ライフサイエンスコーパス: nephrotoxicity

1 (ER) stress contribute to cisplatin-induced nephrotoxicity.

2 fect of combination therapy on mortality and nephrotoxicity.

3 tient variability in the risk of CsA-induced nephrotoxicity.

4 No SNPs were associated with tacrolimus nephrotoxicity.

5 and independently predictive of cyclosporine nephrotoxicity.

6 c factors may also predispose individuals to nephrotoxicity.

7 GAN genes were associated with cyclosporine nephrotoxicity.

8 uded loss of body weight, hepatotoxicity and nephrotoxicity.

9 nts with biopsy-confirmed chronic CsA or TAC nephrotoxicity.

10 al prophylaxis in patients at lower risk for nephrotoxicity.

11 ty of LT recipients converted to SRL for CNI nephrotoxicity.

12 iated with early, acute cyclosporine-related nephrotoxicity.

13 e tumor models while protecting kidneys from nephrotoxicity.

14 wever, its use is dose-limited due to severe nephrotoxicity.

15 with calcineurin inhibitor (CNI)-associated nephrotoxicity.

16 IL-10 ameliorates kidney injury in cisplatin nephrotoxicity.

17 ctive effect of dendritic cells in cisplatin nephrotoxicity.

18 novel targets to reduce calcineurin induced nephrotoxicity.

19 a target of interest to prevent TCE induced nephrotoxicity.

20 ment of iron overload disease because of its nephrotoxicity.

21 ent mechanisms of tissue injury in cisplatin nephrotoxicity.

22 l ischemia/reperfusion and cisplatin-induced nephrotoxicity.

23 l ischemia/reperfusion and cisplatin-induced nephrotoxicity.

24 stage renal failure secondary to calcineurin nephrotoxicity.

25 y their functional significance in cisplatin nephrotoxicity.

26 n, whereas supratherapeutic levels may cause nephrotoxicity.

27 fective dose (BED) with radionuclide-induced nephrotoxicity.

28 atient survival by minimizing CNI-associated nephrotoxicity.

29 r emphasis on calcineurin inhibitor-mediated nephrotoxicity.

30 nt led to downregulation of TonEBP and overt nephrotoxicity.

31 Calcineurin inhibition results in nephrotoxicity.

32 ha or beta isoform to a model of cyclosporin nephrotoxicity.

33 on and renal cell apoptosis during cisplatin nephrotoxicity.

34 en may also improve compliance and limit CNI nephrotoxicity.

35 e direct mediators of experimental cisplatin nephrotoxicity.

36 lated in renal cortex and is responsible for nephrotoxicity.

37 aused by calcineurin inhibitors (CI)-induced nephrotoxicity.

38 horylation and beta-oxidation, would prevent nephrotoxicity.

39 diated renal cell apoptosis during cisplatin nephrotoxicity.

40 cidal properties with minimal or no apparent nephrotoxicity.

41 higher risk of developing CI-induced chronic nephrotoxicity.

42 iperacillin-tazobactam increases the risk of nephrotoxicity.

43 l death can be interceded in vivo to prevent nephrotoxicity.

44 at induced COX-2 expression would lessen ADR nephrotoxicity.

45 tion episodes, renal biopsy, or drug-induced nephrotoxicity.

46 o CsA-treated rats significantly ameliorated nephrotoxicity.

47 r lipotoxic and did not increase CsA-induced nephrotoxicity.

48 ischemic-reperfusion injury, and CsA-induced nephrotoxicity.

49 le of this endonuclease in cisplatin-induced nephrotoxicity.

50 Mycophenolate mofetil (MMF) has no known nephrotoxicity.

51 ur secondary to IVIG treatment or tacrolimus nephrotoxicity.

52 ia-reperfusion (I/R) injury and drug-induced nephrotoxicity.

53 s indicative of tacrolimus (or cyclosporine) nephrotoxicity.

54 ng an additive effect of I/R injury and drug nephrotoxicity.

55 rily in calcineurin inhibitors (CNI)-related nephrotoxicity.

56 st-line" antibiotic scarcely used due to its nephrotoxicity.

57 okine release syndrome and cisplatin-induced nephrotoxicity.

58 8 showed signs of tubular damage, indicating nephrotoxicity.

59 new targets for the inhibition of cisplatin nephrotoxicity.

60 f cytokines in the pathogenesis of cisplatin nephrotoxicity.

61 agent, has a major limitation because of its nephrotoxicity.

62 a-deficient mice were resistant to cisplatin nephrotoxicity.

63 High dosing was associated with more nephrotoxicity.

64 liver transplant recipients with chronic CsA nephrotoxicity.

65 se of CNIs is associated with some degree of nephrotoxicity.

66 erfusion, and the molecular phenotype of CsA nephrotoxicity.

67 sis in NSCLC H460 tumor-bearing mice without nephrotoxicity.

68 ificantly better renal function, that is, no nephrotoxicity.

69 r protecting patients from cisplatin-induced nephrotoxicity.

70 ected on virologic responses, mortality, and nephrotoxicity.

71 monitoring of chronic calcineurin inhibitor nephrotoxicity.

72 skiren may be used for the prevention of CNI nephrotoxicity.

73 mune response, whereas reducing drug-related nephrotoxicity.

74 n for the understanding of polymyxin-induced nephrotoxicity.

75 f DMF has a protective potential against CsA nephrotoxicity.

76 ference, vascular disrupting properties, and nephrotoxicity.

77 Eleven patients (20.0%) developed nephrotoxicity.

78 n injury of the kidney and cisplatin-induced nephrotoxicity.

79 dentified as high-risk patient subgroups for nephrotoxicity.

80 comorbidities reported to predispose them to nephrotoxicity.

81 ith no indication of hematologic toxicity or nephrotoxicity.

82 001) were significant positive predictors of nephrotoxicity.

83 ependently associated with increased odds of nephrotoxicity.

84 2%; 0), fatigue (8%; 0), infection (8%; 2%), nephrotoxicity (2%; 0), and diverticulitis (6%; 2%).

85 s showed predominant features of chronic CNI nephrotoxicity, 27 (43.5%) predominant features of hyper

86 us (45%) and a history of tacrolimus-induced nephrotoxicity (35%) appeared to be prevalent in subject

87 The administration of KBrO(3) resulted in nephrotoxicity, a decline in the specific activities of

88 In ADR nephrotoxicity, a pathologic change in glomeruli could b

89 wever, 7 patients developed adefovir-related nephrotoxicity after >/=20 weeks of treatment; this reso

90 bilities for new methods to prevent or treat nephrotoxicity after contrast medium administration.

91 ent amifostine protected rats from long-term nephrotoxicity after PRRT with (177)Lu-DOTA,Tyr(3)-octre

92 in the urine of mice with cisplatin-induced nephrotoxicity, again preceding the appearance of N-acet

93 Concerns for nephrotoxicity also extend to HIV-negative individuals u

94 dromes were classified including accelerated nephrotoxicity (Amanita proxima, Amanita smithiana), rha

95 rate that endogenous IL-10 reduces cisplatin nephrotoxicity and associated inflammation.

96 usly shown to be a predictor of drug-induced nephrotoxicity and compared its response to Stx2 exposur

97 role in both the development of CNI-induced nephrotoxicity and endothelial vasculopathy in chronic a

98 superior to the CSA era, with less early CNI nephrotoxicity and fewer rejection episodes, but compara

99 significant adverse side effects, including nephrotoxicity and hematological toxicity.

100 h is usually associated with hepatotoxicity, nephrotoxicity and hemolysis.

101 nital malformations but can cause reversible nephrotoxicity and hyperkalemia in the newborn.

102 ociated with immunosuppression, specifically nephrotoxicity and infection risk, significantly affect

103 monstrate that resident DCs reduce cisplatin nephrotoxicity and its associated inflammation.

104 In this article we assess the evidence for nephrotoxicity and its possible mechanisms, provide reco

105 ey development, modeling of kidney diseases, nephrotoxicity and kidney regeneration.

106 neurin inhibitors is associated with chronic nephrotoxicity and lower glomerular filtration rate (GFR

107 arios, especially in light of posttransplant nephrotoxicity and other adverse events associated with

108 ease cisplatin and aspirin to ameliorate the nephrotoxicity and ototoxicity caused by cisplatin.

109 des are clinically useful, they exhibit high nephrotoxicity and ototoxicity, and their overuse has le

110 Large doses of gentamicin cause nephrotoxicity and ototoxicity, entering the cell via th

111 their utility is compromised by significant nephrotoxicity and polymyxin-resistant bacterial strains

112 Lack of nephrotoxicity and possibly an inhibitory effect on the

113 ific effects of RAS stimulation on cisplatin nephrotoxicity and raise the concern that inflammatory m

114 Adriamycin nephrotoxicity and subtotal nephrectomy (SNx) studies in

115 demonstrate a role of PKCdelta in cisplatin nephrotoxicity and support targeting PKCdelta as an effe

116 These effects may explain FQ-induced nephrotoxicity and tendinopathy.

117 opment of novel strategies to ameliorate its nephrotoxicity and to develop safer, new polymyxins.

118 mplication for the prevention of IFO-induced nephrotoxicity and/or mitochondrial diseases secondary t

119 am"] and ["AKI" or "acute renal failure" or "nephrotoxicity"] and registered meta-analysis (PROSPERO:

120 am"] and ["AKI" or "acute renal failure" or "nephrotoxicity"] and registered meta-analysis with relev

121 , glycerol-induced rhabdomyolysis, cisplatin nephrotoxicity, and bilateral ureteral obstruction.

122 IV infection, antiretroviral therapy-related nephrotoxicity, and developments in kidney transplantati

123 F-alpha is a fundamental driver of cisplatin nephrotoxicity, and generation of TNF-alpha is suppresse

124 d transplant ischemia, calcineurin inhibitor nephrotoxicity, and inflammatory response within the all

125 , a metabolite of IFO, is the chief cause of nephrotoxicity, and that agmatine (AGM), which we found

126 r antibacterial effect overlap those causing nephrotoxicity, and there is large inter-patient variabi

127 r antibacterial effect overlap those causing nephrotoxicity, and there is large inter-patient variabi

128 f fibrosis in a chronic cyclosporine A (CsA) nephrotoxicity animal model.

129 of kidney injury associated with ischemia or nephrotoxicity, are the site of oligonucleotide reabsorp

130 gh throughput in vitro method for predictive nephrotoxicity assessment.

131 inhibitors (CNIs) in transplant recipients, nephrotoxicity associated with long-term CNI use remains

132 tion to overcome calcineurin inhibitor (CNI) nephrotoxicity but the evidence base for this approach i

133 or an inflammatory pathogenesis of cisplatin nephrotoxicity, but immune cell-mediated mechanisms in t

134 re significantly protected against cisplatin nephrotoxicity, but it is unknown whether the DNA fragme

135 is known to potentiate cyclosporine-induced nephrotoxicity, but such effect has not been shown with

136 luated the impact of reduced nephron mass on nephrotoxicity by cyclosporine A (CsA) and/or sirolimus

137 ts of dimethyl fumarate (DMF) on CsA-induced nephrotoxicity by enhancing the antioxidant defense syst

138 sEH inhibition attenuates cisplatin-induced nephrotoxicity by modulating nuclear factor-kappaB signa

139 luating the Val effect in alleviation of CsA nephrotoxicity by probable increase in renal Klotho expr

140 ion of Val might lead to amelioration of CsA nephrotoxicity by probably diminishing CsA-induced renal

141 that EET analogs attenuate cisplatin-induced nephrotoxicity by reducing oxidative stress, inflammatio

142 gs (10 mg/kg/d) attenuated cisplatin-induced nephrotoxicity by reducing these renal injury markers by

143 Enhancement of calcineurin inhibitor nephrotoxicity by sirolimus (SRL) is limiting the clinic

144 Nephrotoxicity/calcineurin-inhibitor-related adverse eve

145 negative 'superbugs'; however, dose-limiting nephrotoxicity can occur in up to 60% of patients after

146 Progressive nephrotoxicity caused by calcineurin inhibitor drugs con

147 o the role of miRNAs in cyclosporine-induced nephrotoxicity (CIN) and the gene pathways they regulate

148 l SCr criteria for contrast material-induced nephrotoxicity (CIN; SCr increase >/=0.5 mg/dL [44.20 mu

149 Outcomes included 30-day mortality and nephrotoxicity classified according to the pediatric RIF

150 at this regimen could reduce ototoxicity and nephrotoxicity compared with cisplatin-containing schedu

151 is associated with a decreased likelihood of nephrotoxicity compared with intermittent infusion.

152 therapy had approximately twice the odds of nephrotoxicity compared with those receiving monotherapy

153 oreover, we demonstrated that the attenuated nephrotoxicity correlated with decreased apoptosis that

154 d a significantly higher incidence of severe nephrotoxicity, diarrhea, and thrombocytopenia.

155 Nephrotoxicity due to drugs and environmental chemicals

156 adiolabeled somatostatin analogs may lead to nephrotoxicity during peptide receptor radionuclide ther

157 2011 that contained search terms related to nephrotoxicity following intravenous contrast medium adm

158 ntation include chronic allograft rejection, nephrotoxicity from calcineurin inhibitors (CNIs), and s

159 en implicated in the pathogenesis of chronic nephrotoxicity from CI.

160 The standard method of analyzing nephrotoxicity from existing OOC has majorly consisted o

161 study evaluated histological evidence of CNI nephrotoxicity from normal donor kidneys of successful k

162 Nephrotoxicity from the chemotherapeutic drug cisplatin

163 sed that chronic calcineurin inhibitor (CNI) nephrotoxicity has a central role in chronic kidney dise

164 atment of HIV-1 infection, numerous cases of nephrotoxicity have been reported.

165 ns of aminoglycoside-induced ototoxicity and nephrotoxicity have led to studies of alternate regimens

166 in renal proximal tubules resulting in late nephrotoxicity, highlighting the importance of long-term

167 and elevated CNI levels are associated with nephrotoxicity; however, they do not fully explain the r

168 06 have debilitating side effects, including nephrotoxicity, hypertension, diabetes, and seizures, th

169 During cisplatin nephrotoxicity, hypoxic regions are identified in the ou

170 studied the regulation of TauT in cisplatin nephrotoxicity in a human embryonic kidney cell line and

171 histopathology remains the gold standard for nephrotoxicity in animal systems, serum creatinine (SCr)

172 tibody to ameliorate cyclosporine-associated nephrotoxicity in cardiac transplant recipients.

173 of TGF-beta could ameliorate CsA-associated nephrotoxicity in cardiac transplant recipients.

174 demonstrated that the worsening of cisplatin nephrotoxicity in DC-depleted mice was not a result of t

175 it will be used to help assess the origin of nephrotoxicity in desferrithiocin analogues: is toxicity

176 ajor side effects in normal tissues, notably nephrotoxicity in kidneys.

177 Calcineurin inhibitor nephrotoxicity in nonrenal allograft recipients can lead

178 losporine A (CsA), have been associated with nephrotoxicity in organ transplant patients.

179 e, specific and accurate prediction of human nephrotoxicity in preclinical drug screens.

180 acid containing MMP-13 inhibitors; however, nephrotoxicity in preclinical toxicology species preclud

181 eir prophylactic effect in cisplatin-induced nephrotoxicity in rats.

182 enabled dual-mode monitoring of drug-induced nephrotoxicity in situ.

183 nhibition strategies may improve chronic CNI nephrotoxicity in solid organ transplantation.

184 Combination sirolimus-tacrolimus may cause nephrotoxicity in some patients by mechanisms that are p

185 ay treatment with cyclosporine (CsA)-induced nephrotoxicity in syngeneic kidney transplants correlate

186 long-term lithium therapy is associated with nephrotoxicity in the absence of episodes of acute intox

187 Both Tac and Sir demonstrated evidence of nephrotoxicity in the early posttransplant period includ

188 een SNPs and time to early CNI-related acute nephrotoxicity in the first 6 months posttransplant.

189 isoform reproduces features of cyclosporine nephrotoxicity in vivo and in vitro.

190 protects renal cells from cisplatin-induced nephrotoxicity in vivo.

191 However, its therapeutic use is limited by nephrotoxicity, in part mediated by oxidative stress.

192 istological features common with cyclosporin nephrotoxicity including matrix expansion, arteriole hya

193 Calcineurin inhibitor (CNI)-related acute nephrotoxicity is a common complication of transplantati

194 Calcineurin-inhibitor (CNI) nephrotoxicity is a major cause of morbidity and mortali

195 Nephrotoxicity is a major complication with immunosuppre

196 Nephrotoxicity is a major side effect of cisplatin, a wi

197 Whether this nephrotoxicity is accelerated in diabetic heart transpla

198 Although CNI nephrotoxicity is an important cause of renal failure af

199 Nephrotoxicity is common with the use of the chemotherap

200 Our data demonstrate that cisplatin-induced nephrotoxicity is mitigated by DR3 signaling, suggesting

201 Cyclosporine A-induced nephrotoxicity is multifactorial but oxidative stress ha

202 However, the molecular basis for antibiotic nephrotoxicity is not clearly understood.

203 However, the precise mechanism of nephrotoxicity is not fully understood.

204 ugh the exact mechanism of cisplatin-induced nephrotoxicity is not understood, several studies showed

205 Nephrotoxicity is significantly worsened by reduced neph

206 ut the exact nature of vancomycin-associated nephrotoxicity is unclear, in particular when considerin

207 recipients with calcineurin inhibitor (CNI) nephrotoxicity is unclear.

208 Concerns over nephrotoxicity led to a protocol amendment to an open-la

209 During the course of nephrotoxicity, levels of pVHL, a factor that destabiliz

210 e perceived risk of radiocontrast-associated nephrotoxicity may influence the provision of coronary a

211 In the folic acid nephrotoxicity model of acute tubular necrosis, mice exp

212 e rejection (n=17), or calcineurin inhibitor nephrotoxicity (n=9) based on clinical presentation and

213 iocontrast" and any of the words or phrases "nephrotoxicity," "nephropathy," kidney failure," or "ren

214 to treat several cancers, is associated with nephrotoxicity, neurotoxicity, and ototoxicity, which ha

215 ong-term effects include pulmonary toxicity, nephrotoxicity, neurotoxicity, decreased fertility, hypo

216 include cardiac toxicity, acute and chronic nephrotoxicity, neurotoxicity, hearing loss, infertility

217 o elucidate the reason for the difference in nephrotoxicity observed between the groups and to assess

218 Acute nephrotoxicity occurred in 22.6% of cyclosporine and 19.

219 Nephrotoxicity occurred in 37% of patients treated with

220 Nephrotoxicity occurred more frequently with vancomycin

221 4; 95% CI, 0.54-1.01; p = 0.06; I2 = 25%) or nephrotoxicity (odds ratio, 1.18; 95% CI, 0.76-1.83; p =

222 ng precision-cut tissue slices suggested the nephrotoxicities of 3a-c to be clinically manageable.

223 s in cell culture raise the possibility that nephrotoxicity of APOL1 risk variants may be mediated by

224 probenecid with the infusions to reduce the nephrotoxicity of CDV.

225 Mrp2-null mice reduced the accumulation and nephrotoxicity of cisplatin to levels observed in wild-t

226 An important role for IL-17A in the nephrotoxicity of cisplatin was demonstrated by observin

227 which had previously been shown to block the nephrotoxicity of cisplatin, decreased the binding of Pt

228 We sought to compare the nephrotoxicity of isosmolar contrast medium (IOCM) iodix

229 The nephrotoxicity of methoxyflurane was not realized immedi

230 There is limited data on the potential nephrotoxicity of sirolimus (SRL) and tacrolimus (TAC) i

231 This study assesses the acute nephrotoxicity of tacrolimus (Tac) and sirolimus (Sir) i

232 , is severely limited by a high incidence of nephrotoxicity of unknown etiology.

233 95% CI, .50-1.67; P = .78; I(2) = 34.59%) or nephrotoxicity (OR, 1.14; 95% CI, .59-2.20; P = .69; I(2

234 and 90-day mortality, metastatic infection, nephrotoxicity, or hepatotoxicity.

235 No significant nephrotoxicity, ototoxicity, or cumulative neurologic to

236 creatinine levels (P <0.05) and incidence of nephrotoxicity (P =0.004, conversion from Tac to other a

237 e infusion-related reactions (P<0.01) and of nephrotoxicity (P<0.001).

238 Calcineurin-inhibitor nephrotoxicity plays a role in the pathogenesis of chron

239 role in protecting against cisplatin-induced nephrotoxicity, possibly by attenuating a p53-dependent

240 This data suggests that nephrotoxicity posttransplant is not accelerated in diab

241 Patients with HDMTX-induced nephrotoxicity received one to three doses of intravenou

242 dered for prevention of cisplatin-associated nephrotoxicity, reduction of grade 3 to 4 neutropenia (a

243 95% confidence interval, 1.04-2.14) of acute nephrotoxicity relative to tacrolimus.

244 research, the mechanism of cisplatin-induced nephrotoxicity remains unclear, and renoprotective appro

245 sion to the risk of radiocontrast-associated nephrotoxicity ("renalism") is inappropriate, even if th

246 possible differences in the mechanism(s) of nephrotoxicity requiring further study.

247 Nephrotoxicity (RIFLE injury or higher; OR, 2.12 [95% CI

248 Nephrotoxicity severely limits the use of the anticancer

249 liver transplant recipients with chronic CsA nephrotoxicity showed significantly greater Nox2, alpha-

250 Nephrotoxicity side effect of the immunosuppressive drug

251 l neuropathy, high-dose methotrexate-related nephrotoxicity, sinusoidal obstructive syndrome, thrombo

252 attenuated glomerular disease in adriamycin nephrotoxicity, SNx, and diabetes.

253 We showed that early during cisplatin nephrotoxicity, Src interacted with, phosphorylated, and

254 Here we describe a long term repeat dose nephrotoxicity study conducted on the human renal proxim

255 ociated with a significantly greater risk of nephrotoxicity than continuous infusion (odds ratio = 8.

256 Fewer patients in the ODD group developed nephrotoxicity than the MDD group (5 vs. 12, p =.142).

257 ction and increase graft survival, with less nephrotoxicity than treatment with cyclosporine.

258 rophylactic ABLC in HSCT was associated with nephrotoxicity that could be aggravated by the concomita

259 tic use of cyclosporin A (CsA) is limited by nephrotoxicity that is manifested by reduced GFR, fibros

260 hanges that are characteristic of gentamicin nephrotoxicity that is seen with the native compound.

261 Fears of potential nephrotoxicity that tenofovir would have in common with

262 ential antibacterial benefit against risk of nephrotoxicity the algorithms were designed to achieve t

263 whether CaR could contribute to AGA-induced nephrotoxicity, the acute responses to various AGAs in t

264 Calcineurin inhibitors induce nephrotoxicity through poorly understood mechanisms ther

265 pared lipid emulsion or in liposomes reduced nephrotoxicity to a similar degree, by 18.4% (relative r

266 contribution of calcineurin inhibitors (CNI) nephrotoxicity to progressive kidney transplant injury r

267 us mouse models of ARF were studied: Maleate nephrotoxicity, unilateral ureteral obstruction, and LPS

268 of dendritic cell-derived IL-10 in cisplatin nephrotoxicity using a conditional cell ablation approac

269 The molecular signature of chronic CsA nephrotoxicity using transcriptomic analyses demonstrate

270 e treatment resulted in reduced systemic and nephrotoxicity, validated by decreased biodistribution o

271 Nephrotoxicity was assessed in 173 critically ill patien

272 Nephrotoxicity was associated with tissue hypoxia, espec

273 ling against P. aeruginosa ATCC 27853 and no nephrotoxicity was found after systemic administration,

274 Cisplatin-induced nephrotoxicity was manifested by increases in blood urea

275 Nephrotoxicity was most prominent in the high-dose treat

276 Iopamidol nephrotoxicity was negligible in this cohort of pediatri

277 in 2001, the first case of TDF-induced acute nephrotoxicity was published.

278 The prevalence of new onset nephrotoxicity was reported using Risk, Injury, Failure,

279 Local diagnosis of calcineurin inhibitor nephrotoxicity was spread across all four subgroups and

280 To identify a reliable biomarker of nephrotoxicity, we conducted multiplexed gene expression

281 rrent study, using mouse models of cisplatin nephrotoxicity, we show that the G1/S-regulating cyclin-

282 ily dose and trough concentration at time of nephrotoxicity were 400 mg (400-500 mg) and 228 ng/mL (1

283 Leukopenia, anemia, and allograft nephrotoxicity were addressed by solely decreasing MMF a

284 teria, and independent factors predictive of nephrotoxicity were identified using logistic regression

285 Myelosuppression and nephrotoxicity were not observed.

286 No severe neurotoxicity or nephrotoxicity were observed.

287 No cases of dose-limiting nephrotoxicity were observed.

288 al transplant recipients without the risk of nephrotoxicity, when transplant ultrasound is nondiagnos

289 Clinical use of free AMB is limited by its nephrotoxicity, whereas liposomal AMB is costly and requ

290 KCdelta as a critical regulator of cisplatin nephrotoxicity, which can be effectively targeted for re

291 ules of the kidney and causes dose-dependent nephrotoxicity, which may involve autophagy.

292 that was complicated by cyclosporine-induced nephrotoxicity, which required kidney transplantation.

293 AA-I is largely responsible for the nephrotoxicity while both AA-I and AA-II are genotoxic.

294 rruption of brincidofovir and none developed nephrotoxicity with brincidofovir.

295 rains, poor clinical outcomes, and increased nephrotoxicity with high-dose therapy are challenging it

296 These data suggest potential nephrotoxicity with strategies directed toward inhibitio

297 me more challenging due to recent reports of nephrotoxicity with the combination of vancomycin and pi

298 h level was 4 to 7 ng/mL to reduce long-term nephrotoxicity, with 500 mg twice-daily doses of mycophe

299 Because of nephrotoxicity, withdrawal has been a challenge since th

300 mia in pediatric patients reduces subsequent nephrotoxicity without compromising survival.