ライフサイエンスコーパス: glomerulosclerosis

1 ney ILC2s and ameliorated adriamycin-induced glomerulosclerosis.

2 different strategies, on adriamycin-induced glomerulosclerosis.

3 within the glomerulus in an animal model of glomerulosclerosis.

4 iopsies obtained from individuals with focal glomerulosclerosis.

5 est causality between APOL1 null alleles and glomerulosclerosis.

6 ove that these APOL1 sequence variants cause glomerulosclerosis.

7 onic overactivation leads to focal segmental glomerulosclerosis.

8 process effacement, mesangial expansion, and glomerulosclerosis.

9 thesis increased proteinuria and exacerbated glomerulosclerosis.

10 gravated proteinuria, macrophage influx, and glomerulosclerosis.

11 ons cause autosomal dominant focal segmental glomerulosclerosis.

12 ement activation may slow the progression of glomerulosclerosis.

13 mozygous the G1 and G2 alleles predispose to glomerulosclerosis.

14 echanisms, to promote renal inflammation and glomerulosclerosis.

15 eletal changes, glaucoma and focal segmental glomerulosclerosis.

16 developed significantly less proteinuria and glomerulosclerosis.

17 r kidney; but did produce cortical mesangial glomerulosclerosis.

18 d nephropathy and idiopathic focal segmental glomerulosclerosis.

19 disease that resembles human focal segmental glomerulosclerosis.

20 branous nephropathy, but not focal segmental glomerulosclerosis.

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

22 ch have both tubulointerstitial fibrosis and glomerulosclerosis.

23 enal failure associated with focal segmental glomerulosclerosis.

24 sease mechanism in inherited focal segmental glomerulosclerosis.

25 ension-attributable ESRD and focal segmental glomerulosclerosis.

26 cause the kidney disease focal and segmental glomerulosclerosis.

27 in both diabetic nephropathy and nondiabetic glomerulosclerosis.

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

29 FAT signaling in podocytes, proteinuria, and glomerulosclerosis.

30 podocytes and mediates podocyte depletion in glomerulosclerosis.

31 nal impairment, resulting in proteinuria and glomerulosclerosis.

32 et of podocyte dysfunction, proteinuria, and glomerulosclerosis.

33 erular disease, preceding the development of glomerulosclerosis.

34 riamycin provokes severe podocyte stress and glomerulosclerosis.

35 ing glomerulopathies such as focal segmental glomerulosclerosis.

36 tion barrier structure, and markedly reduced glomerulosclerosis.

37 e RAGE protected against podocyte injury and glomerulosclerosis.

38 lusively in podocytes caused proteinuria and glomerulosclerosis.

39 sangium degeneration with little evidence of glomerulosclerosis.

40 diabetic nephropathy and in focal segmental glomerulosclerosis.

41 role in the pathogenesis of proteinuria and glomerulosclerosis.

42 he podocyte foot processes, albuminuria, and glomerulosclerosis.

43 mesangial expansion, capillary dilation, and glomerulosclerosis.

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

45 mes and intrapair agreement in the degree of glomerulosclerosis.

46 tion of insulin resistance, albuminuria, and glomerulosclerosis.

47 l hypertrophy, which correlate with eventual glomerulosclerosis.

48 histology characteristic of focal segmental glomerulosclerosis.

49 restriction prevents both oxidant injury and glomerulosclerosis.

50 d podocyte injury by 8 wk of age, with later glomerulosclerosis.

51 the progression and potential regression of glomerulosclerosis.

52 tubular atrophy, interstitial fibrosis, and glomerulosclerosis.

53 c background resulted in podocyte injury and glomerulosclerosis.

54 lysis, and focal segmental and early nodular glomerulosclerosis.

55 expressed vpr developed podocyte damage and glomerulosclerosis.

56 cytes, in human kidneys with focal segmental glomerulosclerosis.

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

58 splitting, and secondary focal and segmental glomerulosclerosis.

59 ry and loss that may contribute to worsening glomerulosclerosis.

60 in proteinuria, foot process effacement, and glomerulosclerosis.

61 abnormalities before and during progressive glomerulosclerosis.

62 apoptosis both in vitro and in experimental glomerulosclerosis.

63 identified in association with focal global glomerulosclerosis.

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

65 heir loss causes proteinuria and progressive glomerulosclerosis.

66 drial dysfunction and apoptosis, followed by glomerulosclerosis.

67 modeling by DNA hypermethylation, leading to glomerulosclerosis.

68 genetic disorders manifesting as progressive glomerulosclerosis.

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

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

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

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

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

74 As glomerulosclerosis accumulates, the diseased kidney prog

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

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

77 Only when glomerulosclerosis and arteriosclerosis exceed that expe

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

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

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

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

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

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

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

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

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

87 Glomerulosclerosis and interstitial fibrosis were also s

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

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

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

91 6 lead to autosomal dominant focal segmental glomerulosclerosis and podocyte expression of TRPC6 is i

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

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

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

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

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

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

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

99 ollowing injury underlies the development of glomerulosclerosis and progressive renal failure in a di

100 xpansion and loss of podocytes, resulting in glomerulosclerosis and proteinuria, and is associated wi

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

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

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

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

105 he role of the podocyte in the initiation of glomerulosclerosis and the contribution to glomeruloscle

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

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

108 Glomerulosclerosis and tubulointerstitial fibrosis are a

109 Glomerulosclerosis and tubulointerstitial fibrosis were

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 haracterized by kidney failure, proteinuria, glomerulosclerosis, and retraction of glomerular podocyt

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

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

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

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

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

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

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

133 We also examined the agreement in degree of glomerulosclerosis between paired kidneys.

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

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

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

137 genic mice showed severe podocyte injury and glomerulosclerosis by 4 wk of age.

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

139 Regression of glomerulosclerosis can be induced by angiotensin II anta

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

141 Morphologically, smoking-associated nodular glomerulosclerosis closely resembles diabetic nephropath

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

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

144 Glomerulosclerosis correlates with a reduction in podocy

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

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

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

148 Proteinuria and glomerulosclerosis did not develop if dietary calorie re

149 er than 5% glomerulosclerosis, the degree of glomerulosclerosis did not help predict graft outcomes.

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

151 ity antibodies were more likely to result in glomerulosclerosis during long-term treatment.

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

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

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

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

156 y compared graft survival with the degree of glomerulosclerosis found on donor biopsy.

157 f glomerulosclerosis and the contribution to glomerulosclerosis from capillary hypertension and solub

158 ey disease (ADPKD), familial focal segmental glomerulosclerosis (FSG), hypomagnesemia with secondary

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

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

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

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

163 2 lead to the kidney disease focal segmental glomerulosclerosis (FSGS) and the neurological disorder

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

165 the proteinuric disease focal and segmental glomerulosclerosis (FSGS) compared to control individual

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

167 d sporadic steroid-resistant focal segmental glomerulosclerosis (FSGS) in the pediatric population, b

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

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

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

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

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

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

174 Focal segmental glomerulosclerosis (FSGS) is the most common primary glo

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

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

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

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

179 Focal segmental glomerulosclerosis (FSGS) recurs after kidney transplant

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

181 have been linked to familial focal segmental glomerulosclerosis (FSGS), a common renal disorder in hu

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

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

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

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

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

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

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 opathic and HIV-1-associated focal segmental glomerulosclerosis (FSGS), we carried out an admixture-m

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

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

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

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

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

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

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

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

199 autosomal dominant familial focal segmental glomerulosclerosis (FSGS).

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

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

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

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

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

205 from the same donor was highest for the 0-5% glomerulosclerosis groups (90.6% for pairs with 0-5% glo

206 by endogenous estrogens against progressive glomerulosclerosis (GS) during their reproductive period

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 t research on the pathogenesis of collapsing glomerulosclerosis, human immunodeficiency virus associa

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 reduced proteinuria, cell proliferation, and glomerulosclerosis in HIV-1-transgenic mice.

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

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 Podocyte apoptosis initiates progressive glomerulosclerosis in TGF-beta1 transgenic and CD2AP-kno

226 e relatively modest 17% prevalence of global glomerulosclerosis in the aging group.

227 tion of PAI-1R could slow the progression of glomerulosclerosis in the db/db mouse, a model of type 2

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

229 osclerosis groups (90.6% for pairs with 0-5% glomerulosclerosis in the left kidney vs. 42.5% for pair

230 the left kidney vs. 42.5% for pairs with >5% glomerulosclerosis in the left kidney).

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

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

233 therefore, PAI-1R may prevent progression of glomerulosclerosis in type 2 diabetes.

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

235 enes was observed in the absence of HIV-1 or glomerulosclerosis, indicating that nephropathy suscepti

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

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

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

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

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

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

242 Glomerulosclerosis is a general term for scarring of the

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

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

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

246 that the entity known as idiopathic nodular glomerulosclerosis is not idiopathic.

247 Focal segmental glomerulosclerosis is the leading cause of steroid-unres

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

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

250 otic syndrome, in particular focal segmental glomerulosclerosis, its pathogenesis and alternative the

251 spontaneous proteinuria and focal segmental glomerulosclerosis-like glomerular damage in mice.

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

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

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

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

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

257 Because loss of podocytes associates with glomerulosclerosis, monitoring podocyte loss by measurin

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

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

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

261 Although the degree of glomerulosclerosis on pretransplant donor biopsy is one

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

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

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

265 atinine, mean arterial pressure or scores of glomerulosclerosis or interstitial fibrosis.

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

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

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

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

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

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

275 d expression is decreased in mouse models of glomerulosclerosis, suggesting that beta8 regulates norm

276 Among kidneys with greater than 5% glomerulosclerosis, the degree of glomerulosclerosis did

277 Among the groups with greater than 5% glomerulosclerosis, there was no statistically significa

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

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

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

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

282 y, including glomerular hypertrophy, diffuse glomerulosclerosis, tubular atrophy, interstitial fibros

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

284 iabetic nephropathy that fail to progress to glomerulosclerosis, tubulointerstitial fibrosis, and kid

285 s, and oxidative stress enzymes and decrease glomerulosclerosis, tubulointerstitial fibrosis, and pro

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

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

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

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

290 Donor kidneys with less than 6% glomerulosclerosis were associated with better graft out

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

292 Proteinuria and glomerulosclerosis were linearly related to both increas

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

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

299 discusses the development of focal segmental glomerulosclerosis, with particular attention to the rol

300 J mice developed progressive albuminuria and glomerulosclerosis within 13 weeks, accompanied by incre