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 and Bcl-2 family members in the glomerular, tubulointerstitial, and vascular compartments.

13 s (kidney collagen content and percentage of tubulointerstitial area stained with picrosirius red and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 Amelioration of tubulointerstitial damage in C6-deficient animals was co

37 The tubulointerstitial damage in complement-sufficient rats

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

39 lymphocytes play a dominant role in causing tubulointerstitial damage remains to be elucidated.

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

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

42 renal function, and prevented glomerular and tubulointerstitial damage.

43 umulates and promotes tubular cell death and tubulointerstitial damage.

44 n with more severe arteriolar hyalinosis and tubulointerstitial damage.

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

46 ary kidney disorder with both glomerular and tubulointerstitial damages.

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

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

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

50 Tubulointerstitial disease at that time was accompanied

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

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

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

54 Primary renal tubulointerstitial disease resulting from proximal tubul

55 ent-sufficient animals developed more severe tubulointerstitial disease than did C6-deficient rats.

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

57 Tubulointerstitial disease was conspicuous by its absenc

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

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

60 urine with nonselective proteinuria leads to tubulointerstitial disease, resulting in progressive los

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

62 merulonephritis with crescent formation, and tubulointerstitial disease.

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

64 omechanisms of progression of glomerular and tubulointerstitial disease.

65 etimes of equivalent severity to the chronic tubulointerstitial disease.

66 chemic injury was associated with widespread tubulointerstitial disease.

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

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

69 12M, 1.43 +/- 0.17; P < 0.001) and cortical tubulointerstitial fibrosis (CTIFI: 4M, 0 versus 12M, 57

70 Tubulointerstitial fibrosis (fibrosis), a histologic fea

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

72 Tubulointerstitial fibrosis (TIF) is considered the fina

73 Tubulointerstitial fibrosis (TIF) is recognized as a fin

74 2-treated animals had reduced glomerular and tubulointerstitial fibrosis after subtotal nephrectomy.

75 progressive glomerulonephritis culminates in tubulointerstitial fibrosis and death.

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

77 It also attenuated tubulointerstitial fibrosis and glomerulosclerosis induc

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

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

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

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

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

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

84 Glomerulosclerosis and tubulointerstitial fibrosis are associated with lower re

85 llograft may be partially protected from the tubulointerstitial fibrosis associated with chronic cycl

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

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

88 In this study, aging (24 mo) rats develop tubulointerstitial fibrosis characterized by tubular inj

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

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

91 It is concluded that tubulointerstitial fibrosis in aging is an active proces

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

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

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

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

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

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

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

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

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

101 Tubulointerstitial fibrosis is a chronic and progressive

102 Tubulointerstitial fibrosis is a major characteristic of

103 Tubulointerstitial fibrosis is common with ageing and st

104 Tubulointerstitial fibrosis is considered to be common e

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

106 Renal tubulointerstitial fibrosis is the common end point of p

107 Tubulointerstitial fibrosis is the hallmark of chronic k

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

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

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

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

112 ie the progression to glomerulosclerosis and tubulointerstitial fibrosis that characterize diabetic n

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

114 Tubulointerstitial fibrosis underlies all forms of end-s

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

116 Tubulointerstitial fibrosis was also observed in these m

117 Tubulointerstitial fibrosis was ameliorated in diabetic

118 Glomerulosclerosis and tubulointerstitial fibrosis were similarly reduced with

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

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

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

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

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

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

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

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

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

128 l tubule epithelium, and was associated with tubulointerstitial fibrosis, characterized by excessive

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

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

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

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

133 During progressive tubulointerstitial fibrosis, renal tubular epithelial ce

134 itial fibroblasts are active participants in tubulointerstitial fibrosis, the best correlate of decre

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

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

137 covery, but progressively increased, causing tubulointerstitial fibrosis.

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

139 erized by progressive glomerulosclerosis and tubulointerstitial fibrosis.

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

141 paradigm for renal progression is advancing tubulointerstitial fibrosis.

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

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

144 hronic kidney failure characterized by renal tubulointerstitial fibrosis.

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

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

147 SS rat by attenuating glomerulosclerosis and tubulointerstitial fibrosis.

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

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

150 rates that contribute to this and subsequent tubulointerstitial fibrosis.

151 or receptor in renal proximal tubule induces tubulointerstitial fibrosis.

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

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

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

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

156 radicals, vasoconstrictive thromboxanes, and tubulointerstitial fibrosis.

157 glomerulosclerosis, less is known about the tubulointerstitial fibrosis.

158 glomeruli, microcystic tubular dilation, and tubulointerstitial fibrosis.

159 a major contributor to CKD characterized by tubulointerstitial fibrosis.

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

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

162 pharmacological methods protected mice from tubulointerstitial fibrosis.

163 ore severe capillary rarefaction and greater tubulointerstitial fibrosis.

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

165 quent cellular rejection was associated with tubulointerstitial/glomerular parietal cell expression o

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

167 10:Cr) or not, correlated with the extent of tubulointerstitial (i+t score; all P<0.001) and microvas

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

169 Tubulointerstitial infiltrates were mild, with little or

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

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

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

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

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

175 Tubulointerstitial inflammation and fibrosis are strongl

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

177 Tubulointerstitial inflammation and progression of inter

178 Tubulointerstitial inflammation and progressive fibrosis

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

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

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

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

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

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

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

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

187 However, tubulointerstitial inflammation was more severe among pa

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

189 In the presence of tubulointerstitial inflammation, CCR5 and CXCR4 expressi

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

191 hoid neogenesis in the pathogenesis of lupus tubulointerstitial inflammation.

192 es and vascular congestion without provoking tubulointerstitial inflammation.

193 d BKPyVAN specimens had comparable levels of tubulointerstitial inflammation.

194 ogy accompanied by attenuated glomerular and tubulointerstitial inflammation.

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

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

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

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

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

200 tocopherol has the capacity to modulate both tubulointerstitial injury and glomerulosclerosis, lower

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

202 A correlation between tubulointerstitial injury and the degree of proteinuria

203 Glomerulosclerosis and tubulointerstitial injury are characteristic features se

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

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

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

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

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

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

210 C5b-9, in the pathogenesis of nonimmunologic tubulointerstitial injury induced by proteinuria.

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

212 This tubulointerstitial injury is a direct consequence of hig

213 Tubulointerstitial injury leading to fibrosis is a commo

214 Furthermore, the tubulointerstitial injury may be the consequence of isch

215 Tubulointerstitial injury scores followed a similar patt

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

217 d 30 d after ureter ligation showed that the tubulointerstitial injury was accompanied by a marked an

218 Tubulointerstitial injury was also greater in VEH T26 mi

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

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

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

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

223 -tocopherol modulates glomerulosclerosis and tubulointerstitial injury when it is given 2 wk after re

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

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

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

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

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

229 d infiltrating mononuclear cells in areas of tubulointerstitial injury, with a relative loss of stain

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

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

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

233 uria, and more severe glomerulosclerosis and tubulointerstitial injury.

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

235 of the inflammatory response in progressive tubulointerstitial injury.

236 reased RECA-1 and OX-2 staining) in areas of tubulointerstitial injury.

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

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

239 Autosomal dominant tubulointerstitial kidney disease is characterized by th

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

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

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

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

244 Inflammation contributes to the tubulointerstitial lesions of diabetic nephropathy.

245 a model that is characterized by predominant tubulointerstitial lesions.

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

247 Glomerular and tubulointerstitial mRNAs were microarrayed, followed by

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

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

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

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

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

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

254 Tubulointerstitial nephritis and uveitis (TINU) syndrome

255 Tubulointerstitial nephritis antigen (TIN-Ag) is a recen

256 Tubulointerstitial nephritis antigen (TIN-ag) is an extr

257 467 aa was 46% identical with that of human tubulointerstitial nephritis antigen (TIN-ag), and there

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

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

260 Our findings suggest that tubulointerstitial nephritis developed in these patients

261 Immune complex tubulointerstitial nephritis due to antibodies to brush

262 Tubulointerstitial nephritis is a common cause of kidney

263 a 36-year-old man with AIDS showed a severe tubulointerstitial nephritis with intranuclear inclusion

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

265 ted animals showed renal dysfunction and had tubulointerstitial nephritis with nuclear inclusions, ap

266 from infantile polycystic kidneys to chronic tubulointerstitial nephritis, fibrosis, and cortical mic

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

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

269 and the hamsters that survived showed severe tubulointerstitial nephritis.

270 some forms of immunologically mediated human tubulointerstitial nephritis.

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

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

273 Renal biopsy revealed a chronic tubulointerstitial nephropathy in 100%, with associated

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

275 eported to cause nephronophthisis, a chronic tubulointerstitial nephropathy.

276 s of neutrophils and macrophages that damage tubulointerstitial parenchyma.

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

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

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

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

281 looked inflammatory events that occur in the tubulointerstitial region.

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

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

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

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

291 ectly with the development of glomerular and tubulointerstitial scarring.

292 agents, which greatly reduce glomerular and tubulointerstitial scarring.

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

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

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

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