or without Char

147 ells from 15 (41%) of 36 patients with focal segmental glomerulosclerosis (FSGS), 2 (10%) of 20 patie

148 forms of glomerulonephritis seen were focal segmental glomerulosclerosis (FSGS), 57; immunoglobulin

149 alpha-actinin 4 (ACTN4), are linked to focal segmental glomerulosclerosis (FSGS), a chronic kidney di

150 a tractable therapeutic target for focal and segmental glomerulosclerosis (FSGS), a common cause of k

151 actinin-4 have been linked to familial focal segmental glomerulosclerosis (FSGS), a common renal diso

152 ACTN4) are linked to familial forms of focal segmental glomerulosclerosis (FSGS), a kidney disease ch

153 Dominant INF2 mutations cause focal segmental glomerulosclerosis (FSGS), a kidney disease, a

154 Collapsing focal segmental glomerulosclerosis (FSGS), also known as colla

155 ary nephrotic syndrome (NS), including focal segmental glomerulosclerosis (FSGS), as a primary podocy

156 L), seen in some patients with primary focal segmental glomerulosclerosis (FSGS), comprises prolifera

157 r a dominantly inherited form of human focal segmental glomerulosclerosis (FSGS), evidence supporting

158 tes with increased risk for idiopathic focal segmental glomerulosclerosis (FSGS), HIV-1-associated ne

159 s a susceptibility gene for idiopathic focal segmental glomerulosclerosis (FSGS), HIV-associated neph

160 with the nondiabetic kidney diseases, focal segmental glomerulosclerosis (FSGS), HIV-associated neph

161 In collapsing forms of focal segmental glomerulosclerosis (FSGS), including idiopathi

162 yndrome, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), infection-related G

163 ncies of minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), LN and hepatitis B

164 iopathic nephrotic syndrome, including focal segmental glomerulosclerosis (FSGS), minimal change dise

165 Histologically, 60% exhibited focal segmental glomerulosclerosis (FSGS), often collapsing.

166 et of adults and children with primary focal segmental glomerulosclerosis (FSGS), proteinuria and ren

167 Specific diagnoses included were focal segmental glomerulosclerosis (FSGS), rapidly progressive

168 This approach was applied to study focal segmental glomerulosclerosis (FSGS), the leading cause o

169 Focal segmental glomerulosclerosis (FSGS), the second leading

170 ing to idiopathic and HIV-1-associated focal segmental glomerulosclerosis (FSGS), we carried out an a

171 ific genes are associated with genetic focal segmental glomerulosclerosis (FSGS), yet the potential f

172 iseases of podocytes can result in focal and segmental glomerulosclerosis (FSGS).

173 4) cause an autosomal dominant form of focal segmental glomerulosclerosis (FSGS).

174 l-change nephrotic syndrome (MCNS) and focal segmental glomerulosclerosis (FSGS).

175 a-actinin-4, cause a form of human focal and segmental glomerulosclerosis (FSGS).

176 henotype from CNF to one of congenital focal segmental glomerulosclerosis (FSGS).

177 -Src phosphorylation, proteinuria, and focal segmental glomerulosclerosis (FSGS).

178 ausative factor has been postulated in focal segmental glomerulosclerosis (FSGS).

179 h-range proteinuria and most often focal and segmental glomerulosclerosis (FSGS).

180 nerally accepted treatment for primary focal segmental glomerulosclerosis (FSGS).

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

182 ral forms of kidney disease, including focal segmental glomerulosclerosis (FSGS).

183 es in minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS).

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

185 ted in chronic kidney disease, such as focal segmental glomerulosclerosis (FSGS).

186 omeruli of patients with biopsy-proven focal segmental glomerulosclerosis (FSGS).

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

188 chronic kidney disease (CKD), such as focal segmental glomerulosclerosis (FSGS).

189 e cause of autosomal dominant familial focal segmental glomerulosclerosis (FSGS).

190 in to adriamycin-induced (ADR-induced) focal segmental glomerulosclerosis (FSGS).

191 ucleoside (PAN) and from patients with focal segmental glomerulosclerosis (FSGS).

192 r (suPAR) was associated recently with focal segmental glomerulosclerosis (FSGS).

193 d as a cause of two thirds of cases of focal segmental glomerulosclerosis (FSGS).

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

195 nd a prototypic injury response called focal segmental glomerulosclerosis (FSGS).

196 as HIV nephropathy and idiopathic focal and segmental glomerulosclerosis (FSGS).

197 ible for familial forms of adult onset focal segmental glomerulosclerosis (FSGS).

198 s in all examined glomerular diseases (focal segmental glomerulosclerosis [FSGS], minimal-change dise

199 en (mean age, 6.9 years; 136 boys; 57% focal segmental glomerulosclerosis, FSGS) were followed a medi

200 NA-seq data showed similarity to human focal segmental glomerulosclerosis glomerular RNA-seq data.

201 Two human patients with focal segmental glomerulosclerosis had a mutation predicted to

202 To determine whether patients with focal segmental glomerulosclerosis have a circulating factor c

203 tor) and kidney diseases including focal and segmental glomerulosclerosis, HIV-associated nephropathy

204 ividuals without such variants to have focal segmental glomerulosclerosis, HIV-associated nephropathy

205 erent) and lower for all other groups: focal segmental glomerulosclerosis (HR, 0.80; 95% CI, 0.77-0.8

206 hy (HRa, 0.47; 95% CI, 0.29-0.75), and focal segmental glomerulosclerosis (HRa, 0.69; 95% CI, 0.45-1.

207 osclerosis in idiopathic and secondary focal segmental glomerulosclerosis, hypertensive nephroscleros

208 roteinuria and kidney failure with global or segmental glomerulosclerosis in adulthood.

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

210 podocytes associated with progressive focal-segmental glomerulosclerosis in CD2AP-/- mice.

211 workers identify histopathologic subtypes of segmental glomerulosclerosis in IgA nephropathy showing

212 five families with autosomal dominant focal segmental glomerulosclerosis in which disease segregated

213 Using a model of focal segmental glomerulosclerosis, increased filtration barri

214 Focal segmental glomerulosclerosis is a nonspecific renal lesi

215 ing factor found in some patients with focal segmental glomerulosclerosis is associated with recurren

216 Focal segmental glomerulosclerosis is the leading cause of ste

217 sive nephrotic syndrome, in particular focal segmental glomerulosclerosis, its pathogenesis and alter

218 s the clinical value of subclassifying focal segmental glomerulosclerosis lesions (S1).

219 Renal biopsy demonstrated focal and segmental glomerulosclerosis lesions classified as not o

220 imary podocytopathies manifesting with focal segmental glomerulosclerosis lesions includes glucocorti

221 biopsy are minimal change lesions and focal segmental glomerulosclerosis lesions.

222 to induce spontaneous proteinuria and focal segmental glomerulosclerosis-like glomerular damage in m

223 We found that focal segmental glomerulosclerosis-linked ACTN4 mutants lose t

224 lthy control samples and patients with focal-segmental glomerulosclerosis, membranous glomerulonephri

225 ses, including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, Ig

226 nsion, capsular adhesions (synechiae), focal segmental glomerulosclerosis, mild persistent proteinuri

227 ed from patients with IgA nephropathy, focal segmental glomerulosclerosis, minimal change disease, id

228 c histological patterns, most commonly focal segmental glomerulosclerosis, minimal changes, membranou

229 ve nephrosclerosis (n = 7), idiopathic focal segmental glomerulosclerosis (n = 11), focal sclerosis s

230 e With a Type of Kidney Disease Called Focal Segmental Glomerulosclerosis, NCT05213624.

231 diffuse proliferative lupus nephritis, focal segmental glomerulosclerosis (not collapsing glomerulopa

232 ogic entity that includes proteinuria, focal segmental glomerulosclerosis often of the collapsing var

233 odocytes in glomeruli from humans with focal segmental glomerulosclerosis or diabetic nephropathy exh

234 istry of tissues from individuals with focal segmental glomerulosclerosis or nonalcoholic steatohepat

235 r capillary infiltrates; P values 0.001) and segmental glomerulosclerosis (P value < 0.0001).

236 capillary infiltrates; p-values <=0.001) and segmental glomerulosclerosis (p-value <0.0001).

237 Primary focal segmental glomerulosclerosis (pFSGS) is an acquired kidn

238 jor challenge in patients with primary focal segmental glomerulosclerosis (pFSGS).

239 the biopsies from patients with AS and focal segmental glomerulosclerosis, possibly indicating that t

240 ent progress in the physiopathology of focal segmental glomerulosclerosis recurrence after transplant

241 ular or fibrocellular crescents [C], and for segmental glomerulosclerosis [S] and interstitial fibros

242 dneys examined histologically with the focal segmental glomerulosclerosis score computed from periodi

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

244 increased in human kidneys manifesting focal segmental glomerulosclerosis suggesting a correlation be

245 op of ARHGAP24, a gene associated with focal segmental glomerulosclerosis, suggesting this gene may p

246 ing chronic kidney disease, especially focal segmental glomerulosclerosis -, than European Americans.

247 ent membrane glomerulonephritis, and a focal segmental glomerulosclerosis that is characteristic of s

248 histologically distinct variant of focal and segmental glomerulosclerosis that presents with heavy pr

249 associated with morphologic changes of focal segmental glomerulosclerosis together with interstitial

250 cellularity, endocapillary hypercellularity, segmental glomerulosclerosis, tubular atrophy/interstiti

251 ortional hazards regression, the presence of segmental glomerulosclerosis was the only factor that si

252 eases such as diabetic nephropathy and focal segmental glomerulosclerosis, we observed upregulation o

253 y idiopathic membranous nephropathy or focal segmental glomerulosclerosis were confirmed by gene sequ

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

255 oliferative glomerulonephritis, or (3) focal segmental glomerulosclerosis were studied.

256 Focal segmental glomerulosclerosis, which is a common glomerul

257 ad transplant arteriosclerosis and focal and segmental glomerulosclerosis, while animals treated with

258 ations in actin-binding proteins cause focal segmental glomerulosclerosis, while other organs remain

259 nd a renal biopsy specimen that showed focal segmental glomerulosclerosis with abnormal podocytes con

260 ), is an aggressive form of collapsing focal segmental glomerulosclerosis with accompanying tubular a

261 centic GN, and another had global as well as segmental glomerulosclerosis with features of healed col

262 ic strategy for glomerulonephritis and focal segmental glomerulosclerosis with parietal epithelial ce

263 Histologically, HIVAN is a collapsing focal segmental glomerulosclerosis with prominent tubular dama

264 is review discusses the development of focal segmental glomerulosclerosis, with particular attention