ライフサイエンスコーパス: glomerulosclerosis

1 al age-related changes (arteriosclerosis and glomerulosclerosis).

2 cytes, in human kidneys with focal segmental glomerulosclerosis.

3 splitting, and secondary focal and segmental glomerulosclerosis.

4 ry and loss that may contribute to worsening glomerulosclerosis.

5 in proteinuria, foot process effacement, and glomerulosclerosis.

6 abnormalities before and during progressive glomerulosclerosis.

7 apoptosis both in vitro and in experimental glomerulosclerosis.

8 identified in association with focal global glomerulosclerosis.

9 heir loss causes proteinuria and progressive glomerulosclerosis.

10 tein deposition, which are early features of glomerulosclerosis.

11 drial dysfunction and apoptosis, followed by glomerulosclerosis.

12 modeling by DNA hypermethylation, leading to glomerulosclerosis.

13 genetic disorders manifesting as progressive glomerulosclerosis.

14 f protein aggregates, loss of podocytes, and glomerulosclerosis.

15 terstitial fibrosis and less than 30% to 40% glomerulosclerosis.

16 different strategies, on adriamycin-induced glomerulosclerosis.

17 within the glomerulus in an animal model of glomerulosclerosis.

18 est causality between APOL1 null alleles and glomerulosclerosis.

19 ove that these APOL1 sequence variants cause glomerulosclerosis.

20 S) and streptozotocin (STZ)-induced diabetic glomerulosclerosis.

21 onic overactivation leads to focal segmental glomerulosclerosis.

22 process effacement, mesangial expansion, and glomerulosclerosis.

23 thesis increased proteinuria and exacerbated glomerulosclerosis.

24 gravated proteinuria, macrophage influx, and glomerulosclerosis.

25 ons cause autosomal dominant focal segmental glomerulosclerosis.

26 ement activation may slow the progression of glomerulosclerosis.

27 mozygous the G1 and G2 alleles predispose to glomerulosclerosis.

28 echanisms, to promote renal inflammation and glomerulosclerosis.

29 developed significantly less proteinuria and glomerulosclerosis.

30 r kidney; but did produce cortical mesangial glomerulosclerosis.

31 d nephropathy and idiopathic focal segmental glomerulosclerosis.

32 disease that resembles human focal segmental glomerulosclerosis.

33 branous nephropathy, but not focal segmental glomerulosclerosis.

34 ch have both tubulointerstitial fibrosis and glomerulosclerosis.

35 enal failure associated with focal segmental glomerulosclerosis.

36 sease mechanism in inherited focal segmental glomerulosclerosis.

37 ension-attributable ESRD and focal segmental glomerulosclerosis.

38 cause the kidney disease focal and segmental glomerulosclerosis.

39 in both diabetic nephropathy and nondiabetic glomerulosclerosis.

40 lls and Bowman's capsule in the pathology of glomerulosclerosis.

41 FAT signaling in podocytes, proteinuria, and glomerulosclerosis.

42 podocytes and mediates podocyte depletion in glomerulosclerosis.

43 nal impairment, resulting in proteinuria and glomerulosclerosis.

44 et of podocyte dysfunction, proteinuria, and glomerulosclerosis.

45 erular disease, preceding the development of glomerulosclerosis.

46 not reduce albuminuria or the progression of glomerulosclerosis.

47 th proteinuria, loss of kidney function, and glomerulosclerosis.

48 uria in response to injury, as well as worse glomerulosclerosis.

49 ubular disease and, interestingly, secondary glomerulosclerosis.

50 ney ILC2s and ameliorated adriamycin-induced glomerulosclerosis.

51 s to defects and depletion, albuminuria, and glomerulosclerosis.

52 ion of extracellular matrix (ECM) leading to glomerulosclerosis.

53 iopsies obtained from individuals with focal glomerulosclerosis.

54 th reduced renal function or focal segmental glomerulosclerosis.

55 eletal changes, glaucoma and focal segmental glomerulosclerosis.

56 ensin II (AngII), a peptide known to promote glomerulosclerosis.

57 lial injury, podocyte loss, albuminuria, and glomerulosclerosis.

58 y identified alpha-actinin-4/focal segmental glomerulosclerosis 1 (FSGS1) as an essential factor.

59 0031, and 0.0028 um(3), respectively) and in glomerulosclerosis (18%, 7%, and 11%, respectively).

60 ical abnormalities was 65.8% (19.7% abnormal glomerulosclerosis, 23.9% abnormal interstitial fibrosis

61 approach, we have identified focal segmental glomerulosclerosis 3/CD2-associated protein (FSGS3/CD2AP

62 uman patients with inherited focal segmental glomerulosclerosis, a condition that can lead to end-sta

63 are linked to two diseases: focal segmental glomerulosclerosis, a kidney disease, and Charcot-Marie-

64 As glomerulosclerosis accumulates, the diseased kidney prog

65 To investigate glomerular volume and glomerulosclerosis across different depths of cortex, we

66 obstructive nephropathy and focal segmental glomerulosclerosis (adriamycin nephropathy), we observed

67 ns including extensive apoptotic cell death, glomerulosclerosis, afferent and efferent hyalinosis, an

68 mimetic Actn4 mice developed proteinuria and glomerulosclerosis after subtotal nephrectomy.

69 Only when glomerulosclerosis and arteriosclerosis exceed that expe

70 ated with larger nephrons on biopsy and more glomerulosclerosis and arteriosclerosis than would be ex

71 interstitial fibrosis, tubular atrophy, and glomerulosclerosis and associated independently with gra

72 ropathy with collapsing-type focal segmental glomerulosclerosis and characteristic tubulocystic chang

73 P-KAc-actin, suggesting that focal segmental glomerulosclerosis and Charcot-Marie-Tooth disease resul

74 d in two human diseases, focal and segmental glomerulosclerosis and Charcot-Marie-Tooth disease.

75 e OVE26 type 1 mouse, a model of progressive glomerulosclerosis and decline of renal function.

76 of the major causes of proteinuria, leads to glomerulosclerosis and end stage renal disease, but its

77 Renal tissue showed focal and segmental glomerulosclerosis and extensive effacement and microvil

78 R, and interstitial fibrosis associated with glomerulosclerosis and glomerular volume to a similar ex

79 haracteristic show similar associations with glomerulosclerosis and glomerulomegaly at different cort

80 y attenuated hyperglycemia, albuminuria, and glomerulosclerosis and increased podocyte filtration sli

81 ization and proteinaceous casts, with marked glomerulosclerosis and interstitial fibrosis by 6 weeks

82 nuria as well as lower histologic scores for glomerulosclerosis and interstitial fibrosis than untrea

83 Glomerulosclerosis and interstitial fibrosis were also s

84 associated with lower kidney function, more glomerulosclerosis and interstitial fibrosis, and greate

85 llaries and podocyte structure, and arrested glomerulosclerosis and interstitial fibrosis.

86 mising intervention to retard development of glomerulosclerosis and neointima formation in chronic tr

87 clonal immunoglobulin LC, leading to nodular glomerulosclerosis and nephrotic syndrome.

88 6 lead to autosomal dominant focal segmental glomerulosclerosis and podocyte expression of TRPC6 is i

89 ests that endothelin-1 drives development of glomerulosclerosis and podocyte loss through direct acti

90 buminuria and were completely protected from glomerulosclerosis and podocyte loss, even when uninephr

91 ing diabetic kidney disease, focal segmental glomerulosclerosis and polycystic kidney disease.

92 R) have been associated with focal segmental glomerulosclerosis and poor clinical outcomes in patient

93 ctivation of Rap1a and Rap1b induced massive glomerulosclerosis and premature death.

94 ts beyond the first year of engraftment, and glomerulosclerosis and progression to ESRD are caused by

95 ity to levels below a threshold value drives glomerulosclerosis and progression to ESRD.

96 ties, including albuminuria, focal segmental glomerulosclerosis and progressive kidney disease, and m

97 rregularities that manifested as adult-onset glomerulosclerosis and proteinuria.

98 flect glomerular damage, which culminates in glomerulosclerosis and proteinuria.

99 the podocytes of transgenic mice resulted in glomerulosclerosis and proteinuria.

100 h GS-444217 significantly inhibited diabetic glomerulosclerosis and reduced renal dysfunction but had

101 fly review new insights into focal segmental glomerulosclerosis and the role of podocytes in health a

102 ficantly lower baseline eGFR, more segmental glomerulosclerosis and total glomerulosclerosis, and mor

103 Glomerulosclerosis and tubulointerstitial fibrosis are a

104 Glomerulosclerosis and tubulointerstitial fibrosis were

105 n a 500-fold increase in albuminuria, marked glomerulosclerosis and tubulointerstitial fibrosis, and

106 dney disease is characterized by progressive glomerulosclerosis and tubulointerstitial fibrosis.

107 ia), structural (foot-process effacement and glomerulosclerosis) and molecular (gene-expression) chan

108 increased ectopic lipid accumulation (ELA), glomerulosclerosis, and albuminuria.

109 may therefore directly lead to focal global glomerulosclerosis, and all progressive glomerular disea

110 that the Elmo1 hypermorphs have albuminuria, glomerulosclerosis, and changes in the ultrastructure of

111 e higher creatinine at biopsy, percentage of glomerulosclerosis, and degree of interstitial fibrosis

112 model, 20-mg/kg 4SC-101 reduced proteinuria, glomerulosclerosis, and fibrosis with decreased IL-17 me

113 is at presentation, the presence of diabetic glomerulosclerosis, and greater tubular atrophy and inte

114 more segmental glomerulosclerosis and total glomerulosclerosis, and more tubular atrophy/interstitia

115 the mTORC1 pathway can trigger proteinuria, glomerulosclerosis, and progression to ESRD.

116 e, accompanied by tubulointerstitial damage, glomerulosclerosis, and proteinuria.

117 te density was associated with reduced eGFR, glomerulosclerosis, and proteinuria.

118 n of CCN3 resulted in decreased albuminuria, glomerulosclerosis, and reduced cortical collagen type I

119 jury leads to progressive loss of podocytes, glomerulosclerosis, and renal failure.

120 ed ROS prevented podocyte loss, albuminuria, glomerulosclerosis, and renal failure.

121 , whereas endocapillary proliferation, focal glomerulosclerosis, and tubulointerstitial abnormalities

122 oves renal injury by decreasing proteinuria, glomerulosclerosis, and tubulointerstitial fibrosis, and

123 G1 and G2 correlate best with glomerulosclerosis as recessive alleles, which suggests

124 es performed from 1995 to 2011 with diabetic glomerulosclerosis as the only glomerular disease diagno

125 rats, lesions of focal segmental and global glomerulosclerosis as well as tubulointerstitial lesions

126 Glomerulosclerosis associated more strongly with arterio

127 Interstitial fibrosis, tubular atrophy, and glomerulosclerosis associated significantly with death-c

128 d focal podocyte foot process effacement and glomerulosclerosis at 3 months.

129 inhibitor can induce regression of existing glomerulosclerosis, at least in part by decreasing matri

130 e caspase-3 increased in focal and segmental glomerulosclerosis biopsies, and both proteins displayed

131 ntly accompany idiopathic FSGS and secondary glomerulosclerosis, but it is unknown whether IgM activa

132 nel cause autosomal-dominant focal segmental glomerulosclerosis, but the molecular components involve

133 Podocyte depletion leads to glomerulosclerosis, but whether an impaired capacity of

134 tal epithelial cells, which together promote glomerulosclerosis by enhancing podocyte loss while supp

135 y elevated biomarkers of kidney dysfunction, glomerulosclerosis, C3/C5b-9 deposition, and reduced cir

136 Regression of glomerulosclerosis can be induced by angiotensin II anta

137 h kidney diseases, including focal segmental glomerulosclerosis, characterized by proteinuria and pod

138 associated with a secondary focal segmental glomerulosclerosis coined obesity-related glomerulopathy

139 Kidney glomerulosclerosis commonly progresses to end-stage kidn

140 ely invaded segments of the tuft affected by glomerulosclerosis, consistent with our previous finding

141 lomerulosclerosis, suggesting age-associated glomerulosclerosis could be caused by a similar mechanis

142 e K255E mutation that causes focal segmental glomerulosclerosis) demonstrated increased actin binding

143 Our studies indicate that segmental glomerulosclerosis develops as a result of podocyte-endo

144 Proteinuria and glomerulosclerosis did not develop if dietary calorie re

145 eficient mice, which develop proteinuria and glomerulosclerosis, display lower beta-catenin expressio

146 MYH9 disorders characterized by progressive glomerulosclerosis (Epstein and Fechtner syndromes).

147 te that secretes excess collagen in diabetic glomerulosclerosis), ET-1 increased mRNA and protein for

148 and tubuli and was associated with increased glomerulosclerosis even in a different set of DKD sample

149 Patients with focal segmental glomerulosclerosis exhibited specific TMEM63C loss in po

150 ngial sclerosis (focally approaching nodular glomerulosclerosis), focal arteriolar hyalinosis, mesang

151 cribes five patients who had focal segmental glomerulosclerosis (FSGS) (four with recurrent FSGS afte

152 of extracapillary lesions in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephri

153 that, in African Americans, focal segmental glomerulosclerosis (FSGS) and hypertension-attributed en

154 al change disease (MCD), focal and segmental glomerulosclerosis (FSGS) and membranous nephropathy.

155 identified an association of focal segmental glomerulosclerosis (FSGS) and proteinuria in a cohort of

156 ic syndrome characterized by focal segmental glomerulosclerosis (FSGS) and proteinuria.

157 adriamycin (ADR)-induced focal and segmental glomerulosclerosis (FSGS) and streptozotocin (STZ)-induc

158 2 lead to the kidney disease focal segmental glomerulosclerosis (FSGS) and the neurological disorder

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

160 ctivator receptor (suPAR) in focal segmental glomerulosclerosis (FSGS) as the circulating factor or a

161 Familial forms of focal segmental glomerulosclerosis (FSGS) have been linked to gain-of-fu

162 n autosomal dominant form of focal segmental glomerulosclerosis (FSGS) in affected humans.

163 esions that mimic collapsing focal segmental glomerulosclerosis (FSGS) in humans with collapse of the

164 Focal segmental glomerulosclerosis (FSGS) is a cause of proteinuric kidn

165 Focal segmental glomerulosclerosis (FSGS) is a common form of idiopathic

166 Focal and segmental glomerulosclerosis (FSGS) is a histological pattern freq

167 Focal segmental glomerulosclerosis (FSGS) is a leading cause of nephroti

168 Focal segmental glomerulosclerosis (FSGS) is a pattern of kidney injury

169 Focal segmental glomerulosclerosis (FSGS) is a relatively prevalent glom

170 Focal segmental glomerulosclerosis (FSGS) is a syndrome that involves ki

171 ticipate in the formation of focal segmental glomerulosclerosis (FSGS) lesions.

172 Primary focal segmental glomerulosclerosis (FSGS) often causes nephrotic protein

173 yed elevated TNF levels, and focal segmental glomerulosclerosis (FSGS) patients, whose TNF levels res

174 n) was found in PAN rats and focal segmental glomerulosclerosis (FSGS) patients.

175 nsplantation recipients with focal segmental glomerulosclerosis (FSGS) recurrence.

176 Focal segmental glomerulosclerosis (FSGS) recurs after kidney transplant

177 nin 4 (ACTN4), are linked to focal segmental glomerulosclerosis (FSGS), a chronic kidney disease char

178 e therapeutic target for focal and segmental glomerulosclerosis (FSGS), a common cause of kidney fail

179 linked to familial forms of focal segmental glomerulosclerosis (FSGS), a kidney disease characterize

180 ominant INF2 mutations cause focal segmental glomerulosclerosis (FSGS), a kidney disease, and FSGS+Ch

181 tic syndrome (NS), including focal segmental glomerulosclerosis (FSGS), as a primary podocytopathy.

182 he podocytic kidney disease focal segemental glomerulosclerosis (FSGS), as well as to cases of the ne

183 ntly inherited form of human focal segmental glomerulosclerosis (FSGS), evidence supporting mechanism

184 ncreased risk for idiopathic focal segmental glomerulosclerosis (FSGS), HIV-1-associated nephropathy

185 nondiabetic kidney diseases, focal segmental glomerulosclerosis (FSGS), HIV-associated nephropathy (H

186 tibility gene for idiopathic focal segmental glomerulosclerosis (FSGS), HIV-associated nephropathy (H

187 inimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), LN and hepatitis B associated

188 ts and children with primary focal segmental glomerulosclerosis (FSGS), proteinuria and renal dysfunc

189 Focal segmental glomerulosclerosis (FSGS), the second leading cause of e

190 autosomal dominant familial focal segmental glomerulosclerosis (FSGS).

191 amycin-induced (ADR-induced) focal segmental glomerulosclerosis (FSGS).

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

193 was associated recently with focal segmental glomerulosclerosis (FSGS).

194 se of two thirds of cases of focal segmental glomerulosclerosis (FSGS).

195 cause of autosomal dominant focal segmental glomerulosclerosis (FSGS).

196 typic injury response called focal segmental glomerulosclerosis (FSGS).

197 phropathy and idiopathic focal and segmental glomerulosclerosis (FSGS).

198 amilial forms of adult onset focal segmental glomerulosclerosis (FSGS).

199 podocytes can result in focal and segmental glomerulosclerosis (FSGS).

200 horylation, proteinuria, and focal segmental glomerulosclerosis (FSGS).

201 oteinuria and most often focal and segmental glomerulosclerosis (FSGS).

202 onic kidney disease, such as focal segmental glomerulosclerosis (FSGS).

203 patients with biopsy-proven focal segmental glomerulosclerosis (FSGS).

204 ion unit, a condition called focal segmental glomerulosclerosis (FSGS).

205 idney disease (CKD), such as focal segmental glomerulosclerosis (FSGS).

206 nd B2R, including urinary albumin excretion, glomerulosclerosis, glomerular basement membrane thicken

207 In preclinical models of renal fibrosis and glomerulosclerosis, high podocyte [Ca(2)(+)]i correlated

208 idney diseases including focal and segmental glomerulosclerosis, HIV-associated nephropathy and hyper

209 ithout such variants to have focal segmental glomerulosclerosis, HIV-associated nephropathy, or ESRD,

210 ociated lipocalin, NGAL), kidney growth, and glomerulosclerosis, however, were not improved with empa

211 lower for all other groups: focal segmental glomerulosclerosis (HR, 0.80; 95% CI, 0.77-0.82), membra

212 .47; 95% CI, 0.29-0.75), and focal segmental glomerulosclerosis (HRa, 0.69; 95% CI, 0.45-1.06).

213 and kidney failure with global or segmental glomerulosclerosis in adulthood.

214 important finding was the presence of severe glomerulosclerosis in alpha7(-/-) mice in this early pha

215 tion of the renin-angiotensin system reduces glomerulosclerosis in animals with less tightly adherent

216 m often decreases the rate of progression of glomerulosclerosis in chronic kidney diseases.

217 diating podocyte detachment and accelerating glomerulosclerosis in experimental crescentic glomerulon

218 itical event associated with proteinuria and glomerulosclerosis in glomerular diseases including DN.

219 ignaling in podocytes causes proteinuria and glomerulosclerosis in humans and rodents, but the underl

220 ey podocytes-have been linked to proteinuric glomerulosclerosis in humans.

221 Second, we evaluated adriamycin-induced glomerulosclerosis in Jh mice, a strain that lacks matur

222 nt to induce Kimmelstiel-Wilson-like nodular glomerulosclerosis in mice through a process that involv

223 Damage or loss of podocytes causes glomerulosclerosis in murine models, and mutations in po

224 sible for the development of proteinuria and glomerulosclerosis in radiation nephropathy remain large

225 nd proteinuria more strongly associated with glomerulosclerosis in the deep and middle regions, respe

226 r preventing podocyte apoptosis and eventual glomerulosclerosis in the kidney; however, the transcrip

227 de definitive conclusions but the absence of glomerulosclerosis in this unique population is consiste

228 e of vascular congestion, and attenuation of glomerulosclerosis in treated mice.

229 Using a model of focal segmental glomerulosclerosis, increased filtration barrier permeab

230 r PAR2 inhibitors attenuated albuminuria and glomerulosclerosis (indicators of diabetic nephropathy)

231 o attenuated tubulointerstitial fibrosis and glomerulosclerosis induced by HFD feeding in kidney.

232 We evaluated specimens for the degree of glomerulosclerosis, interstitial fibrosis and tubular at

233 pid accumulation and renal injury, including glomerulosclerosis, interstitial fibrosis, and albuminur

234 (arteriosclerosis/arteriolosclerosis, global glomerulosclerosis, interstitial fibrosis, and tubular a

235 y there is nephron loss and lesions of focal glomerulosclerosis, interstitial fibrosis, tubular atrop

236 d reduced histological end points, including glomerulosclerosis, interstitial fibrosis, tubular injur

237 We used global glomerulosclerosis, interstitial fibrosis/tubular atroph

238 cate that the development and progression of glomerulosclerosis involve loss of podocyte DAF, trigger

239 Glomerulosclerosis is a general term for scarring of the

240 uction, podocyte number is better preserved, glomerulosclerosis is ameliorated, and proteinuria is re

241 mice and BALB/c mice with Adriamycin-induced glomerulosclerosis is associated with endothelin-1 (EDN1

242 t with the possibility that African-American glomerulosclerosis is caused, not by loss of APOL1 funct

243 In the kidney, glomerulosclerosis is the underlying pathology in approx

244 o respond to hypertrophic stress also causes glomerulosclerosis is unknown.

245 cytopathies manifesting with focal segmental glomerulosclerosis lesions includes glucocorticoids and

246 e minimal change lesions and focal segmental glomerulosclerosis lesions.

247 We found that focal segmental glomerulosclerosis-linked ACTN4 mutants lose their abili

248 f mean nonsclerotic glomerular volume and of glomerulosclerosis (measured as the percentage of global

249 anced glomerular ROS production, accelerated glomerulosclerosis, mesangial expansion, and ECM protein

250 nary albumin excretion, mesangial expansion, glomerulosclerosis, mesangiolysis, and glomerular filtra

251 nction in eNOS(-/-) mice resulted in nodular glomerulosclerosis, mesangiolysis, microaneurysms, and a

252 , renal insufficiency, and extensive nodular glomerulosclerosis, mimicking advanced DN in humans.

253 stic features of LCDD, including progressive glomerulosclerosis, nephrotic-range proteinuria, and fin

254 ng, this APOL1 null individual does not have glomerulosclerosis, nor do his relatives who carry APOL1

255 ns of mouse models that lack the progressive glomerulosclerosis observed in humans, we studied the co

256 Glomerulosclerosis occurred when podocyte density reache

257 The peak prevalence of ESRD from glomerulosclerosis occurs at 70 to 79 years.

258 nephron loss with aging by either increased glomerulosclerosis or by cortical volume decline is cons

259 n glomeruli from humans with focal segmental glomerulosclerosis or diabetic nephropathy exhibited dim

260 However, LSKL did not alter glomerulosclerosis or glomerular structure.

261 te in the LAT group was the extent of global glomerulosclerosis (P = 0.0001).

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

263 and other kidney diseases featuring diffuse glomerulosclerosis, particularly diabetic nephropathy.

264 e models of disease and kidney biopsies from glomerulosclerosis patients exhibited increased RAP1GAP,

265 ix remodeling represented the first steps of glomerulosclerosis, paving the way for future therapeuti

266 renal insufficiency and the diabetic nodular glomerulosclerosis phenotype of diabetic Sema3a(+) mice.

267 had additive protective effects on DeltaGFR, glomerulosclerosis, podocyte density in juxtamedullary n

268 es from patients with AS and focal segmental glomerulosclerosis, possibly indicating that the same me

269 podocytes in utero developed proteinuria and glomerulosclerosis postnatally, resembling FSGS.

270 tion of >40% of podocytes led to progressive glomerulosclerosis, profound tubular injury, and renal f

271 r hyalinosis correlated with contemporaneous glomerulosclerosis (r = 0.44, P < 0.001), and subsequent

272 may be a primary event followed by secondary glomerulosclerosis, raising the possibility that focusin

273 me into glomerular capillary rarefaction and glomerulosclerosis, recapitulating the phenotype of prog

274 ss in the physiopathology of focal segmental glomerulosclerosis recurrence after transplantation and

275 reported in multiple disease models, such as glomerulosclerosis, renal fibrosis, and acute kidney inj

276 renal function and halted the progression of glomerulosclerosis, renal inflammation, and tubular inju

277 In model systems, podocyte depletion causes glomerulosclerosis, suggesting age-associated glomerulos

278 ter role in the pathogenesis of hypertensive glomerulosclerosis than previously thought.

279 docyte loss and irreversible FSGS and global glomerulosclerosis, this study points to an important ro

280 teinuria contributes directly to progressive glomerulosclerosis through the suppression of podocyte r

281 slit diaphragm-associated ion channel, cause glomerulosclerosis; TRPC6 expression is increased in acq

282 ar sclerosing GN with extensive focal global glomerulosclerosis, tubular atrophy, and interstitial fi

283 d is characterized on renal biopsy by global glomerulosclerosis, tubular atrophy, interstitial fibros

284 and serum creatinine and significantly less glomerulosclerosis, tubular damage, and interstitial inf

285 ma creatinine and urea nitrogen levels; less glomerulosclerosis, tubulointerstitial injury, and extra

286 azards regression, the presence of segmental glomerulosclerosis was the only factor that significantl

287 multivariate analysis, higher percentage of glomerulosclerosis was the only independent predictor of

288 as diabetic nephropathy and focal segmental glomerulosclerosis, we observed upregulation of Wnt1 and

289 ic membranous nephropathy or focal segmental glomerulosclerosis were confirmed by gene sequencing to

290 rtensive arterionephrosclerosis and diabetic glomerulosclerosis were frequent but typically mild.

291 Proteinuria and glomerulosclerosis were linearly related to both increas

292 ed role in many fibrotic diseases, including glomerulosclerosis, where it increases collagen I deposi

293 Exceptions include age-related glomerulosclerosis, which appears to be an ischemic proc

294 Focal segmental glomerulosclerosis, which is a common glomerular disorde

295 ocyte-deleted mice developed proteinuria and glomerulosclerosis, while control mice were resistant.

296 biopsy specimen that showed focal segmental glomerulosclerosis with abnormal podocytes containing cy

297 ggressive form of collapsing focal segmental glomerulosclerosis with accompanying tubular and interst

298 There was a marked increase in glomerulosclerosis with age in the superficial region, b

299 and another had global as well as segmental glomerulosclerosis with features of healed collapsing gl

300 cally, HIVAN is a collapsing focal segmental glomerulosclerosis with prominent tubular damage.