ライフサイエンスコーパス: nephrotoxic

1 Calcineurin inhibitors are known to be nephrotoxic.

2 osporine and tacrolimus are both known to be nephrotoxic.

3 , a commonly used chemotherapeutic agent, is nephrotoxic.

4 However, it is severely nephrotoxic.

5 limination of compounds that are potentially nephrotoxic.

6 Nephrotoxic Ab and TLR2 ligation caused a neutrophil inf

7 mmation induced by passive administration of nephrotoxic Ab does not occur in the absence of TLR2 sti

8 sh renal injury induced by complement-fixing nephrotoxic Ab.

9 rular basement membrane after conjugation to nephrotoxic Ab.

10 by intraperitoneal injections of folic acid (nephrotoxic acute kidney injury) or by IM injections of

11 tions of rHuEPO can ameliorate ischaemic and nephrotoxic acute renal failure, Bahlmann's work is the

12 interval, 1.07-1.31) and the number of other nephrotoxic agents (odds ratio, 1.38; 95% confidence int

13 nts likely involves rapid elimination of the nephrotoxic agents from the kidney by promoting diuresis

14 zing injury from radiocontrast dyes or other nephrotoxic agents, and optimizing cardiovascular functi

15 t often a result of sepsis, hypotension, and nephrotoxic agents.

16 e aggravated by the concomitant use of other nephrotoxic agents.

17 AAs are nephrotoxic and carcinogenic compounds found in Aristolo

18 Aristolochic acids (AA) are nephrotoxic and carcinogenic.

19 was upregulated in damaged tubular cells in nephrotoxic and ischemia reperfusion (IRI) induced AKI.

20 cal tubules and in the blood and urine after nephrotoxic and ischemic injury.

21 Chloroacetaldehyde (CA) is a nephrotoxic and neurotoxic metabolite of the anticancer

22 The anticancer drug cisplatin is nephrotoxic and neurotoxic.

23 ately 40% of lupus patient sera and are both nephrotoxic and neurotoxic.

24 conjugates of a variety of hydroquinones are nephrotoxic, and because 2-tert-butyl-5-(glutathion-S-yl

25 We previously demonstrated that a subset of nephrotoxic anti-dsDNA antibodies also recognizes the pe

26 eased susceptibility to glomerular injury by nephrotoxic antibodies or immune complexes.

27 the glomerular injury and proteinuria which nephrotoxic antibodies produce.

28 glomeruli rarely contained DCs, injury with nephrotoxic antibodies resulted in accumulation of ZBTB4

29 merular mesangial activity after fixation of nephrotoxic antibodies to the glomerular basement membra

30 RNA sequencing 7 days after nephrotoxic antibody injection showed that CD11b(+) DCs

31 Administration of nephrotoxic antibody resulted in significant glomerular

32 Cumulative doses of nephrotoxic antimicrobial drugs were recorded, as well a

33 Patients on potentially nephrotoxic antiretrovirals or at high risk of chronic k

34 the risks and benefits of adding potentially nephrotoxic antiretrovirals to a treatment regimen and w

35 ark of the maintenance phase of ischemic and nephrotoxic ARF, and can reflect its severity.

36 xposures are widespread, and both metals are nephrotoxic at high exposure levels.

37 nerability to superimposed ATP depletion and nephrotoxic attack.

38 Severity of disease and the global nephrotoxic burden were risk factors for acute kidney in

39 Sirolimus (SRL) is not nephrotoxic, but it has been shown to increase transform

40 hylation, which generates the neurotoxic and nephrotoxic byproduct chloroacetaldehyde.

41 To reduce long-term nephrotoxic calcineurin inhibitor dosage, adjunctive sir

42 il (MMF) and reduction or discontinuation of nephrotoxic calcineurin inhibitors (CNI).

43 ttempt to reduce both initial and long-term (nephrotoxic) calcineurin inhibitor maintenance dosage an

44 , and express kidney injury molecule-1 after nephrotoxic chemical injury.

45 Finally, internalization of this non-nephrotoxic component was unaltered, but the subcellular

46 The known nephrotoxic compound djenkolic acid was found to be pres

47 rd; and chloroacetaldehyde, a neurotoxic and nephrotoxic compound, arising from the oxidation of the

48 ow high throughput quantitative screening of nephrotoxic compounds using HO-1 as a sensitive biomarke

49 itional panel of 39 mechanistically distinct nephrotoxic compounds.

50 ial resolution and avoids use of potentially nephrotoxic contrast agent or radiation.

51 Benefits of this procedure include lack of nephrotoxic contrast, what is especially important in ch

52 stresses, such as type 1 interferons (IFN), nephrotoxic damage, and bacterial infection.

53 algia); and three delayed syndromes (delayed nephrotoxic, delayed neurotoxic, rhabdomyolysis).

54 tion, possibly through the addition of a non-nephrotoxic dose of CNI.

55 suggest that the administration of a single nephrotoxic dose of KBrO(3) inhibits brush border membra

56 Sepsis, major surgery, and nephrotoxic drugs are the most common causes of acute ki

57 ine eGFR, comorbidities, co-prescriptions of nephrotoxic drugs, and episodes of lithium toxicity; how

58 tributed to multiorgan failure or the use of nephrotoxic drugs, but AKI is rarely considered a direct

59 ecies (ROS), produced under renal failure or nephrotoxic drugs, may influence renal function as well

60 simulation of the human kidney's response to nephrotoxic drugs.

61 nosuppression and delaying the initiation of nephrotoxic drugs.

62 atients who received caspofungin sustained a nephrotoxic effect (2.6 percent vs. 11.5 percent, P<0.00

63 ICAM-1 antisense ME/PS-oligo alleviated the nephrotoxic effect and decreased ICAM-1 expression and l

64 Nephrotoxic effects (defined by a serum creatinine level

65 The risks of nephrotoxic effects and opportunistic infection were sim

66 Awareness of these potential nephrotoxic effects is crucial to prevention of serious

67 Because of the nephrotoxic effects of aminoglycosides, the Danish guide

68 ncreased lean body mass and potential direct nephrotoxic effects of anabolic steroids.

69 cluding traditional risk factors for CKD and nephrotoxic effects of antiretroviral therapy.

70 ypothermic organ preservation and reduce the nephrotoxic effects of calcineurin inhibitors.

71 TLR4, rather than myeloid TLR4, mediated the nephrotoxic effects of cisplatin.

72 xposure of renal allograft recipients to the nephrotoxic effects of CsA.

73 part mediates both the immunosuppressive and nephrotoxic effects of cyclosporine, recipients were tre

74 ther anti-TGF-beta antibody could reduce the nephrotoxic effects of cyclosporine.

75 n 6 and 12 months, presumably due to ongoing nephrotoxic effects of cyclosporine.

76 on patterns associated with acute rejection, nephrotoxic effects of drugs, chronic allograft nephropa

77 c or hepatic failure, prolonged surgery, and nephrotoxic effects of immunosuppression.

78 pite the past theoretical concerns about the nephrotoxic effects of several clinically utilized volat

79 changes can presumably be attributed to the nephrotoxic effects of this drug combined with the progr

80 sess potential drug-drug interactions and/or nephrotoxic effects of various therapeutics, and to scre

81 s not associated with detectable ototoxic or nephrotoxic effects or with accumulation of the drug in

82 and lipid abnormalities, it had no apparent nephrotoxic effects to exacerbate CsA-induced renal dysf

83 emonstrated markedly reduced cardiotoxic and nephrotoxic effects, as well as better tolerance, relati

84 ewer fluorinated anesthetics might also have nephrotoxic effects, three currently used agents (isoflu

85 s with cyclosporine (CsA) results in chronic nephrotoxic effects, which frequently lead to progressiv

86 dom coefficient models were used to estimate nephrotoxic effects.

87 cyclosporine concentrations and avoiding the nephrotoxic effects.

88 c allograft survival may be curtailed by its nephrotoxic effects.

89 ree late syndromes (hepatotoxic, accelerated nephrotoxic, erythromelalgia); and three delayed syndrom

90 Ochratoxin A (OTA) is a widely spread nephrotoxic food contaminant mycotoxin.

91 tis (NTN) that is induced by a small dose of nephrotoxic globulin, WKY rats developed crescents in 80

92 lock the metabolic activation of a series of nephrotoxic halogenated alkenes.

93 h improved HRQoL, suggesting that use of non-nephrotoxic immunosuppressants may affect the patient's

94 hat replacement of their lymphocytotoxic and nephrotoxic immunosuppression (combination of mycophenol

95 Nephrotoxic immunosuppression (IS) may exacerbate diabet

96 he rejection; thus, the incorporation of non-nephrotoxic immunosuppressive agents, such as sirolimus,

97 Eliminating the need for nephrotoxic immunosuppressive drugs during the early pos

98 The once daily regimen might be less nephrotoxic in children.

99 Both Tac and Sir may be nephrotoxic in the early posttransplant period, especial

100 Conversely, whether TDF is nephrotoxic in the long term is a highly debated questio

101 The data show that cisplatin was nephrotoxic in wild-type mice but not in GGT-deficient m

102 Ischemic and nephrotoxic injuries are induced more readily in sodium-

103 The mechanism by which proteinuria leads to nephrotoxic injury is unclear, but a role for complement

104 Acute nephrotoxic injury was induced in wa-2 and wild-type mic

105 mice from cisplatin- and doxorubicin-induced nephrotoxic injury.

106 plus Ca2+ overload) or a clinically relevant nephrotoxic insult (myoglobin exposure).

107 Strategies to minimize nephrotoxic insults and retard progressive renal injury

108 New publications on a wide variety of nephrotoxic insults are presented, including antifibrino

109 tential therapeutic benefit for ischemic and nephrotoxic kidney injury.

110 in digestion in the presence or absence of a nephrotoxic LC known to bind THP.

111 of binding or aggregation of five different nephrotoxic LCs with THP.

112 x-dependent, complement- and FcR-independent nephrotoxic mechanism, and suggest that isotypes that po

113 tion, using preventive measures and avoiding nephrotoxic medications are paramount in reducing the ov

114 51 orders were written on renally cleared or nephrotoxic medications, of which 14 440 (15%) had at le

115 infection and its subsequent treatment with nephrotoxic medications.

116 tris-(glutathion-S-yl)hydroquinone, a potent nephrotoxic metabolite of hydroquinone, and 2-bromo-bis-

117 o study the transepithelial transport of the nephrotoxic mycotoxin ochratoxin A.

118 Citrinin is a nephrotoxic mycotoxin which can be synthesized by Monasc

119 A) to prolong allograft survival, it was not nephrotoxic, myelotoxic, or lipotoxic and did not increa

120 e complex disease induced in the accelerated nephrotoxic nephritis (ANTN) model.

121 During the development of nephrotoxic nephritis (NTN) in the mouse, we find that a

122 Nephrotoxic nephritis (NTN) is characterized by acute ma

123 also unknown, we studied these cells in the nephrotoxic nephritis (NTN) model of acute crescentic GN

124 e effects have been observed for IL-6 in the nephrotoxic nephritis (NTN) model of acute crescentic GN

125 e studied the function of these cells in the nephrotoxic nephritis (NTN) model of cGN.

126 We studied the function of Treg17 in the nephrotoxic nephritis (NTN) model of crescentic GN.

127 In the model of nephrotoxic nephritis (NTN) that is induced by a small d

128 ents and reverses proteinuria in accelerated nephrotoxic nephritis (NTN).

129 acerbated disease following the induction of nephrotoxic nephritis (NTN).

130 ges isolated from the glomeruli of rats with nephrotoxic nephritis also induced apoptosis and suppres

131 ophages infiltrating glomeruli in telescoped nephrotoxic nephritis are programmed.

132 s, were significantly increased in mice with nephrotoxic nephritis as compared to control-injected mi

133 te the development of disease in accelerated nephrotoxic nephritis by influencing the development of

134 L in antibody-mediated nephritis, we induced nephrotoxic nephritis by passive antibody transfer to 12

135 trast, glomerular macrophages from rats with nephrotoxic nephritis did not express beta-glucuronidase

136 entic glomerulonephritis by inducing passive nephrotoxic nephritis in SPARC(+/+) and SPARC(-/-) mice.

137 Induction of nephrotoxic nephritis in the double-congenic rats (WKY.L

138 d (late treatment study) after induction of nephrotoxic nephritis in Wistar Kyoto rats.

139 In nephrotoxic nephritis in WKY rats, recombinant rat IFN-b

140 tive immune responses, we use the autologous nephrotoxic nephritis model with two disease induction p

141 Inhibition of miR-193a in a mouse model of nephrotoxic nephritis resulted in reduced crescent forma

142 Injury in nephrotoxic nephritis was also decreased when assessed m

143 Nephrotoxic nephritis was induced in Wistar-Kyoto rats a

144 using a mouse model of acute crescentic GN (nephrotoxic nephritis), we identified CD4(+) T cells and

145 ntic GN and a murine model of crescentic GN (nephrotoxic nephritis).

146 ceptibility of the Wistar-Kyoto (WKY) rat to nephrotoxic nephritis, a rat model of Crgn.

147 t to ICAM-1, is not up-regulated by day 2 of nephrotoxic nephritis, and plays little part in early le

148 In a rat model of nephrotoxic nephritis, glomerular expression of VCAM-1,

149 y 10, during the early inflammatory phase of nephrotoxic nephritis, had no effect on albuminuria or g

150 By using the murine model of nephrotoxic nephritis, we investigated the role of S100A

151 decreased in the first week of experimental nephrotoxic nephritis, whereas reduction in glomerular n

152 In nephrotoxic nephritis, wild-type (WT) mice with glomerul

153 d lipid A on the development of heterologous nephrotoxic nephritis.

154 unization on disease severity in accelerated nephrotoxic nephritis.

155 ctivated naturally in glomeruli of rats with nephrotoxic nephritis.

156 ation within the kidney by accelerated serum nephrotoxic nephritis.

157 nd NGAL-knockout mice following induction of nephrotoxic nephritis.

158 pecific basal expression) were injected with nephrotoxic (NTS) or control serum.

159 triglycerides, sirolimus did not augment the nephrotoxic or hypertensive proclivities of cyclosporine

160 rease in tubular cell damage in kidneys with nephrotoxic or IRI induced AKI.

161 tic dose of each drug may be synergistically nephrotoxic, perhaps due to hyperglycemia.

162 Numerous studies confirm the nephrotoxic potential of high-dose mannitol, especially

163 model to understand the hematopathologic and nephrotoxic potential of the inert ingredient mixture (t

164 d from human kidneys to better predict their nephrotoxic potential.

165 re mitochondrial biogenesis and toxicity and nephrotoxic potential.

166 chanism for the immunosuppressive as well as nephrotoxic properties of tacrolimus, as the multifuncti

167 d with a reduced systemic immune response to nephrotoxic rabbit IgG.

168 have a history of congestive heart failure, nephrotoxic (rather than ischemic or multifactorial) ori

169 f risk factors for contrast material-induced nephrotoxic reactions.

170 In such cases, conversion to a less nephrotoxic regimen may be beneficial.

171 ninvasive urinary biomarker for ischemic and nephrotoxic renal injury.

172 IV LOCM does not appear to be a nephrotoxic risk factor in patients with a pre-CT eGFR o

173 IV LOCM is a nephrotoxic risk factor in patients with a stable eGFR l

174 -osmolality iodinated contrast material is a nephrotoxic risk factor, but not in patients with a stab

175 ith rabbit anti-glomerular basement membrane nephrotoxic sera (NTS), to induce renal disease.

176 e mechanism potentiated the pathogenicity of nephrotoxic sera.

177 inducible model of LN in which mice receive nephrotoxic serum (NTS) containing anti-glomerular antib

178 dies were designed to explore the effects of nephrotoxic serum (NTS) in rats on the uptake and proces

179 We induced nephrotoxic serum (NTS) nephritis in Daf1(-/-), CD59a(-/

180 In nephrotoxic serum (NTS) nephritis, injected antibodies (

181 Nephrotoxic serum (NTS) or passive Heymann nephritis (PH

182 ase-8, Pod-ATTAC mice) and mice treated with nephrotoxic serum (NTS), which triggers immune-mediated

183 te injury in vivo using protamine sulfate or nephrotoxic serum (NTS).

184 The administration of nephrotoxic serum and lipid A caused a neutrophil influx

185 oxygenase (HO-1) mRNA was induced 6 h after nephrotoxic serum and renal tubules were identified as t

186 Nephrotoxic serum did not protect against ischemic acute

187 , CSA, tacrolimus, ischemia-reperfusion, and nephrotoxic serum each induced dramatic CE +/- FC elevat

188 lupus nephritis, we compared the severity of nephrotoxic serum glomerulonephritis in wild-type (WT),

189 from T cell-dependent nephritis, we induced nephrotoxic serum nephritis (NSN) in IL-15-/- and wild-t

190 tubular and/or glomerular injury, we induced nephrotoxic serum nephritis (NSN) in MCP-1 genetically d

191 For this purpose, we compared nephrotoxic serum nephritis (NSN) in mice lacking PD-L1

192 We used nephrotoxic serum nephritis as a model of immune-mediate

193 CL10-/- C57BL/6 mice were not protected from nephrotoxic serum nephritis compared with WT mice.

194 y kidney injury and renal disease in a mouse nephrotoxic serum nephritis model was inhibited by amino

195 ediated nephritis (MRL-Fas(lpr) mice and the nephrotoxic serum nephritis model), but evidence suggest

196 urse microarray analysis of glomeruli during nephrotoxic serum nephritis revealed significant upregul

197 Nephrotoxic serum nephritis was induced in wild-type (WT

198 With nephrotoxic serum nephritis, CXCR3-/- and CXCL9-/- mice

199 ent and reduced levels of proteinuria during nephrotoxic serum nephritis, whereas TRPC6 null mice exh

200 imus therapy, or 48 hours after induction of nephrotoxic serum nephritis.

201 0-/- B6 mice were compared with WT mice with nephrotoxic serum nephritis.

202 Thus, nephrotoxic serum protects against glycerol-induced acut

203 ALB/c APA-knockout (KO) mice injected with a nephrotoxic serum showed persistent glomerular hyalinosi

204 In mice treated with nephrotoxic serum to induce crescentic nephritis (rapidl

205 Nephrotoxic serum, administered to rats 24 h before the

206 ably, 2 weeks after the induction of GN with nephrotoxic serum, mice with a heterozygous deletion of

207 anti-glomerular basement membrane antiserum (nephrotoxic serum, NTS) into presensitized mice triggers

208 r glomerular injury induced by either LPS or nephrotoxic serum, the podocyte GR knockout mice demonst

209 Strategies to rapidly remove nephrotoxic serum-free light chains combined with novel

210 ed DC and Th cell activation and ameliorated nephrotoxic serum-induced GN in mice.

211 In contrast, Axl-deficient nephrotoxic serum-injected mice showed decreased Akt pho

212 However, nephrotoxic serum-treated Axl-KO mice had significantly

213 ygenase prevented the protection afforded by nephrotoxic serum.

214 ygenase underlies the protection afforded by nephrotoxic serum.

215 In contrast, induction of nephrotoxic stress (acute and chronic folic acid-induced

216 a-cell toxicity, allowing for single low non-nephrotoxic STZ doses (70 mg/kg).

217 that nucleic acid-specific B cells activate nephrotoxic T cells.

218 Vemurafenib seems to be more nephrotoxic than dabrafenib.

219 eover, indolyl-ASC was at least twofold less nephrotoxic than tacrolimus upon 3-week oral treatment i

220 e ODD tobramycin regimen appeared to be less nephrotoxic than the MDD regimen despite significantly h

221 once daily treatment was significantly less nephrotoxic than was thrice daily (mean% change in creat

222 may facilitate rapid assessment of potential nephrotoxic therapeutics and environmental chemicals.

223 ric patients with FR-SSNS, but may be a less nephrotoxic treatment option.

224 ication in vitro; however, this analogue was nephrotoxic when tested in vivo.

225 Aminoglycoside antibiotics (AGAs) are nephrotoxic, with most of the damage confined to the pro