ライフサイエンスコーパス: tubulointerstitial

1 proliferation, focal glomerulosclerosis, and tubulointerstitial abnormalities were uncommon.

2 Tubulointerstitial and glomerular cells derived from the

3 tes, and both M1 and M2 macrophages; reduced tubulointerstitial and glomerular injuries; delayed fata

4 , we suggest that IL-15 is a therapeutic for tubulointerstitial and glomerular kidney diseases.

5 d PPARgamma as major regulatory nodes in the tubulointerstitial and glomerular networks, respectively

6 nd stage renal failure characterized by both tubulointerstitial and glomerular pathology.

7 h glucose contributes to the accumulation of tubulointerstitial and matrix proteins in diabetic nephr

8 ion, urinary CXCL10:Cr ratio associates with tubulointerstitial and microvascular inflammation of the

9 the increase in plasma creatinine levels and tubulointerstitial and microvascular pathology.

10 uveitis (TINU) syndrome is characterized by tubulointerstitial and ocular inflammation.

11 were accompanied by augmented perivascular, tubulointerstitial, and glomerular fibrosclerosis, infla

12 tronectin and PAI-1 co-localized to the same tubulointerstitial area.

13 cells and expanded in both SLE blood and the tubulointerstitial areas of individuals with proliferati

14 mice (2.0 +/- 0.2 versus 1.2 +/- 0.2 per 100 tubulointerstitial cells, day 14 UUO) while the number o

15 Our genetic analysis suggests that tubulointerstitial cellular crosstalk modulates renal EP

16 r renal cells to high glucose contributes to tubulointerstitial changes in diabetic nephropathy.

17 p16(INK4a) expression, associate with these tubulointerstitial changes, but it is unknown whether th

18 ng kidney transplantation and developed less tubulointerstitial changes.

19 ion in surveillance biopsies with or without tubulointerstitial chronic lesions is associated with an

20 APOL1 tubulointerstitial coexpression analysis showed coexpres

21 All therapies prevented tubulointerstitial collagen deposition, but glomerular m

22 kidney model ameliorated renal fibrosis and tubulointerstitial collagen deposition.

23 LN often concomitantly affects the tubulointerstitial compartment of the kidney, leading fi

24 The tubulointerstitial compartment showed strong enrichment

25 identified eGFP-L10a expressing cells in the tubulointerstitial compartment which stained positive fo

26 f extracellular matrix in the glomerular and tubulointerstitial compartments and by the thickening an

27 leukocyte infiltration in the glomerular and tubulointerstitial compartments in both human and experi

28 ound strong Jak-2 staining in glomerular and tubulointerstitial compartments in diabetic nephropathy

29 has been demonstrated in the glomerular and tubulointerstitial compartments of experimental diabetic

30 ted on epithelium in diseased glomerular and tubulointerstitial compartments when compared with norma

31 e, control wild-type mice had an increase in tubulointerstitial complement C3 deposition and neutroph

32 Tubulointerstitial damage (TID) is a key feature of chro

33 ells, but they do not directly contribute to tubulointerstitial damage and fibrosis.

34 on of vessel patency alone failed to reverse tubulointerstitial damage and partly explains the limite

35 ing in obstructed kidneys, thus ameliorating tubulointerstitial damage and renal fibrosis.

36 docyte effacement or reversed glomerular and tubulointerstitial damage in 1,25-vitamin D3-deficient a

37 SPARC contributes to glomerulosclerosis and tubulointerstitial damage in response to hyperglycemia t

38 iabetic glomerular disease and their role in tubulointerstitial damage that accompanies progression.

39 glomerular microvasculature, accompanied by tubulointerstitial damage, glomerulosclerosis, and prote

40 stologic groups, and appeared to result from tubulointerstitial damage.

41 renal function, and prevented glomerular and tubulointerstitial damage.

42 umulates and promotes tubular cell death and tubulointerstitial damage.

43 ary kidney disorder with both glomerular and tubulointerstitial damages.

44 and elastase expression result in increased tubulointerstitial deposition of elastin in diabetic nep

45 ing hyperuricemia is associated with chronic tubulointerstitial disease and intrarenal vasoconstricti

46 In summary, rapamycin ameliorates the tubulointerstitial disease associated with chronic prote

47 tudy highlights the prognostic importance of tubulointerstitial disease for long-term graft loss.

48 pathogenesis of systemic lupus erythematosus tubulointerstitial disease is not known.

49 ndemic (Balkan) nephropathy, a chronic renal tubulointerstitial disease of previously unknown cause t

50 Primary renal tubulointerstitial disease resulting from proximal tubul

51 Proteinuric rats developed tubulointerstitial disease that was most severe in rats

52 eritubular capillary loss in adult models of tubulointerstitial disease, although, in one study, this

53 emic or toxic injury, as well as in cases of tubulointerstitial disease, polycystic kidney disease, a

54 phritis, with crescent formation, as well as tubulointerstitial disease, with these phenotypes being

55 merulonephritis with crescent formation, and tubulointerstitial disease.

56 n of the collapsing variant, and microcystic tubulointerstitial disease.

57 omechanisms of progression of glomerular and tubulointerstitial disease.

58 of atubular glomeruli is even more common in tubulointerstitial disorders, such as obstructive nephro

59 ted the renal EGF receptor and increased the tubulointerstitial expression of matrix metalloproteinas

60 12M, 1.43 +/- 0.17; P < 0.001) and cortical tubulointerstitial fibrosis (CTIFI: 4M, 0 versus 12M, 57

61 Tubulointerstitial fibrosis (fibrosis), a histologic fea

62 ke response, which culminates in progressive tubulointerstitial fibrosis (TIF) and renal failure.

63 Tubulointerstitial fibrosis (TIF) is considered the fina

64 Tubulointerstitial fibrosis (TIF) is recognized as a fin

65 ulation of proximal tubular DsbA-L for renal tubulointerstitial fibrosis (TIF) remains unclear.

66 2-treated animals had reduced glomerular and tubulointerstitial fibrosis after subtotal nephrectomy.

67 Whether or how Rac promotes tubulointerstitial fibrosis and chronic kidney disease (

68 ne or TMAO directly led to progressive renal tubulointerstitial fibrosis and dysfunction.

69 It also attenuated tubulointerstitial fibrosis and glomerulosclerosis induc

70 transgenic mice (Tg26 mice), which have both tubulointerstitial fibrosis and glomerulosclerosis.

71 results revealed a strong link between renal tubulointerstitial fibrosis and glycerophospholipid meta

72 ediating the molecular and cellular basis of tubulointerstitial fibrosis and highlight new insights t

73 s, low expression of miR-192 correlated with tubulointerstitial fibrosis and low estimated GFR.

74 sh the importance of the circadian rhythm in tubulointerstitial fibrosis and suggest CLOCK/TGF-beta s

75 acement (OVX+E(2)) on glomerulosclerosis and tubulointerstitial fibrosis and the mechanisms contribut

76 Glomerulosclerosis and tubulointerstitial fibrosis are associated with lower re

77 unilateral ureteral obstruction, a model of tubulointerstitial fibrosis associated with TGF-beta up-

78 orated the increases in oxidative stress and tubulointerstitial fibrosis caused by diabetes.

79 Chimeric animal models also reveal that tubulointerstitial fibrosis develops, even in the absenc

80 , we found that humans and mouse models with tubulointerstitial fibrosis had lower expression of key

81 Tissue samples from kidneys with tubulointerstitial fibrosis had significantly elevated n

82 of glomerular apoptosis before the onset of tubulointerstitial fibrosis in 2-week-old animals.

83 nal propeptide (PIIINP) mark the severity of tubulointerstitial fibrosis in biopsy studies, but the a

84 functional changes, kidney inflammation, and tubulointerstitial fibrosis in mice.

85 cts leading to dramatic attenuation of renal tubulointerstitial fibrosis in obstructive nephropathy i

86 gial cells and to be highly expressed during tubulointerstitial fibrosis in rat angiotensin (ANG) II

87 inhibition of Smad2 and Smad3 activation and tubulointerstitial fibrosis in terms of tubulointerstiti

88 severity of glomerulosclerosis and cortical tubulointerstitial fibrosis in the 12M group was augment

89 n the inhibition of tubular inflammation and tubulointerstitial fibrosis in these mice.

90 ointerstitium was positively correlated with tubulointerstitial fibrosis in tissue samples from patie

91 lial Hif-1alpha inhibited the development of tubulointerstitial fibrosis in UUO kidneys, which was as

92 ection rate, Smad7 transgene expression, and tubulointerstitial fibrosis including alpha-smooth muscl

93 Tubulointerstitial fibrosis is a chronic and progressive

94 Tubulointerstitial fibrosis is a major characteristic of

95 etic nephropathy (DN), and progressive renal tubulointerstitial fibrosis is an important mediator of

96 Tubulointerstitial fibrosis is common with ageing and st

97 Tubulointerstitial fibrosis is considered to be common e

98 trated at the corticomedullary junction, and tubulointerstitial fibrosis is dominant.

99 Renal tubulointerstitial fibrosis is the common end point of p

100 Tubulointerstitial fibrosis is the hallmark of chronic k

101 al function at baseline, and the presence of tubulointerstitial fibrosis on renal biopsy as independe

102 mmation and decreased renal perivascular and tubulointerstitial fibrosis relative to wild-type hypert

103 e of circadian rhythm in the pathogenesis of tubulointerstitial fibrosis remains unclear.

104 percentage of sclerotic glomeruli and worse tubulointerstitial fibrosis than those of the group with

105 ation of dynamics between key populations in tubulointerstitial fibrosis that demonstrates how these

106 Here, we used a mouse model of tubulointerstitial fibrosis to determine whether adipone

107 Tubulointerstitial fibrosis underlies all forms of end-s

108 the FXR agonist EDP-305 in a mouse model of tubulointerstitial fibrosis via unilateral ureteral obst

109 Importantly, the degree of tubulointerstitial fibrosis was also markedly lower in U

110 Tubulointerstitial fibrosis was also observed in these m

111 Tubulointerstitial fibrosis was ameliorated in diabetic

112 Glomerulosclerosis and tubulointerstitial fibrosis were similarly reduced with

113 Further, the robust induction of tubulointerstitial fibrosis without increase in activate

114 n albuminuria, marked glomerulosclerosis and tubulointerstitial fibrosis, and induction of many of th

115 that fail to progress to glomerulosclerosis, tubulointerstitial fibrosis, and kidney failure.

116 reasing proteinuria, glomerulosclerosis, and tubulointerstitial fibrosis, and modulating renal lipid

117 ut of podocytes, albuminuria, glomerular and tubulointerstitial fibrosis, and progressive renal failu

118 ess enzymes and decrease glomerulosclerosis, tubulointerstitial fibrosis, and proteinuria.

119 both diffuse and nodular glomerulosclerosis, tubulointerstitial fibrosis, and vascular sclerosis.

120 to promote spontaneous and progressive renal tubulointerstitial fibrosis, as characterized by increas

121 lopathy, albuminuria, loss of podocytes, and tubulointerstitial fibrosis, but female Dsk5 mice had mi

122 idney tubule-specific Cul3 disruption causes tubulointerstitial fibrosis, but little is known about t

123 y play important roles in the development of tubulointerstitial fibrosis, by promoting epithelial cel

124 ction, TbetaRII(endo+/-) mice exhibited less tubulointerstitial fibrosis, enhanced preservation of re

125 covery and redifferentiation, and subsequent tubulointerstitial fibrosis, eventually leading to chron

126 ient to cause spontaneous, progressive renal tubulointerstitial fibrosis, evident by epithelial dedif

127 aCO(3) in preventing renal Ca deposition and tubulointerstitial fibrosis, including better preservati

128 tained on weeks 8 to 24 revealed progressive tubulointerstitial fibrosis, inflammation, renal dysfunc

129 During progressive tubulointerstitial fibrosis, renal tubular epithelial ce

130 uate MAIT cells in human native kidneys with tubulointerstitial fibrosis, the hallmark of CKD, we use

131 ion of PDGF-BB and PDGF-DD on glomerular and tubulointerstitial fibrosis, these data suggest that fai

132 nd XBP1 (ER stress markers), and accelerated tubulointerstitial fibrosis.

133 pharmacological methods protected mice from tubulointerstitial fibrosis.

134 ore severe capillary rarefaction and greater tubulointerstitial fibrosis.

135 covery, but progressively increased, causing tubulointerstitial fibrosis.

136 erized by progressive glomerulosclerosis and tubulointerstitial fibrosis.

137 uction (UUO) in mice, a model of progressive tubulointerstitial fibrosis.

138 paradigm for renal progression is advancing tubulointerstitial fibrosis.

139 ent of new strategies for treatment of renal tubulointerstitial fibrosis.

140 ama4-/- mice have progressive glomerular and tubulointerstitial fibrosis.

141 hronic kidney failure characterized by renal tubulointerstitial fibrosis.

142 erteporfin significantly attenuated diabetic tubulointerstitial fibrosis.

143 ism of EMT and likely to be a contributor to tubulointerstitial fibrosis.

144 SS rat by attenuating glomerulosclerosis and tubulointerstitial fibrosis.

145 estive heart failure, and renal failure with tubulointerstitial fibrosis.

146 rates that contribute to this and subsequent tubulointerstitial fibrosis.

147 ase in Smad2 and Smad3 activation and severe tubulointerstitial fibrosis.

148 activation of TGF-beta1 can protect against tubulointerstitial fibrosis.

149 ria, renal function, glomerulosclerosis, and tubulointerstitial fibrosis.

150 o be a key contributor to the progression of tubulointerstitial fibrosis.

151 radicals, vasoconstrictive thromboxanes, and tubulointerstitial fibrosis.

152 hallenges, including damage to the kidney by tubulointerstitial fibrosis.

153 ed age-associated renal function decline and tubulointerstitial fibrosis.

154 nal diseases characterized by glomerular and tubulointerstitial fibrosis.

155 SASP) that coincided with the development of tubulointerstitial fibrosis.

156 glomeruli, microcystic tubular dilation, and tubulointerstitial fibrosis.

157 nic kidney diseases (CKD) by producing renal tubulointerstitial fibrosis.

158 s were identified in PARN in 2 probands with tubulointerstitial fibrosis.

159 ed podocyte injury, mesangial expansion, and tubulointerstitial fibrosis.

160 or receptor in renal proximal tubule induces tubulointerstitial fibrosis.

161 a major contributor to CKD characterized by tubulointerstitial fibrosis.

162 ming growth factor (TGF)-beta contributes to tubulointerstitial fibrosis.

163 ellular matrix (ECM), and the development of tubulointerstitial fibrosis.

164 tubule is known to play an important role in tubulointerstitial fibrosis; however, the underlying mol

165 rker discovery and a greater appreciation of tubulointerstitial histopathology and the role of tubula

166 10:Cr) or not, correlated with the extent of tubulointerstitial (i+t score; all P<0.001) and microvas

167 a cohort of 68 lupus nephritis biopsies, the tubulointerstitial infiltrate was organized into well-ci

168 n mice with severe glomerular disease, renal tubulointerstitial infiltrates were very limited, and in

169 ) with high accuracy, even in the absence of tubulointerstitial inflammation (AUC=0.70; 95% CI, 0.61

170 ute Banff scores = 0), and C4d staining with tubulointerstitial inflammation (i > 0 with or without t

171 The presence of tubulointerstitial inflammation (i-t) meeting TCMR crite

172 predict poorer graft survival; the extent of tubulointerstitial inflammation (TI) is of no prognostic

173 Tubulointerstitial inflammation and fibrosis are strongl

174 rosis, afferent and efferent hyalinosis, and tubulointerstitial inflammation and fibrosis.

175 Tubulointerstitial inflammation and progression of inter

176 Tubulointerstitial inflammation and progressive fibrosis

177 nPP exerted divergent effects: SnPP provoked tubulointerstitial inflammation and up-regulation of inj

178 terstitial inflammation in 6 patients (12%), tubulointerstitial inflammation in 6 patients (12%), and

179 ction in 7 patients (14%), C4d staining with tubulointerstitial inflammation in 6 patients (12%), tub

180 ediates NF-kappaB activation and may promote tubulointerstitial inflammation in chronic kidney diseas

181 est that a TLR4-mediated pathway may promote tubulointerstitial inflammation in diabetic nephropathy.

182 scents, neutrophils, fibrinoid necrosis, and tubulointerstitial inflammation in the kidneys as well a

183 diated rejection (TCMR) are characterized by tubulointerstitial inflammation in the renal allograft,

184 mation or C4d-positive staining or intensive tubulointerstitial inflammation played a less significan

185 be a mathematical model of the progress from tubulointerstitial inflammation to fibrosis.

186 However, tubulointerstitial inflammation was more severe among pa

187 frequently in patients with C4d staining and tubulointerstitial inflammation when compared to patient

188 bute to progressive renal damage by inducing tubulointerstitial inflammation, fibrosis, and tubular c

189 ogy accompanied by attenuated glomerular and tubulointerstitial inflammation.

190 hoid neogenesis in the pathogenesis of lupus tubulointerstitial inflammation.

191 es and vascular congestion without provoking tubulointerstitial inflammation.

192 d BKPyVAN specimens had comparable levels of tubulointerstitial inflammation.

193 on except in renal grafts, where it causes a tubulointerstitial inflammatory response similar to acut

194 ospho-Smad2/3 levels and improved markers of tubulointerstitial injury (fibronectin) and podocytes (n

195 a is an important mediator of glomerular and tubulointerstitial injury and can induce tubular epithel

196 ted molecular pathways may set the stage for tubulointerstitial injury and diabetic nephropathy.

197 ly features of diabetic nephropathy, whereas tubulointerstitial injury and fibrosis are critical for

198 ed to the tubular epithelium protect against tubulointerstitial injury and renal dysfunction in a rat

199 A correlation between tubulointerstitial injury and the degree of proteinuria

200 , while its deficiency shields kidneys from, tubulointerstitial injury by dampening oxidant and ER st

201 histology, available in 55 patients, showed tubulointerstitial injury in 86%, cholemic nephrosis in

202 erular hypertension, renal inflammation, and tubulointerstitial injury in animals.

203 em has been implicated in the development of tubulointerstitial injury in clinical and animal studies

204 lood glucose with insulin completely blocked tubulointerstitial injury in diabetic eNOSKO mice.

205 nal HIF-1alpha expression is associated with tubulointerstitial injury in patients with chronic kidne

206 the relationships between these factors and tubulointerstitial injury in the poststenotic kidney are

207 ens III and IV and attenuated glomerular and tubulointerstitial injury indices, despite the presence

208 AMPK and tuberin activation prevent tubulointerstitial injury induced by TGF-beta.

209 This tubulointerstitial injury is a direct consequence of hig

210 Tubulointerstitial injury leading to fibrosis is a commo

211 ays an important role in the pathogenesis of tubulointerstitial injury through binding of PDGF-Rbeta

212 A model of proteinuria-associated tubulointerstitial injury was developed and was used to

213 of mesangiolysis and microaneurysms, whereas tubulointerstitial injury was not prevented in these mic

214 of high glucose levels on the development of tubulointerstitial injury was suggested by the observati

215 crescent formation, sclerotic glomeruli, and tubulointerstitial injury were significantly reduced com

216 ea nitrogen levels; less glomerulosclerosis, tubulointerstitial injury, and extracellular matrix; and

217 xpression in obstructed kidneys and enhanced tubulointerstitial injury, apoptosis, and NADPH oxidase.

218 at serum glucose levels were correlated with tubulointerstitial injury, as well as with the expressio

219 in the proximal tubule of the kidney causes tubulointerstitial injury, but how this process occurs i

220 erglycemia may have a more important role in tubulointerstitial injury, possibly due to the stimulati

221 Flk-sel also induced tubulointerstitial injury, with some tubular epithelial

222 sement membrane protein, in the UUO model of tubulointerstitial injury.

223 MAC plays a key role in proteinuria-induced tubulointerstitial injury.

224 uria, and more severe glomerulosclerosis and tubulointerstitial injury.

225 AF/MAPK/ERK has largely been associated with tubulointerstitial injury.

226 itium, which correlated with the severity of tubulointerstitial injury.

227 each other's activities, thereby augmenting tubulointerstitial injury/fibrosis.

228 ditions to enable examination of mechanistic tubulointerstitial interactions.

229 iltration rate significantly correlated with tubulointerstitial Jak-1, -2, and -3 and Stat-1 expressi

230 e data suggest a direct relationship between tubulointerstitial Jak/Stat expression and progression o

231 Autosomal dominant tubulointerstitial kidney disease (ADTKD) is a recently

232 Autosomal dominant tubulointerstitial kidney disease is characterized by th

233 OD are the major cause of autosomal dominant tubulointerstitial kidney disease, a condition that lead

234 MUC1) were found to cause autosomal dominant tubulointerstitial kidney disease, the same disease caus

235 Autosomal dominant tubulointerstitial kidney diseases (ADTKDs) are a group

236 ouse offers a novel genetic model of chronic tubulointerstitial kidney injury, using collecting duct

237 Glomerular and tubulointerstitial laminin subunit gamma-1 (LAMC1) expre

238 displayed severe glomeruli (P < 0.0001) and tubulointerstitial lesions (P < 0.001) compared to kidne

239 ty, but the role of IL-36 signaling in renal tubulointerstitial lesions (TILs), a major prognostic fe

240 Inflammation contributes to the tubulointerstitial lesions of diabetic nephropathy.

241 Tubulointerstitial lesions were frequent: acute tubular

242 tal and global glomerulosclerosis as well as tubulointerstitial lesions were prominent while podocyte

243 a model that is characterized by predominant tubulointerstitial lesions.

244 ltered with cisplatin exposure, but cortical tubulointerstitial mass decreased.

245 Glomerular and tubulointerstitial mRNAs were microarrayed, followed by

246 and tubulointerstitial fibrosis in terms of tubulointerstitial myofibroblast accumulation (85% downw

247 This disease may manifest as tubulointerstitial nephritis (IgG4-TIN), but its clinico

248 polyendocrine syndrome type 1 who developed tubulointerstitial nephritis and ESRD in association wit

249 ains, develop ESRD associated with prominent tubulointerstitial nephritis and fibrosis within 3 month

250 ic interstitial nephropathy characterized by tubulointerstitial nephritis and formation of enlarged n

251 ed glomerular filtration rate (GFR), chronic tubulointerstitial nephritis and ultrastructural changes

252 Tubulointerstitial nephritis and uveitis (TINU) syndrome

253 Tubulointerstitial nephritis and uveitis syndrome is und

254 Tubulointerstitial nephritis and uveitis syndrome should

255 Here, we studied the tubulointerstitial nephritis antigen (TINag), a tubular

256 therapeutic delivery of the secreted protein Tubulointerstitial nephritis antigen-like 1 (Tinagl1) su

257 athy is characterized by rapidly progressive tubulointerstitial nephritis culminating in end-stage re

258 Our findings suggest that tubulointerstitial nephritis developed in these patients

259 Immune complex tubulointerstitial nephritis due to antibodies to brush

260 Tubulointerstitial nephritis is a common cause of kidney

261 Tubulointerstitial nephritis was the dominant lesion in

262 for immune and genetic causes of microcystic tubulointerstitial nephritis with little attention to it

263 2, 21.1%), infectious uveitis (6/52, 11.5%), tubulointerstitial nephritis with uveitis (6/52, 11.5%),

264 trogen levels, more severe histologic GN and tubulointerstitial nephritis, increased glomerular cresc

265 phronophthisis (NPH), an autosomal-recessive tubulointerstitial nephritis, is the most common cause o

266 69% were concurrently receiving a potential tubulointerstitial nephritis-causing medication.

267 h worse renal prognosis, whereas concomitant tubulointerstitial nephritis-causing medications and tre

268 and the hamsters that survived showed severe tubulointerstitial nephritis.

269 kidneys and urinary tract (n = 637 [70.9%]), tubulointerstitial nephropathies (n = 92 [10.2%]), glome

270 renal injury in multiple myeloma is chronic tubulointerstitial nephropathy associated with casts in

271 eported to cause nephronophthisis, a chronic tubulointerstitial nephropathy.

272 at model of CRF with adenine-induced chronic tubulointerstitial nephropathy.

273 s of neutrophils and macrophages that damage tubulointerstitial parenchyma.

274 e TGF-beta as key mediator of glomerular and tubulointerstitial pathobiology in chronic kidney diseas

275 e nephropathy with glomerular, vascular, and tubulointerstitial pathology.

276 ns were scored for glomerular, vascular, and tubulointerstitial pathology.

277 C of differentially-expressed glomerular and tubulointerstitial proteins can be used to help discrimi

278 al of 107 of 2026 glomerular and 112 of 2399 tubulointerstitial proteins was significantly differenti

279 ACR; 112 of 2026 glomerular and 181 of 2399 tubulointerstitial proteins were significantly dysregula

280 In contrast, the tubulointerstitial proteomes were markedly different in

281 tion (pATM(Ser1981)) increased 4-fold in the tubulointerstitial region of the unilateral ureteral obs

282 , and older mutant mice eventually developed tubulointerstitial renal disease.

283 ed by progressive interstitial nephritis and tubulointerstitial renal fibrosis in 3-, 6-, and 8-week

284 ns (FLCs) are usually directly involved, and tubulointerstitial renal injury and fibrosis are promine

285 In human glomeruli and tubulointerstitial samples, the Janus kinase (Jak)-signa

286 There was progressively higher average tubulointerstitial scarring (ci+ct) from 3 to 6 to 12 mo

287 nd control rats showed marked glomerular and tubulointerstitial scarring at day 32.

288 iorated vasculopathy with lipid deposits and tubulointerstitial scarring, inflammation, and upregulat

289 rophages, but no difference in glomerular or tubulointerstitial scarring.

290 ectly with the development of glomerular and tubulointerstitial scarring.

291 ast cell states, and previously unidentified tubulointerstitial signaling pathways.

292 escribe the presence of B1-like cells in the tubulointerstitial space of human lupus kidney biopsies.

293 nts with IFTANOS, rat allografts had greater tubulointerstitial staining for Nox-2 and alpha-SMA.

294 e did not reduce expression levels of either tubulointerstitial thrombospondin-1 or transforming grow

295 2 levels in tumor necrosis factor-stimulated tubulointerstitial tissue in vitro.

296 tive tissue growth factor) and histological (tubulointerstitial total collagen and glomerular collage

297 variants were genotyped, and glomerular and tubulointerstitial transcriptomes from protocol renal bi

298 es of chronic kidney disease associated with tubulointerstitial upregulation of FAT10.

299 Whether early glomerular, tubulointerstitial, vascular, and global glomerulosclero

300 Tubulointerstitial volume was significantly decreased in