ライフサイエンスコーパス: renal injury

1 tial as a strategy for improving outcomes of renal injury.

2 nd the progression is further accelerated by renal injury.

3 hropathy and mice with hyperglycemia-induced renal injury.

4 7A in innate leukocytes in cisplatin-induced renal injury.

5 -17A from those cells does not contribute to renal injury.

6 rted into proximal tubules, leading to acute renal injury.

7 nergy metabolism and attenuating I/R-induced renal injury.

8 conditions and fostering macrophage-mediated renal injury.

9 ed in wild-type mice after cisplatin-induced renal injury.

10 sed albuminuria and histological measures of renal injury.

11 nflammation, thereby attenuating I/R-induced renal injury.

12 ession protected animals from L-NAME-induced renal injury.

13 lication in protection from ischemic-induced renal injury.

14 ich in turn contribute to the progression of renal injury.

15 oteins, can attenuate both acute and chronic renal injury.

16 nhibitors in the setting of acute or chronic renal injury.

17 malities and those with sustained iatrogenic renal injury.

18 rization in ARAS on renal tissue hypoxia and renal injury.

19 rstitial injury, and decreased biomarkers of renal injury.

20 ry response to IRI exacerbates the resultant renal injury.

21 ells (Tregs) help protect against autoimmune renal injury.

22 ause hemolytic anemia, thrombocytopenia, and renal injury.

23 ly demonstrated in the pathogenesis of acute renal injury.

24 development but increased susceptibility to renal injury.

25 TL1A), and TNF in TECs, as observed in human renal injury.

26 is in five mouse models of acute and chronic renal injury.

27 recruitment into the kidney and ameliorated renal injury.

28 a target for novel therapeutic approaches to renal injury.

29 in Ins2(Akita) mice or STZ-induced diabetic renal injury.

30 dies in the broader context of immunological renal injury.

31 um reabsorption, proliferation, fibrosis and renal injury.

32 gesting that it may protect against ischemic renal injury.

33 ported to be markedly induced in response to renal injury.

34 fter renal I/R and contributes to functional renal injury.

35 orted MCP-1 gene activation in patients with renal injury.

36 hat becomes deposited in the kidney, causing renal injury.

37 icantly reduced blood pressure and prevented renal injury.

38 gesting ER stress as a causal factor for the renal injury.

39 ophagy induction during hypoxic and ischemic renal injury.

40 ney function regardless of the exact site of renal injury.

41 n contribute to the pathogenesis of ischemic renal injury.

42 d renal function and reduced the severity of renal injury.

43 o the renal Fanconi syndrome and progressive renal injury.

44 pattern and pathophysiology of some forms of renal injury.

45 al that promotes inflammation after ischemic renal injury.

46 flammatory response that exacerbate ischemic renal injury.

47 omprised of regenerated cells in response to renal injury.

48 ietic cells was responsible for the enhanced renal injury.

49 alocorticoid aldosterone induces cardiac and renal injury.

50 le in the repair process in animal models of renal injury.

51 suspected mechanism of vancomycin-associated renal injury.

52 L) has been implicated in the development of renal injury.

53 mmation are integral to hypertension-induced renal injury.

54 ase Shp2 to lipopolysaccharide (LPS)-induced renal injury.

55 otected against ischemia-reperfusion-induced renal injury.

56 nsplantation (RTx) and in vitro cold hypoxic renal injury.

57 il dwell time and ROS production, as well as renal injury.

58 )CD25(+) cells were also found as increasing renal injury.

59 del of human salt-sensitive hypertension and renal injury.

60 into the kidney exacerbates hypertension and renal injury.

61 , which might inhibit or potentially reverse renal injury.

62 wild-type mice, with respect to survival and renal injury.

63 , and whether the kidneys were challenged by renal injury.

64 he feasibility of a novel therapy to curtail renal injury.

65 increases the hazard rate of having rash and renal injury.

66 irected to recipient-dependent mechanisms of renal injury.

67 of Rhophilin-1 knockout mice exacerbated the renal injury.

68 tment normalized blood pressure and reversed renal injury.

69 cant attenuation of intestinal, hepatic, and renal injuries.

70 ated in patients with both acute and chronic renal injuries.

71 ration was associated with increased risk of renal injury (6.2% vs. 2.9%; absolute risk difference 13

72 Severe renal injuries after blunt trauma cause diagnostic and t

73 ntly and attenuated intestinal, hepatic, and renal injury after AKI.

74 ocardial infarction, bleeding, and recurrent renal injury after discharge.

75 Our results indicate that octreotide reduced renal injury after HIR due to its induction of autophagy

76 However, nonperitoneal B cells attenuate renal injury after I/R, possibly through the production

77 the glomeruli after renal I/R and attenuated renal injury after I/R.

78 We also assessed hepatic and renal injury after intestinal IRI.

79 th S1P(2)R small interfering RNA had reduced renal injury after IR.

80 ay a critical role in the pathophysiology of renal injury after obstruction.

81 ore IRI protects from both acute and chronic renal injuries and may have clinical application in prot

82 ssment of altered redox capacity in diabetic renal injury and after successful treatment.

83 erlipidemia acted reciprocally, accentuating renal injury and altering renal function.

84 ed renal function, and attenuated histologic renal injury and apoptosis after IRI.

85 eceptor agonist exendin-4 reduced CP-induced renal injury and apoptosis, and suppression of renal GLP

86 and multiple organ failure, including acute renal injury and ARDS.

87 monstrated equal efficacy but with decreased renal injury and bone mineral density loss compared with

88 Calcineurin inhibitors cause vascular and renal injury and can trigger hemolytic uremic syndrome.

89 Interestingly, both the renal injury and dysfunction in wild-type mice undergoin

90 ent with the three rhubarb extracts improved renal injury and dysfunction, either fully or partially

91 cisplatin, Tlr9(-/-) mice developed enhanced renal injury and exhibited fewer intrarenal regulatory T

92 ly directly involved, and tubulointerstitial renal injury and fibrosis are prominent histologic featu

93 ther TLR-4 deficiency reduces Ang-II-induced renal injury and fibrosis by attenuating reactive oxygen

94 CL16 plays a key role in the pathogenesis of renal injury and fibrosis in salt-sensitive hypertension

95 e TGFbeta signaling pathway to contribute to renal injury and fibrosis.

96 /min or slower is also effective in reducing renal injury and has the added benefit of improving ston

97 esults strongly support a role for IRAK-M in renal injury and identify IRAK-M as a possible modulator

98 psy calls for treatment strategies to reduce renal injury and improve the efficiency of stone breakag

99 NOSKO mice, aging eNOSKO mice showed greater renal injury and in particular developed a thrombotic mi

100 igh) population associated with the onset of renal injury and increase in proinflammatory cytokines,

101 n the glomerulus is sufficient to accelerate renal injury and inflammation in the absence of hyperten

102 hypertension, microvascular rarefaction, and renal injury and led to greater recovery of renal functi

103 pletion significantly attenuated IRI-induced renal injury and leukocyte accumulation.

104 recipients who showed evidence of reversible renal injury and limited chronicity on pre-LT kidney bio

105 and dedifferentiation, which associate with renal injury and may also influence the rate of cystogen

106 h mortality at lower doses, but Stx2-induced renal injury and mortality were delayed 2 to 3 days comp

107 acute changes in creatinine lag behind both renal injury and recovery.

108 iptin (AG), significantly reduced CP-induced renal injury and reduced the renal mRNA expression ratio

109 Both renal injury and renal IL-1beta and IL-17A production we

110 is central to tubular repair using an acute renal injury and repair model, ischemia/reperfusion (I/R

111 therefore define a molecular fingerprint of renal injury and suggest miR-21 may play a role in prote

112 plays a major role in induction of diabetic renal injury and that blocking arginase-2 activity or ex

113 mplification of PD1 circuits restrains acute renal injury and that short-term changes in dietary omeg

114 f the pathogenesis of alcohol-induced hepato-renal injury and the development of new approaches to it

115 e found that induction of HO attenuated both renal injury and the rate of cystogenesis, whereas inhib

116 mmation, endothelial damage, thrombosis, and renal injury and underscore ongoing risk for systemic TM

117 ays, had increased biochemical indicators of renal injury, and exhibited severe pathological injury w

118 ificantly reduced TRL, as well as markers of renal injury, and improved endothelial-dependent vasorel

119 associated with increased aortic stiffness, renal injury, and incident cardiovascular events.

120 t mortality, worse structural and functional renal injury, and increased levels of apoptosis in rhabd

121 xpression normalized systolic BP, attenuated renal injury, and inhibited RPTC Nrf2, Agt, and heme oxy

122 t they exhibit proteinuria, signs of chronic renal injury, and kidney inflammation.

123 subsequent HSRs, including documented rash, renal injury, and liver injury.

124 ated in urine samples of patients with acute renal injury, and macrophage inflammatory protein-1Delta

125 cteria capable of causing pyelonephritis and renal injury, and to selectively target the gastrointest

126 Novel biomarkers of renal injury appear inconsistent in identifying a creati

127 and age, hemoglobin and markers of liver and renal injury are associated with inflammation.

128 Acute renal injury (ARI) and acute renal failure (ARF) are ser

129 yte infiltration, and inflammation following renal injury as determined by light microscopy, immunohi

130 that were produced in a mouse model of acute renal injury (as a result of kidney-specific ablation of

131 irectly to mice with ischemic AKI attenuated renal injury, as assessed by plasma creatinine, tubular

132 ression was measured using real-time PCR and renal injury assessed with histological analysis.

133 ney disease in blacks, but the mechanisms of renal injury associated with APOL1 risk variants are unk

134 tion of Epac as a therapeutic application in renal injury associated with oxidative stress.

135 Soluble apyrase reduced acute renal injury at 24 hours and renal fibrosis at 4 weeks p

136 39 transgenic mice were protected from acute renal injury at 24 hours, but had increased renal fibros

137 suggest that the VDR attenuates obstructive renal injury at least in part by suppressing the renin-a

138 alin and varying creatinine-based metrics of renal injury at multiple time points associated with car

139 py attenuated MV damage, but did not resolve renal injury at practical clinical doses.

140 he right kidney accounted for differences in renal injury between the two kidneys, measured by percen

141 Doses>/=0.1 mg/kg DA elevated the renal injury biomarkers kidney injury molecule-1 and neu

142 measured in air, urine, and serum, and early renal injury biomarkers were measured in urine.

143 human tubular epithelial cells (TECs) during renal injury, but its function in this setting remains u

144 Bone marrow-derived stem cells may modulate renal injury, but the effects may depend on the age of t

145 -214 and miR-21 are upregulated in models of renal injury, but the function of miR-214 in this settin

146 atment with the FXR agonist INT-747 improves renal injury by decreasing proteinuria, glomeruloscleros

147 s were matched with patients without post-LT renal injury by gender, creatinine, and body mass index.

148 PAR-gamma agonists may benefit aging-related renal injury by improving mitochondrial function.

149 hat is distinguishable from typical ischemic renal injury by its paucity of tubular cell death.

150 ies) limits the progression of pulmonary and renal injury by reducing activation of the AGEs-RAGE pat

151 type and eNOS knockout mice and then induced renal injury by uninephrectomy.

152 Renal injury can also markedly accelerate the renal cyst

153 echanism that may be involved in progressive renal injury caused by chronic exposure to Ang II.

154 fering from greater oxidative DNA damage and renal injury compared with Nrf2(+/+) mice.

155 n kidney injury and repair and indicate that renal injury constitutes a 'third hit' resulting in rapi

156 malfunction, tissue failure, and progressive renal injury despite cystine-depletion therapies.

157 However, renal injury did not induce the expression of Bpifa2 in

158 w biomarkers that provide better measures of renal injury, especially in patients with sepsis.

159 s in mice fed an adenine diet known to cause renal injury followed by fibrosis.

160 In addition, intestinal, hepatic, and renal injury following AKI was attenuated without affect

161 ficantly attenuated intestinal, hepatic, and renal injury following liver IR.

162 can Association for Surgery of Trauma (AAST) renal injury grading scale.

163 ther hyperuricemia can induce chronic direct renal injury has been argued for many decades.

164 Warfarin-associated calciphylaxis without renal injury has been described, but whether it is a sub

165 ine system, blood lipids, and the liver, but renal injury has not been described.

166 Several biomarkers of renal injury have been identified but the utility of the

167 In mice, GTCs injected after ischemic renal injury homed to the renal parenchyma, and GTC-trea

168 HR], 4.16; 95% CI, 2.54-6.83; P < .0001) and renal injury (HR, 2.13; 95% CI, 1.36-3.33; P = .0009) bu

169 AC6 is a key mediator of cyst formation and renal injury in a model of PKD.

170 about environmental exposure to melamine and renal injury in adults is lacking.

171 gamma agonist pioglitazone protected against renal injury in aging; it reduced proteinuria, improved

172 ls separated from diseased kidney aggravated renal injury in AN mice.

173 butes to the development of hypertension and renal injury in Dahl salt-sensitive (SS) rats, a widely

174 effects of diet supplementation of AS-IV on renal injury in db/db mice, a type 2 diabetic mouse mode

175 Renal injury in diabetes is associated with elevated sys

176 in the kidney plays a key role in mediating renal injury in diabetes.

177 sion and the development of hypertension and renal injury in diabetic Akita transgenic mice.

178 telmisartan were less effective at reducing renal injury in diabetic eNOSKO mice compared with diabe

179 pril also failed to prevent hypertension and renal injury in diabetic eNOSKO mice.

180 The present study demonstrates accelerated renal injury in diabetic FXR KO mice.

181 The enhanced renal injury in diabetic mice caused by lack of B1R and

182 which hyperglycemia induces hypertension and renal injury in diabetic mice.

183 iated glomerular neutrophil accumulation and renal injury in experimental, crescentic anti-GBM nephri

184 for promoting these effects and aggravating renal injury in HIV-transgenic mice.

185 ibution of IgG Fcgamma receptors to diabetic renal injury in hyperglycemic, hypercholesterolemic mice

186 Polygenic susceptibility to renal injury in hypertension arises in association with

187 that contrast strongly in susceptibility to renal injury in hypertension.

188 isplatin-induced functional and histological renal injury in Il17a(-/-) and Rorgammat(-/-) mice, as w

189 nd the factors influencing susceptibility to renal injury in individuals with congenital solitary kid

190 ar events promoting chronic inflammation and renal injury in individuals with DN.

191 of the N- and L-type calcium channel lessens renal injury in kidney disease patients.

192 utant proteins in kidneys caused progressive renal injury in male transgenic mice as evidenced by an

193 and coexpressed with CSF-1 in TECs following renal injury in mice and humans.

194 mulation of VEGFR2 can potentiate subsequent renal injury in mice, an effect enhanced in the setting

195 sion-induced increases in blood pressure and renal injury in mice.

196 ibitor trametinib prevents endotoxin-induced renal injury in mice.

197 podocytes, contributes to the progression of renal injury in mouse GN, and myeloid deficiency of MR p

198 d injury to Fanconi syndrome and progressive renal injury in nephropathic cystinosis.

199 om April 2013 through June 2014, 13 cases of renal injury in patients receiving dabrafenib therapy we

200 Furthermore, renal injury in preeclampsia associated with an elevated

201 Cisplatin induced more renal injury in PT-S1P1-null mice than in controls.

202 at treating with aluminum citrate attenuates renal injury in rats with severe ethylene glycol toxicit

203 nd Mas expression, associated with increased renal injury in response to Ang II.

204 1,25-vitamin D3 deficiency directly leads to renal injury in rodents.

205 Analogs of vitamin D attenuate renal injury in several models of kidney disease, but th

206 modulate the susceptibility to hypertensive renal injury in SHR-A3 rats.

207 iron accumulation occurs and contributes to renal injury in SLE.

208 butes to the development of hypertension and renal injury in SS rats.

209 te its effects on diabetic macrovascular and renal injury in streptozotocin-induced diabetic apolipop

210 histologic data indicated similar degrees of renal injury in survivin(ptKO) and control mice 24 hours

211 ndothelial nitric oxide synthase accelerates renal injury in the aging kidney.

212 Renal injury in the Dahl salt-sensitive rat mimics human

213 llele is defective and likely contributes to renal injury in the FHH rat.

214 and a vitamin D analog markedly ameliorated renal injury in the streptozotocin (STZ)-induced diabete

215 rfusion pressure (RPP) on the development of renal injury in this model.

216 nd may serve as a marker of diverse forms of renal injury in tissues from mice and humans.

217 To evaluate the effect of IRAK-M in chronic renal injury in vivo, a mouse model of unilateral ureter

218 induced acute tubular necrosis worsened peak renal injury in vivo.

219 We used cisplatin to induce renal injury in wild-type (DR3(+/+)) or congenitally def

220 which was associated with cisplatin-induced renal injury in wild-type mice, was significantly blunte

221 wed decreased levels of plasma biomarkers of renal injury including Cystatin C, Osteopontin, Tissue I

222 Antiretroviral drugs also cause renal injury, including crystals and tubular injury, acu

223 with subsequent renal lipid accumulation and renal injury, including glomerulosclerosis, interstitial

224 he immune system contribute to the resultant renal injury, including the complement system.

225 eatinine and CP caused remarkable pathologic renal injury, including tubular necrosis.

226 6 months after Pkd1 deletion, and additional renal injury increased the likelihood of cyst formation

227 with COPD and/or CS-exposed mice had chronic renal injury, increased urinary albumin/creatinine ratio

228 hat miR-214 functions to promote fibrosis in renal injury independent of TGF-beta signaling in vivo a

229 That genetic reduction of TF prevents renal injury induced by different aPL antibodies indicat

230 nary biomarkers in rats during recovery from renal injury induced by exposure to carbapenem A or gent

231 deletion of the MR gene in SMCs, limited the renal injury induced by IR through effects on Rac1-media

232 Renal injury induced by ischemia was associated with inc

233 Uremia, in the absence of renal injury, induced the NGAL gene, but not MCP-1, sugg

234 In mice, renal injury-induced activation of pericytes, which are

235 cteria make targeted probiotic prevention of renal injury-inducing UTIs a potential therapeutic reali

236 The renal injury inflicted by expression of the folding muta

237 Nur77-mediated renal injury involved a conformational change of Bcl2 an

238 portant role in the pathogenesis of ischemic renal injury (IRI), which is the major cause of intrinsi

239 Ischemic renal injury is a complex syndrome; multiple cellular ab

240 This attenuated renal injury is associated with reduced oxidative stress

241 of immunological mechanisms in hypertensive renal injury is incompletely understood.

242 urrence of lupus nephritis (LN) before overt renal injury is needed to optimize and individualize tre

243 ciated HUS, and the mechanism of Stx-induced renal injury is not well understood primarily due to a l

244 Tubular damage following ischemic renal injury is often reversible, and tubular epithelial

245 ion, but the role of integrin alpha2beta1 in renal injury is unclear.

246 During renal injury, kidney-localized proteinases can signal by

247 ssment of polytrauma patients with suspected renal injury, leading to timely diagnosis and urgent sur

248 n together, these data suggest that ischemic renal injury leads to a rise in antibody production, whi

249 This finding motivated a novel hypothesis: renal injury leads to activation of an extracellular 2',

250 Here we show that renal injury leads to massive cystic disease in the same

251 l complement activation (C5a and sC5b-9) and renal injury markers (clusterin, cystatin-C, beta2-micro

252 Villin 1 levels were compared with other renal injury markers (creatinine, aspartate transaminase

253 -1alpha, resulted in increased expression of renal injury markers and inflammatory cell infiltration

254 tin-induced nephrotoxicity by reducing these renal injury markers by 40-80% along with a 50-70% reduc

255 The increased susceptibility to renal injury may be due, in part, to reduced nephron num

256 Addition of biomarkers of renal injury may provide additional prognostic value to

257 ulation of Mpv17l is a consistent feature in renal injury models.

258 rotic cytokine expression in two independent renal injury models: folate nephropathy and unilateral u

259 with eosinophilia, including rash (n = 32), renal injury (n = 31), and liver injury (n = 13).

260 ypokalemia, three reported CTC grade 3 acute renal injury, none of which were deemed directly attribu

261 Neither strategy to reduce renal injury -- not power ramping with 'pause-protection

262 velopment of target organ injury, especially renal injury, obesity-associated hypertension becomes mo

263 In the HES and saline groups, renal injury occurred in 34.6% and 38.0% of patients, re

264 ons with special emphasis on the 5 grades of renal injury on a CT according to the AAST scale.

265 eptor blockade attenuates cardiovascular and renal injury, only recently have we learned that mineral

266 CRP administration did not reduce renal injury or alter disease in the ANTN model.

267 es and tubular epithelial cells, accompanied renal injury; paricalcitol largely abolished this induct

268 tion of autoantibody production, reversal of renal injury, preservation of biochemical renal function

269 create a therapeutic target in hypertensive renal injury, rats of both lines were treated with the i

270 d hepatocyte death, cerebral infarction, and renal injury relative to wild-type.

271 We discovered that renal injury releases 2',3'-cAMP (positional isomer of 3

272 However, its role in hypertension induced renal injury remains unexplored.

273 eated with the FXR agonist obeticholic acid, renal injury, renal lipid accumulation, apoptosis, and c

274 on of the EMT program in TECs during chronic renal injury represents a potential anti-fibrosis therap

275 is a thrombotic microangiopathy with severe renal injury secondary to an overactive alternative comp

276 dministration of a monoclonal antibody after renal injury stimulated bone formation rates, corrected

277 venile than adult kidneys and increase after renal injury, suggesting that cell proliferation may enh

278 enal I/R and found that they sustained worse renal injury than wild-type controls.

279 tibodies, we developed a new animal model of renal injury that shares many features with thrombotic m

280 further renal hypoxia and hypoxia-associated renal injury, there is concern that high altitude may ac

281 ity that kidney DDAH1 expression exacerbates renal injury through uromodulin-related mechanisms.

282 lateral urinary obstruction model of chronic renal injury to decipher the role of these enzymes using

283 es the CKD-MBD in diabetic mice subjected to renal injury to induce stage 2 CKD (CKD-2 mice).

284 gleaned from the temporal change markers of renal injury (urine neutrophil gelatinase-associated lip

285 H2 S treatment mitigates cold IRI-associated renal injury via mitochondrial actions and could represe

286 e control of salt-sensitive hypertension and renal injury via Rac1, which is one of the small GTPases

287 Acute tubular and glomerular renal injury was accompanied by nonheme iron deposition

288 Progress of renal injury was compared with nephropathy-resistant wil

289 Renal injury was more common in men (85 men vs 47 women;

290 To confirm that a lack of Tregs potentiated renal injury, we co-transferred isolated Tregs and Scurf

291 n this haplotype block and susceptibility to renal injury, we examined the effect of SHR-A3 and SHR-B

292 uld alter susceptibility to hypertension and renal injury, we infused mice with angiotensin II contin

293 To assess renal injury, we performed the renal pelvis injections o

294 ignal transduction pathways mis-regulated in renal injury, we studied the modulation of mammalian tar

295 Serum markers of renal injury were significantly decreased in the CD47mAb

296 tendant complications of multiple myeloma is renal injury, which contributes significantly to morbidi

297 dney/glomerular hypertrophy, and progressive renal injury, which culminates in reduced renal function

298 tension and renal hyperfiltration as well as renal injury with heightened TGF-beta1 expression in adu

299 Mice receiving Adriamycin developed renal injury with loss of podocytes and hyperplastic les

300 Renal injury with metabolic inhibitors increased the mea