ライフサイエンスコーパス: renal tubular

1 Autosomal recessive distal renal tubular acidosis (dRTA) is a severe disorder of ac

2 cally reduced renal acid excretion in distal renal tubular acidosis (dRTA) may lead to nephrocalcinos

3 ercalated cells (ICs) leads to type I distal renal tubular acidosis (dRTA), a disease associated with

4 ne ATP6V1B1 cause autosomal-recessive distal renal tubular acidosis (dRTA).

5 meostasis and, when defective, causes distal renal tubular acidosis (dRTA).

6 calated cell cause autosomal dominant distal renal tubular acidosis (dRTA).

7 he consequent development of complete distal renal tubular acidosis (dRTA).

8 lenge showed the child has incomplete distal renal tubular acidosis (dRTA).

9 ions of the human ATP6V1B1 gene cause distal renal tubular acidosis (dRTA; OMIM #267300) often associ

10 Proximal renal tubular acidosis (pRTA) is a rare, recessively-inh

11 Proximal renal tubular acidosis (pRTA) is a syndrome caused by ab

12 ecessive mutations in SLC4A4 causes proximal renal tubular acidosis (pRTA), a disease characterized b

13 in the bicarbonate-wasting disease proximal renal tubular acidosis (pRTA).

14 e mutations in NBCe1-A cause severe proximal renal tubular acidosis (pRTA).

15 99Val) in an individual with severe proximal renal tubular acidosis (pRTA; usually associated with de

16 terized by low molecular weight proteinuria, renal tubular acidosis (RTA), aminoaciduria, and hyperca

17 main of NBCe1 (SLC4A4) is linked to proximal renal tubular acidosis and results in impaired transport

18 discuss why not all gene defects that cause renal tubular acidosis are associated with hypercalciuri

19 Glaucoma, cataracts, and proximal renal tubular acidosis are diseases caused by point muta

20 on of renal concentration defects and distal renal tubular acidosis as a result of impaired V-ATPase

21 The form of renal tubular acidosis associated with hyperkalemia is u

22 ith a clinical diagnosis of inherited distal renal tubular acidosis has no identified causative mutat

23 d as a potential cause of unexplained distal renal tubular acidosis or decreased gastric acid secreti

24 bulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea.

25 monogenic kidney stone disorders, including renal tubular acidosis with deafness, Bartter syndrome,

26 It has been implicated in tumor metastasis, renal tubular acidosis, and osteoporosis.

27 cystic fibrosis, growth hormone deficiency, renal tubular acidosis, and small for gestational age wi

28 eletion of Slc26a7 expression develop distal renal tubular acidosis, as manifested by metabolic acido

29 ions including primary aldosteronism, distal renal tubular acidosis, Liddle's disease, apparent miner

30 on, and various disease processes, including renal tubular acidosis, osteopetrosis, and tumor metasta

31 , poor growth, gastrointestinal dysmotility, renal tubular acidosis, seizures, and episodic metabolic

32 f hereditary hemolytic anemias and/or distal renal tubular acidosis.

33 nic mechanism of S427L in mediating proximal renal tubular acidosis.

34 thy, primary hyperparathyroidism, and distal renal tubular acidosis.

35 TM1 impairs ion transport, causing proximal renal tubular acidosis.

36 lead to the human diseases osteopetrosis and renal tubular acidosis.

37 sed serum pH, consistent with a diagnosis of renal tubular acidosis.

38 ing both hereditary spherocytosis and distal renal tubular acidosis.

39 is prevented and the animals develop distal renal tubular acidosis.

40 arly-onset sensorineural deafness and distal renal tubular acidosis.

41 ogether, these data demonstrate that reduced renal tubular ADMA metabolism protects against progressi

42 urine, leading to mild metabolic alkalosis ("renal tubular alkalosis").

43 he pathophysiology of AKI is orchestrated by renal tubular and endothelial cell necrosis and apoptosi

44 62Gln) at the DDC gene that affects multiple renal tubular and glomerular traits, and predicts accele

45 passes a group of disorders characterized by renal tubular and interstitial abnormalities, leading to

46 ) has an important role in the regulation of renal tubular and vascular function and has been implica

47 ys have essential roles in the regulation of renal tubular and vascular function.

48 We harvested CD4+ T cells from renal tubular antigen (Fx1A) -immunized rats and activat

49 n this study, the effects of high glucose on renal tubular apoptosis and the potential ability for Ra

50 PK) heterozygous background showed extensive renal tubular apoptosis by approximately 10 weeks of age

51 Renal tubular atrophy accompanies many proteinuric renal

52 nic inhibition of CaSR selectively increased renal tubular calcium absorption and blood calcium conce

53 entration, independent of PTH, and modulates renal tubular calcium transport in the TAL via the perme

54 s by 40-80% along with a 50-70% reduction in renal tubular cast formation.

55 Bax and Bak from proximal tubules attenuated renal tubular cell apoptosis and suppressed renal inters

56 production, with increased kidney injury and renal tubular cell apoptosis.

57 t of miR-26a on apoptosis was evaluated in a renal tubular cell culture.

58 ional intervention reduced hemolysis-related renal tubular cell damage, hepatocyte damage, ileal leak

59 f mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, rem

60 nistered to donor or recipient decreased the renal tubular cell death, inflammation, and MHC II expre

61 f persistent Cav-EGFR-ERK signaling mediates renal tubular cell dedifferentiation and identifies a no

62 with acute tubular necrosis, apoptosis, and renal tubular cell desquamation, with toxic vacuolizatio

63 n of renal vessels and induces hypertension, renal tubular cell hypertrophy, and podocyte apoptosis.

64 Primary cilia dysfunction alters renal tubular cell proliferation and differentiation and

65 ulated proinflammatory macrophages, promoted renal tubular cell proliferation.

66 y involved in the circadian clock system, in renal tubular cells (Bmal1(lox/lox)/Pax8-rtTA/LC1 mice).

67 romising therapeutic strategy for protecting renal tubular cells against cisplatin-induced AKI by enh

68 ll types including the vascular endothelium, renal tubular cells and erythrocytes.

69 Whereas murine renal tubular cells and freshly isolated renal tubules r

70 sue remodeling using cultured human proximal renal tubular cells and half-nephrectomized mice treated

71 cisplatin accumulates preferentially in the renal tubular cells and is a frequent cause of drug-indu

72 NGAL is a glycoprotein released by damaged renal tubular cells and is a sensitive maker of both cli

73 ologic analysis revealed Pals1 expression in renal tubular cells and podocytes of human kidneys.

74 In vitro, SCFAs modulated inflammation in renal tubular cells and podocytes under hyperglycemic co

75 asure the significant uptake of polymyxin in renal tubular cells and provides crucial information for

76 d ADV may cause mitochondrial dysfunction in renal tubular cells and reprogramming of glucose metabol

77 e proteins shows a predominant expression in renal tubular cells and the localization of immunoreacti

78 common in sepsis but presents focally; most renal tubular cells appear normal.

79 Myofibroblasts produced from EMT of renal tubular cells are responsible for the deposition o

80 he regenerative capacity of actively cycling renal tubular cells by decreasing the number of cells in

81 mmed necrosis (necroptosis), which occurs in renal tubular cells during AKI.

82 he expression of membrane sodium channels in renal tubular cells in a manner dependent on the metabol

83 ty is associated with a beneficial effect on renal tubular cells in AKI.

84 owed iron accumulation on the apical side of renal tubular cells in Heph/Cp KO mice.

85 Factor H was present on the urinary side of renal tubular cells in proteinuric, but not in normal re

86 is effects of kaempferol and esculetin using renal tubular cells in vitro and in vivo in a mouse Unil

87 Consistently, in cisplatin-injured renal tubular cells in vitro, lithium enhanced autophagi

88 lation and concentration of polymyxin within renal tubular cells is essential for the development of

89 capacity for autophagy in both podocytes and renal tubular cells is markedly impaired in type 2 diabe

90 primary cultures treated with cyclosporin A, renal tubular cells isolated from Nupr1-deficient mice e

91 Knockdown of Fat1 in renal tubular cells reduces migration, decreases active

92 r in situ We now show that EV from adult rat renal tubular cells significantly improved renal functio

93 HIF-2alpha activation in renal tubular cells upregulated mRNA and protein express

94 Albumin induced features of ER stress in renal tubular cells with ATF3/ATF4 activation.

95 on of cell cycle pathways was seen in murine renal tubular cells with NOTCH overexpression, and molec

96 -beta) plays an essential role in the EMT of renal tubular cells, but the molecular mechanism governi

97 ATP depletion or cisplatin treatment of rat renal tubular cells, mitochondrial fragmentation was obs

98 In renal tubular cells, TGF-beta1 administration upregulate

99 nhibitors might modulate glucose influx into renal tubular cells, thereby regulating the metabolic co

100 cyte-macrophage colony-stimulating factor by renal tubular cells, which directly stimulates expressio

101 abundantly expressed in podocytes but not in renal tubular cells.

102 nction caused by ischemic or toxic injury to renal tubular cells.

103 ion and fibrosis that is highly expressed in renal tubular cells.

104 ot induce apoptosis or regulated necrosis of renal tubular cells.

105 Gas6 receptor Axl in the apical membrane of renal tubular cells.

106 pathways leading to apoptosis or survival in renal tubular cells.

107 l-mesenchymal transition induced by FGF-2 in renal tubular cells.

108 n in mouse inner medullary collecting duct-3 renal tubular cells.

109 rkers of M2 macrophages when cocultured with renal tubular cells.

110 ithelial sodium channel alpha, ENaCalpha, in renal tubular cells.

111 s a critical role in TGF-beta-induced EMT of renal tubular cells.

112 created by knocking out Tsc1 in a subset of renal tubular cells.

113 glucose-induced mitochondrial dysfunction in renal tubular cells.

114 an integral part of the injury phenotype of renal tubular cells.

115 nal protection required both macrophages and renal tubular cells.

116 iates albumin-induced profibrotic effects in renal tubular cells.

117 rker for detecting ER stress in podocytes or renal tubular cells.

118 Acute kidney injury evokes renal tubular cholesterol synthesis.

119 hropathy showed a decrease in AIF within the renal tubular compartment and lower AIFM1 renal cortical

120 nalysis of CCRCCs and matched microdissected renal tubular controls revealed overexpression of NOTCH

121 cts on the expression and activity of distal renal tubular cotransporter proteins and to discuss the

122 How perturbations in Notch signaling cause renal tubular cysts remains unclear.

123 decreasing oxidative stress, leading to less renal tubular damage during cold preservation of porcine

124 m pretreatment prominently ameliorated acute renal tubular damage in mice exposed to cisplatin insult

125 ionally, EV treatment significantly improved renal tubular damage, 4-hydroxynanoneal adduct formation

126 In addition, MitoQ blunted oxidative stress, renal tubular damage, and cell death after 48 hours.

127 ly induced oxidative stress (nitrotyrosine), renal tubular damage, and cell death.

128 sociated lipocalin (NGAL), a novel marker of renal tubular damage, in patients with heart failure wit

129 include crystals and uromodulin released by renal tubular damage.

130 hypertension, and attenuated glomerular and renal tubular damage.

131 urinary concentrating abnormalities but also renal tubular defects that lead to neonatal mortality fr

132 , but whether these fragments originate from renal tubular degradation of filtered albumin is unknown

133 rosophila share some similar features during renal tubular development.

134 (aOR = 5.8; 95% CI = 3.7-9.0), and proximal renal tubular dysfunction (aOR = 7.0; 95% CI = 4.9-10.2]

135 creatinine ratio >/=3 mg/mmol), and proximal renal tubular dysfunction (retinol-binding protein/creat

136 vascular disease and mortality, but focus on renal tubular dysfunction as a potential risk factor is

137 e; hearing loss; pigmentary maculopathy; and renal tubular dysfunction.

138 ntal delay, hypertrophic cardiomyopathy, and renal tubular dysfunction.

139 renal impairment, albuminuria, and proximal renal tubular dysfunction.

140 lume and potassium homeostasis by regulating renal tubular electrolyte transport.

141 h activation of renal AMPK and inhibition of renal tubular ENaC.

142 aily and determined urinary excretion of the renal tubular enzymes fructose-1,6-bisphosphatase and gl

143 ween aberrantly increased AGS3 expression in renal tubular epithelia affected by PKD and epithelial c

144 te that postischemic NF-kappaB activation in renal tubular epithelia aggravates tubular injury and ex

145 I induced widespread NF-kappaB activation in renal tubular epithelia and in interstitial cells that p

146 nhanced Bcl-2 and HSP-70 expression in human renal tubular epithelial (HK-2) cells and prevented mito

147 mic injury to the kidney is characterized by renal tubular epithelial apoptosis and inflammation.

148 In human renal tubular epithelial cell line (HK-2), VAN induced p

149 receptor-independent mechanism to facilitate renal tubular epithelial cell proliferation and renal tu

150 The intracellular mechanisms underlying renal tubular epithelial cell proliferation and tubular

151 Similar reductions in renal tubular epithelial cell proliferation were observe

152 In a separate arm, renal tubular epithelial cells (HK-2) were directly stim

153 Here, using renal tubular epithelial cells (RTECs) derived from FAT1

154 We hypothesized that renal tubular epithelial cells (RTECs) isolated from hib

155 Renal tubular epithelial cells (RTECs) perform the essen

156 a, cytotoxicity, and inflammatory insults to renal tubular epithelial cells (RTECs), resulting in the

157 autophagosome and autolysosome formation in renal tubular epithelial cells (RTECs).

158 ptor (TNFR) superfamily, is induced in human renal tubular epithelial cells (TEC) in response to inju

159 ng factor (CSF)-1 and its receptor CSF-1R on renal tubular epithelial cells (TEC) will promote prolif

160 To elucidate the mechanisms by which renal tubular epithelial cells (TECs) control the comple

161 ller (NK) cell-mediated cytotoxicity against renal tubular epithelial cells (TECs) plays a crucial ro

162 We hypothesize that human renal tubular epithelial cells (TECs) trigger selective

163 NLRP3 expression in renal tubular epithelial cells (TECs) was found to be an

164 These results suggest that netrin-1 protects renal tubular epithelial cells against ischemia reperfus

165 However, Mif gene deletion restricted to renal tubular epithelial cells aggravated these effects.

166 d production of proinflammatory mediators by renal tubular epithelial cells and inflammatory cells (e

167 nflammatory responses through acting on both renal tubular epithelial cells and inflammatory cells an

168 ion induced inflammatory mediators from both renal tubular epithelial cells and macrophages after hyp

169 est that Dragon may enhance BMP signaling in renal tubular epithelial cells and maintain normal renal

170 DOT1L expression and H3K79 dimethylation in renal tubular epithelial cells and myofibroblasts in a m

171 infected with fluorescently tagged HIV with renal tubular epithelial cells and observed efficient vi

172 TMIGD1 is expressed in renal tubular epithelial cells and promotes cell surviva

173 tion (UUO), HDAC8 was primarily expressed in renal tubular epithelial cells and time-dependently upre

174 ed cell cycle dysregulation and apoptosis of renal tubular epithelial cells are important components

175 CI34051 treatment also reduced the number of renal tubular epithelial cells arrested at the G2/M phas

176 During proteinuria, renal tubular epithelial cells become exposed to ultrafi

177 eceptor 2 (TNFR2) is strongly upregulated on renal tubular epithelial cells by acute cell-mediated re

178 Damage to renal tubular epithelial cells by genetic, environmental

179 However, podocytes and renal tubular epithelial cells do not express CD4 recept

180 Nearly all renal tubular epithelial cells express insulin receptor.

181 Studies have shown that podocytes and renal tubular epithelial cells from patients with HIV-as

182 Renal tubular epithelial cells from SIRP-alpha(mut) mice

183 We found that Nod1 and Nod2 were present in renal tubular epithelial cells in both mouse and human k

184 biquitin-like protein that is upregulated in renal tubular epithelial cells in HIVAN.

185 Oxidative damage to renal tubular epithelial cells is a fundamental pathogen

186 During kidney morphogenesis and repair, renal tubular epithelial cells lacking the transmembrane

187 he increased expression of IL-36alpha in the renal tubular epithelial cells of a mouse model of unila

188 showed that the absence of C3aR and C5aR on renal tubular epithelial cells or circulating leukocytes

189 kdown of endogenous AGS3 mRNA and protein in renal tubular epithelial cells reduced cell proliferatio

190 beta1 integrin was required for renal tubular epithelial cells to mediate GDNF- and FGF-

191 ing progressive tubulointerstitial fibrosis, renal tubular epithelial cells transform into alpha-smoo

192 Murine renal tubular epithelial cells were studied in response

193 of transmembrane TNF-alpha in cultured CD4- renal tubular epithelial cells, 293T cells, and HeLa cel

194 l synapses between HIV-harboring T cells and renal tubular epithelial cells, allowing viral uptake an

195 und on many epithelial cell types, including renal tubular epithelial cells, in which they are felt t

196 beta-catenin in the cytoplasm and nuclei of renal tubular epithelial cells, indicating activation of

197 cking complex, localizes to primary cilia of renal tubular epithelial cells, is required for ciliogen

198 facilitated NLRP3 inflammasome activation in renal tubular epithelial cells, macrophages, and dendrit

199 r kidney injury induces cell cycle arrest in renal tubular epithelial cells, resulting in the secreti

200 First, FBP1 antagonizes glycolytic flux in renal tubular epithelial cells, the presumptive ccRCC ce

201 In vascular smooth muscle cells and renal tubular epithelial cells, treatment with thrombosp

202 le deletion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC

203 und on many epithelial cell types, including renal tubular epithelial cells, where they participate i

204 eta1 induced a biphasic activation of ILK in renal tubular epithelial cells, with rapid activation st

205 Hypoxia significantly increased HE4 in renal tubular epithelial cells.

206 ch for the sustained in-vivo modification of renal tubular epithelial cells.

207 ecule expression, and internalization within renal tubular epithelial cells.

208 cells and by inhibiting bacteria invasion of renal tubular epithelial cells.

209 ut also reduced bacterial internalization by renal tubular epithelial cells.

210 creased larval survival and proliferation of renal tubular epithelial cells.

211 FkappaB-mediated cyclooxygenase-2 (COX-2) in renal tubular epithelial cells.

212 human BK polyomavirus in primary cultures of renal tubular epithelial cells.

213 ngle-pass transmembrane protein expressed in renal tubular epithelial cells.

214 1 via a redox-dependent activation of Akt in renal tubular epithelial cells.

215 quencing on glomerular endothelial cells and renal tubular epithelial cells.

216 ydrophilic norursodeoxycholic acid inhibited renal tubular epithelial injury in CBDL mice.

217 ed toxic BAs represent a pivotal trigger for renal tubular epithelial injury leading to cholemic neph

218 day common bile duct ligation (CBDL) induced renal tubular epithelial injury predominantly at the lev

219 contributes to the maintenance and repair of renal tubular epithelium and may be a novel therapeutic

220 ntributes to renal IRI by a direct effect on renal tubular epithelium and that this effect is indepen

221 TNF-alpha production specifically within the renal tubular epithelium attenuated the AKI and the incr

222 ile beta-catenin is induced predominantly in renal tubular epithelium in CKD, surprisingly, depletion

223 Both Nlrp3 and Asc were highly expressed in renal tubular epithelium of humans and mice, and the abs

224 bstruction induced Shh, predominantly in the renal tubular epithelium of the fibrotic kidneys.

225 The presence of viral particles in the renal tubular epithelium that were morphologically ident

226 may be processed by urokinase, released from renal tubular epithelium, to generate active plasmin.

227 nd amelioration of hypoxia through increased renal tubular expression of VEGF and its isoforms.

228 of mTORC1 inhibitors, the role of mTORC1 in renal tubular function and kidney homeostasis remains el

229 essential for normal kidney development and renal tubular function.

230 ibility that these miRNAs could modulate key renal tubular functions in a paracrine manner.

231 egulator of FoxM1 because GSK3 inhibition or renal tubular GSK3beta gene deletion significantly incre

232 dies implicate a series of genes involved in renal tubular handling of lithogenic substrates, such as

233 Renal tubular handling of uric acid is dependent on tubu

234 (a) To examine the latest information about renal tubular handling of uric acid, its genetic backgro

235 In conclusion, late-stage renal tubular HIF-2alpha activation has protective effec

236 nal profiling revealed that mTORC1 maintains renal tubular homeostasis by controlling mitochondrial m

237 hemic acute kidney injury (AKI) by promoting renal tubular inflammation after ischemia and reperfusio

238 Furthermore, renal tubular inflammation, necrosis, and apoptosis were

239 Patients in the urinary renal tubular injury biomarker substudy (NAG [N-acetyl-b

240 erandomization WRF was unrelated to baseline renal tubular injury biomarkers ( r=0.14; P=0.17).

241 RF was strongly associated with worsening in renal tubular injury biomarkers (odds ratio, 12.6; P=0.0

242 Increase in renal tubular injury biomarkers was associated with a hi

243 3 (TFF3) and urinary albumin to detect acute renal tubular injury have never been evaluated with suff

244 In addition, we provide evidence for renal tubular injury in cholestatic patients with cholem

245 increase the levels of urinary biomarkers of renal tubular injury in this occupational setting.

246 Renal tubular injury is common in sepsis but presents fo

247 more sensitive and robust diagnosis of acute renal tubular injury than traditional biomarkers.

248 can cause vascular and renal calcification, renal tubular injury, and premature death in multiple an

249 ction, PAR2-deficient mice displayed reduced renal tubular injury, fibrosis, collagen synthesis, conn

250 eexisting worsening renal function (WRF) and renal tubular injury, postdischarge renal function, and

251 al expansion) glomerular injury and improves renal tubular injury.

252 bumin were markedly increased in response to renal tubular injury.

253 pulation, which are increased in response to renal tubular injury.

254 DOCA-salt treatment significantly increased renal tubular lesions from day 2 and mRNA expression of

255 atment, Nupr1-deficient mice exhibited worse renal tubular lesions than wild-type mice.

256 n be differentiated into functionally active renal tubular-like cells that therapeutically prevent ch

257 F) with tenofovir alafenamide (TAF) improves renal tubular markers in HIV-infected individuals but th

258 ficantly decreased the protein expression of renal tubular megalin, which inversely correlated with t

259 NAD(+)-dependent maintenance of renal tubular metabolic health may also attenuate long-t

260 cells in vitro and in vivo Our data identify renal tubular MIF as an endogenous renoprotective factor

261 hance the activity of transporters mediating renal tubular Na(+) reabsorption are well established ca

262 Aldosterone increases renal tubular Na+ absorption in large part by increasing

263 oxicities in two patients at 70 mg/m(2) were renal tubular necrosis and proteinuria (both grade 3).

264 se protects against ischemic AKI by reducing renal tubular necrosis, apoptosis, and inflammation, and

265 Other lesions included progressive renal tubular necrosis, glomerular fibrin thrombosis, an

266 t ischemic AKI with significantly attenuated renal tubular necrosis, inflammation, and apoptosis when

267 r reperfusion, Slit2 significantly inhibited renal tubular necrosis, neutrophil and macrophage infilt

268 loss, cecal luminal fluid accumulation, and renal tubular necrosis.

269 To determine the role of renal tubular NEDD4-2 in adult mice, we generated tetrac

270 compared with control littermates, inducible renal tubular NEDD4-2 knockout (Nedd4L(Pax8/LC1) ) mice

271 We evaluated the role of renal tubular Nox-2 in the pathogenesis of epithelial-to

272 A subset of these patients have renal tubular obstruction by casts of red blood cells, p

273 modynamics, direct tubular injury or causing renal tubular obstruction.

274 and PVT1 expression specifically in cells of renal tubular origins.

275 Previously described markers of renal tubular progenitor cells were analyzed using immun

276 ecognized a high molecular weight protein in renal tubular protein extracts that we identified as LDL

277 reperfusion injury, and transgenic mice with renal tubular QLalpha12 (activated mutant) expression we

278 s rapidly increase renal excretion or reduce renal tubular reabsorption and thus blunt large increase

279 Angiotensin II (ANG II) stimulates renal tubular reabsorption of NaCl by targeting Na(+)/H(

280 owth factor 23 (FGF23) axis, creatinine, and renal tubular reabsorption of phosphate (TRP).

281 Conceptually, modest inhibition of renal tubular reabsorption should provide effective reli

282 in the expression of AGS3 exhibited impaired renal tubular recovery 7 d following IRI compared to wil

283 ults demonstrate that FoxM1 is important for renal tubular regeneration following AKI and that GSK3be

284 eterotrimeric G-protein function, influences renal tubular regeneration following IRI.

285 al tubular epithelial cell proliferation and renal tubular regeneration.

286 Renal tubular repair in the outer medulla 7 days after I

287 In such individuals, the renal tubular response to FGF23 may be suboptimal.

288 icate that miR-146a is a key mediator of the renal tubular response to IRI that limits the consequenc

289 Renal tubular secretion is an active efflux pathway for

290 Our results suggest that mIBG undergoes renal tubular secretion mediated by hOCT2 and hMATE1/2-K

291 Increased renal tubular sodium reabsorption impairs pressure natri

292 scular compartment and gaining access to the renal tubular space, we reasoned that a kidney allograft

293 principle repressor of PPM1A, as conditional renal tubular-specific induction of TGF-beta1 in mice dr

294 ical utility of urinary dickkopf-3 (DKK3), a renal tubular stress marker, for preoperative identifica

295 cal and physiological characteristics of the renal tubular system.

296 also had greater macrophage infiltration and renal tubular TGF-beta1 expression than wild-type mice.

297 KRN23 significantly increased the maximum renal tubular threshold for phosphate reabsorption (TmP/

298 se-dependent but usually reversible proximal renal tubular toxicity.

299 ity within the ABCC10 gene may influence TFV renal tubular transport and contribute to the developmen

300 ry albumin fragments occurs independently of renal tubular uptake and degradation of albumin, suggest