ライフサイエンスコーパス: nephrotoxic

1 limination of compounds that are potentially nephrotoxic.

2 osporine and tacrolimus are both known to be nephrotoxic.

3 , a commonly used chemotherapeutic agent, is nephrotoxic.

4 tility effects in males, while (R)-3-MCPD is nephrotoxic.

5 eatment, as many chemotherapeutic agents are nephrotoxic.

6 antigen receptor T cell therapy, can also be nephrotoxic.

7 Calcineurin inhibitors are known to be nephrotoxic.

8 However, it is severely nephrotoxic.

9 Nephrotoxic Ab and TLR2 ligation caused a neutrophil inf

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

11 rular basement membrane after conjugation to nephrotoxic Ab.

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

13 lls mediate the pathogenesis of ischemic and nephrotoxic acute kidney injury (AKI).

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

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

16 CKD was induced in C57BL/6J mice using a nephrotoxic adenine diet.

17 olling for patient age, comorbidities, other nephrotoxic agent use, and patient and procedure charact

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

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

20 igens, tumor antigens, ischemic reperfusion, nephrotoxic agents, and aging.

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

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

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

24 t mice had protection from both ischemic and nephrotoxic AKI.

25 In particular, cisplatin is nephrotoxic and can cause acute kidney injury and chroni

26 developed cancer chemotherapeutic agents are nephrotoxic and can promote kidney dysfunction, which fr

27 AAs are nephrotoxic and carcinogenic compounds found in Aristolo

28 Aristolochic acids (AAs) are nephrotoxic and carcinogenic nitrophenanthrene carboxyli

29 Aristolochic acids (AA) are nephrotoxic and carcinogenic.

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

31 r pharmacological Cdkl5 inhibition mitigates nephrotoxic and ischemia-associated AKI.

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

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

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

35 The anticancer drug cisplatin is nephrotoxic and neurotoxic.

36 hey are often cationic and can be cytotoxic, nephrotoxic and/or ototoxic, which has limited their cli

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

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

39 R: 1.95; 95% CI: 1.004, 3.78; P = .049), and nephrotoxic antibiotic exposure (OR: 2.86; 95% CI: 1.55,

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

41 the glomerular injury and proteinuria which nephrotoxic antibodies produce.

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

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

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

45 Administration of nephrotoxic antibody resulted in significant glomerular

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

47 usative organism, bacteremia, and the use of nephrotoxic antimicrobials, vasopressin, or specific ino

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

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

50 ilar to clinical D:A:D score and potentially nephrotoxic antiretrovirals.

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

52 ells (PTCs) of mice subjected to ischemic or nephrotoxic (aristolochic acid) injury resulted in a red

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

54 Ingested U accumulates in kidneys and is nephrotoxic at high levels.

55 nerability to superimposed ATP depletion and nephrotoxic attack.

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

57 Both drugs are nephrotoxic, but CsA has been associated with greater re

58 and vancomycin (VAN) has been identified as nephrotoxic, but existing studies focus on extended dura

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

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

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

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

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

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

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

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

67 drug, ganciclovir, and aristolochic acid, a nephrotoxic compound found in some herbal medicines, wer

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

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

70 itional panel of 39 mechanistically distinct nephrotoxic compounds.

71 Scanning electron microscopy showed that sub-nephrotoxic concentrations of colistin had no effect on

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

73 ile avoiding repeated exposure to radiation, nephrotoxic contrast material, or gadolinium-based contr

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

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

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

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

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

79 tive biological effectiveness [RBE], 5) as a nephrotoxic dose, as no such histologic findings were ob

80 nging, including appropriate volume control, nephrotoxic drug management, and the timing and type of

81 correction of hypovolaemia and avoidance of nephrotoxic drugs (for example, hydroxocobalamin), where

82 olume status and haemodynamics, avoidance of nephrotoxic drugs and radiocontrast agents, and preventi

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

84 In addition, use of nephrotoxic drugs to treat parasitic infections is assoc

85 ion, infectious disease, immune disease, and nephrotoxic drugs use at baseline.

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

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

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

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

90 nosuppression and delaying the initiation of nephrotoxic drugs.

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

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

93 ximal tubular (PT) cell damage has a greater nephrotoxic effect when combined with cyanuric and uric

94 Nephrotoxic effects (defined by a serum creatinine level

95 The risks of nephrotoxic effects and opportunistic infection were sim

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

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

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

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

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

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

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

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

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

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

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

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

108 scordant findings have been published on the nephrotoxic effects of lithium therapy.

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

110 However, the nephrotoxic effects of these therapies continue to pose

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

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

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

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

115 nd assessments for safety (ototoxic effects, nephrotoxic effects, and autoimmune response).

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

117 ompleted the study, and no ototoxic effects, nephrotoxic effects, or anti-laminin 332 antibodies were

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

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

120 dom coefficient models were used to estimate nephrotoxic effects.

121 cyclosporine concentrations and avoiding the nephrotoxic effects.

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

123 polymyxin analogues, aimed at reducing their nephrotoxic effects.

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

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

126 motherapy to rapidly reduce the secretion of nephrotoxic free light chains.

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

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

129 cotoxins have shown harmful effects, such as nephrotoxic, hepatotoxic, and genotoxic effects, in huma

130 Radiocontrast has long been thought of as nephrotoxic; however, a number of recent observational s

131 lves oligoclonal or polyclonal production of nephrotoxic IgG3 and may not derive from a clonal B-cell

132 tion of the Hippo pathway in podocytes after nephrotoxic immune injury.

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

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

135 Nephrotoxic immunosuppression (IS) may exacerbate diabet

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

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

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

139 ociated lipocalin, suggesting that A+Z maybe nephrotoxic in patients with severe alcohol-associated h

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

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

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

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

144 ificantly reduced kidney injury after IR and nephrotoxic injury compared with WT mice.

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

146 s do not progress to fibrosis, we employed a nephrotoxic injury model using aristolochic acid I to as

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

148 ds thus acquire function, and on exposure to nephrotoxic injury, display tubular collapse and DNA dam

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

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

151 KI), commonly caused by ischemia, sepsis, or nephrotoxic insult, is associated with increased mortali

152 Strategies to minimize nephrotoxic insults and retard progressive renal injury

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

154 h baseline risk, monitoring and reduction of nephrotoxic insults, whereas treatment involves the appl

155 tential therapeutic benefit for ischemic and nephrotoxic kidney injury.

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

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

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

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

160 51 orders were written on renally cleared or nephrotoxic medications, of which 14 440 (15%) had at le

161 infection and its subsequent treatment with nephrotoxic medications.

162 rs include maternal comorbidities and use of nephrotoxic medications.

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

164 generation by argatroban in a serum-transfer nephrotoxic model identified thrombin as a surrogate pat

165 lonal proliferative disorder that produces a nephrotoxic monoclonal immunoglobulin and does not meet

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

167 Citrinin is a hepato-nephrotoxic mycotoxin produced by fungal species.

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

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

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

171 ntravascular monocyte subset behavior during nephrotoxic nephritis (NTN) in a novel WKY-hCD68-GFP mon

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

173 Nephrotoxic nephritis (NTN) is characterized by acute ma

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

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

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

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

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

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

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

181 ted, then three disease models were induced: nephrotoxic nephritis (NTN, a model for crescentic GN),

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

183 ophages infiltrating glomeruli in telescoped nephrotoxic nephritis are programmed.

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

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

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

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

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

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

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

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

192 The nephrotoxic nephritis model of GN was studied in AREG(-/

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

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

195 Injury in nephrotoxic nephritis was also decreased when assessed m

196 Nephrotoxic nephritis was induced in Wistar-Kyoto rats a

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

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

199 T cell-intrinsic IL-6R signaling, we induced nephrotoxic nephritis, a mouse model for crescentic GN,

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

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

202 Similarly, in a mouse model of nephrotoxic nephritis, besides reducing inflammatory cyt

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

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

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

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

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

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

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

210 unization on disease severity in accelerated nephrotoxic nephritis.

211 ctivated naturally in glomeruli of rats with nephrotoxic nephritis.

212 fic T cell reactivity in the murine model of nephrotoxic nephritis.

213 duced kidney injury during accelerated serum nephrotoxic nephritis.

214 ation within the kidney by accelerated serum nephrotoxic nephritis.

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

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

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

218 No nephrotoxic or ototoxic effects were detected after intr

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

220 pective trials are warranted to estimate the nephrotoxic potential of (177)Lu-PSMA.

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

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

223 re mitochondrial biogenesis and toxicity and nephrotoxic potential.

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

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

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

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

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

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

230 Here, using doxorubicin-induced nephrotoxic renal injury model, we investigated whether

231 ninvasive urinary biomarker for ischemic and nephrotoxic renal injury.

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

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

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

235 Associations between eGFR changes (%) and nephrotoxic risk factors, prior treatment lines, and num

236 compromised kidney function due to perceived nephrotoxic risks, called contrast-induced nephropathy o

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

238 e mechanism potentiated the pathogenicity of nephrotoxic sera.

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

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

241 ize podocyte biology during MMF treatment in nephrotoxic serum (NTS) nephritis (NTN).

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

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

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

245 pathy in mice injured by adriamycin (ADR) or nephrotoxic serum (NTS), as demonstrated by increased al

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

247 In a nephrotoxic serum (NTS)-induced glomerulonephritis model

248 mates injured by either protamine sulfate or nephrotoxic serum (NTS).

249 were challenged with two different doses of nephrotoxic serum (NTS).

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

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

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

253 Nephrotoxic serum did not protect against ischemic acute

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

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

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

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

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

259 nondiabetic, T-cell-mediated murine model of nephrotoxic serum nephritis (NTS).

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

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

262 vivo studies were performed by induction of nephrotoxic serum nephritis in wild type, CD30OX40(- /-)

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

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

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

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

267 tibodies against CD30L and OX40L ameliorated nephrotoxic serum nephritis without affecting pan-effect

268 n three independent proteinuric models (LPS, nephrotoxic serum nephritis, and HIV-1 transgenic mice).

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

270 mice and from four different disease models (nephrotoxic serum nephritis, diabetes, doxorubicin toxic

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

272 0-/- B6 mice were compared with WT mice with nephrotoxic serum nephritis.

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

274 ds were upregulated on various leukocytes in nephrotoxic serum nephritis.

275 0(-/-) or OX40(-/-) mice were protected from nephrotoxic serum nephritis.

276 Thus, nephrotoxic serum protects against glycerol-induced acut

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

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

279 Nephrotoxic serum, administered to rats 24 h before the

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

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

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

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

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

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

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

287 ygenase prevented the protection afforded by nephrotoxic serum.

288 ygenase underlies the protection afforded by nephrotoxic serum.

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

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

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

292 nic toxic effect and proved to be mutagenic, nephrotoxic, teratogenic, immunosuppressive, and carcino

293 Vemurafenib seems to be more nephrotoxic than dabrafenib.

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

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

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

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

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

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

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