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

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

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

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

8 ne ATP6V1B1 cause autosomal-recessive 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 e mutations in NBCe1-A cause severe proximal renal tubular acidosis (pRTA).

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

14 99Val) in an individual with severe proximal renal tubular acidosis (pRTA; usually associated with de

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

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

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

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

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

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

21 NBC1 mutations cause proximal renal tubular acidosis in humans, consistent with its ro

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

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

24 t disease in patients lacking the cataracts, renal tubular acidosis, and neurological abnormalities t

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

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

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

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

29 tosis, south-east Asian ovalocytosis, distal renal tubular acidosis, Rhnull), associated with both st

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

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

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

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

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

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

36 ing both hereditary spherocytosis and distal renal tubular acidosis.

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

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

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

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

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

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

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

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

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

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

47 Renal tubular apoptosis is a major factor leading to tub

48 Renal tubular atrophy accompanies many proteinuric renal

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

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

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

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

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

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

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

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

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

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

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

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

61 in a doxycycline-regulated Smad7-expressing renal tubular cell line.

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

63 ulated proinflammatory macrophages, promoted renal tubular cell proliferation.

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

65 was found for cell fusion between indigenous renal tubular cells and BMDC, but this was infrequent an

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

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

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

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

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

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

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

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

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

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

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

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

78 Renal tubular cells do not express any of the known HIV-

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

80 Renal tubular cells elicit adaptive responses following

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

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

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

84 d secreted by immune cells, hepatocytes, and renal tubular cells in various pathologic states.

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

86 viability of islets and HK-2 human proximal renal tubular cells in vitro.

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

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

89 Renal biopsy data further suggest that renal tubular cells may serve as reservoir for HIV-1.

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

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

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

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

94 In cultured renal tubular cells, 20 microM cisplatin induced approxi

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

96 t mediates internalization of the virus into renal tubular cells, from which the virus can be rescued

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 nal protection required both macrophages and renal tubular cells.

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

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

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

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

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

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

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

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

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

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

110 glucose-induced mitochondrial dysfunction in renal tubular cells.

111 s on the viability of islets, podocytes, and renal tubular cells.

112 the mechanism that enables viral entry into renal tubular cells.

113 eases in GAPDH and pax2 abundance in NRK-52E renal tubular cells.

114 ss 1 phosphatidylinositol 3-kinase (PI3K) in renal tubular cells.

115 or against oxidative and apoptotic damage in 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 abundantly expressed in podocytes but not in renal tubular cells.

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

120 Acute kidney injury evokes renal tubular cholesterol synthesis.

121 lated to whether lethal infection or chronic renal tubular colonization occurs remains to be tested.

122 hage in guinea pigs and asymptomatic chronic renal tubular colonization with urinary shedding in rats

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

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

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

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

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

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

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

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

131 include crystals and uromodulin released by renal tubular damage.

132 hypertension, and attenuated glomerular and renal tubular damage.

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

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

135 rosophila share some similar features during renal tubular development.

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

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

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

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

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

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

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

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

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

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

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

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

148 ion and that loss of mechanosensation in the renal tubular epithelia is a feature of PKD cysts.

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

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

151 signaling pathways, mediates Ang II-induced renal tubular epithelial cell hypertrophy.

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

153 In microarray studies that used a novel renal tubular epithelial cell line from a patient with H

154 BMDC contributed to the renal tubular epithelial cell population, although most

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

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

157 Similar reductions in renal tubular epithelial cell proliferation were observe

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

159 Dysregulated apoptosis of renal tubular epithelial cells (RTEC) is an important co

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

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

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

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

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

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

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

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

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

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

170 cally important because it typically damages renal tubular epithelial cells and glomerular cells and

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

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

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

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

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

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

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

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

179 Damage to renal tubular epithelial cells by genetic, environmental

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

181 Nearly all renal tubular epithelial cells express insulin receptor.

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

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 Renal tubular epithelial cells in S-phase were scored as

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

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

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

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

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

191 Renal tubular epithelial cells synthesize laminin (LN)5

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

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

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

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

196 In renal tubular epithelial cells, decreased Smad3 levels w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 1 via a redox-dependent activation of Akt in renal tubular epithelial cells.

212 njury is followed by regeneration of damaged renal tubular epithelial cells.

213 posing regenerating tubules are derived from renal tubular epithelial cells.

214 ated caspase 3 expression, present mostly on renal tubular epithelial cells.

215 s-inducing factor (AIF) in cisplatin-treated renal tubular epithelial cells.

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

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

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

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

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

221 d frizzled-related protein 4 (sFRP4), during renal tubular epithelial injury initiated by unilateral

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

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

224 uced exclusively in the degenerated, dilated renal tubular epithelium after unilateral ureteral obstr

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

226 layer in mediating cell dedifferentiation of renal tubular epithelium and suggest that EMT is a multi

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

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

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

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

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

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

233 r cells and might facilitate the recovery of renal tubular epithelium.

234 type and were intimately associated with the renal tubular epithelium.

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

236 activity in kidneys in situ, thus modulating renal tubular fluid and electrolyte transport.

237 Renal tubular fluid in the distal nephron of the kidney

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

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

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

241 Renal tubular handling of uric acid is dependent on tubu

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

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

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

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

246 ion that NGAL is massively upregulated after renal tubular injury and may participate in limiting kid

247 3 (TFF3) and urinary albumin to detect acute renal tubular injury have never been evaluated with suff

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

249 val genes protects against TNF-alpha-induced renal tubular injury in diabetes.

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

251 Renal tubular injury is common in sepsis but presents fo

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

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

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

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

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

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

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

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

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

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

262 ycystin-1 (PC1) has an essential function in renal tubular morphogenesis and disruption of its functi

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

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

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

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

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

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

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

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

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

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

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

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

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

276 nd chloride transport, and new insights into renal tubular physiology.

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

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

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

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

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

282 factor 23, a hormone that inhibits proximal renal tubular reabsorption of phosphate and down-regulat

283 t NHERF-1 exerts a significant effect on the renal tubular reabsorption of uric acid in the mouse by

284 ibed transporter that is responsible for the renal tubular reabsorption of uric acid.

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

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

287 thelial cell population, although most (90%) renal tubular regeneration came from female indigenous c

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

289 al tubular epithelial cell proliferation and renal tubular regeneration.

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

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

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

293 Increased renal tubular sodium reabsorption impairs pressure natri

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

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