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1 trough monitoring is associated with higher nephrotoxicity.
2 skiren may be used for the prevention of CNI nephrotoxicity.
3 mune response, whereas reducing drug-related nephrotoxicity.
4 iver transplantation (LT) is associated with nephrotoxicity.
5 n for the understanding of polymyxin-induced nephrotoxicity.
6 f DMF has a protective potential against CsA nephrotoxicity.
7 ference, vascular disrupting properties, and nephrotoxicity.
8 Eleven patients (20.0%) developed nephrotoxicity.
9 n injury of the kidney and cisplatin-induced nephrotoxicity.
10 dentified as high-risk patient subgroups for nephrotoxicity.
11 comorbidities reported to predispose them to nephrotoxicity.
12 ith no indication of hematologic toxicity or nephrotoxicity.
13 001) were significant positive predictors of nephrotoxicity.
14 ependently associated with increased odds of nephrotoxicity.
15 (ER) stress contribute to cisplatin-induced nephrotoxicity.
16 fect of combination therapy on mortality and nephrotoxicity.
17 tient variability in the risk of CsA-induced nephrotoxicity.
18 rosuvastatin protects against aminoglycoside nephrotoxicity.
19 s often fail to accurately and timely detect nephrotoxicity.
20 No SNPs were associated with tacrolimus nephrotoxicity.
21 and independently predictive of cyclosporine nephrotoxicity.
22 c factors may also predispose individuals to nephrotoxicity.
23 GAN genes were associated with cyclosporine nephrotoxicity.
24 uded loss of body weight, hepatotoxicity and nephrotoxicity.
25 nts with biopsy-confirmed chronic CsA or TAC nephrotoxicity.
26 al prophylaxis in patients at lower risk for nephrotoxicity.
27 ection of transplanted organs but also cause nephrotoxicity.
28 ty of LT recipients converted to SRL for CNI nephrotoxicity.
29 iated with early, acute cyclosporine-related nephrotoxicity.
30 e tumor models while protecting kidneys from nephrotoxicity.
31 predict and prevent chemotherapeutic-induced nephrotoxicity.
32 wever, its use is dose-limited due to severe nephrotoxicity.
33 with calcineurin inhibitor (CNI)-associated nephrotoxicity.
34 IL-10 ameliorates kidney injury in cisplatin nephrotoxicity.
35 ytes to control transplant rejection without nephrotoxicity.
36 ctive effect of dendritic cells in cisplatin nephrotoxicity.
37 a target of interest to prevent TCE induced nephrotoxicity.
38 ment of iron overload disease because of its nephrotoxicity.
39 ent mechanisms of tissue injury in cisplatin nephrotoxicity.
40 l ischemia/reperfusion and cisplatin-induced nephrotoxicity.
41 l ischemia/reperfusion and cisplatin-induced nephrotoxicity.
42 stage renal failure secondary to calcineurin nephrotoxicity.
43 y their functional significance in cisplatin nephrotoxicity.
44 fective dose (BED) with radionuclide-induced nephrotoxicity.
45 atient survival by minimizing CNI-associated nephrotoxicity.
46 r emphasis on calcineurin inhibitor-mediated nephrotoxicity.
47 nt led to downregulation of TonEBP and overt nephrotoxicity.
48 Calcineurin inhibition results in nephrotoxicity.
49 ha or beta isoform to a model of cyclosporin nephrotoxicity.
50 on and renal cell apoptosis during cisplatin nephrotoxicity.
51 en may also improve compliance and limit CNI nephrotoxicity.
52 e direct mediators of experimental cisplatin nephrotoxicity.
53 lated in renal cortex and is responsible for nephrotoxicity.
54 aused by calcineurin inhibitors (CI)-induced nephrotoxicity.
55 horylation and beta-oxidation, would prevent nephrotoxicity.
56 diated renal cell apoptosis during cisplatin nephrotoxicity.
57 cidal properties with minimal or no apparent nephrotoxicity.
58 higher risk of developing CI-induced chronic nephrotoxicity.
59 l death can be interceded in vivo to prevent nephrotoxicity.
60 at induced COX-2 expression would lessen ADR nephrotoxicity.
61 tion episodes, renal biopsy, or drug-induced nephrotoxicity.
62 o CsA-treated rats significantly ameliorated nephrotoxicity.
63 r lipotoxic and did not increase CsA-induced nephrotoxicity.
64 ischemic-reperfusion injury, and CsA-induced nephrotoxicity.
65 le of this endonuclease in cisplatin-induced nephrotoxicity.
66 Mycophenolate mofetil (MMF) has no known nephrotoxicity.
67 on attributed to calcineurin inhibitor (CNI) nephrotoxicity.
68 Capsaicin also ameliorates cisplatin-induced nephrotoxicity.
69 d other comparable KIs with varying risks of nephrotoxicity.
70 splants related to immunosuppression-related nephrotoxicity.
71 all-cause mortality, and treatment-emergent nephrotoxicity.
72 ron overload without demonstrating DFO's own nephrotoxicity.
73 n, whereas supratherapeutic levels may cause nephrotoxicity.
74 novel targets to reduce calcineurin induced nephrotoxicity.
75 iperacillin-tazobactam increases the risk of nephrotoxicity.
76 sure, and it is associated with high risk of nephrotoxicity.
77 st-line" antibiotic scarcely used due to its nephrotoxicity.
78 8 showed signs of tubular damage, indicating nephrotoxicity.
79 High dosing was associated with more nephrotoxicity.
80 liver transplant recipients with chronic CsA nephrotoxicity.
81 se of CNIs is associated with some degree of nephrotoxicity.
82 erfusion, and the molecular phenotype of CsA nephrotoxicity.
83 sis in NSCLC H460 tumor-bearing mice without nephrotoxicity.
84 ificantly better renal function, that is, no nephrotoxicity.
85 r protecting patients from cisplatin-induced nephrotoxicity.
86 ected on virologic responses, mortality, and nephrotoxicity.
87 monitoring of chronic calcineurin inhibitor nephrotoxicity.
88 2%; 0), fatigue (8%; 0), infection (8%; 2%), nephrotoxicity (2%; 0), and diverticulitis (6%; 2%).
89 s showed predominant features of chronic CNI nephrotoxicity, 27 (43.5%) predominant features of hyper
90 us (45%) and a history of tacrolimus-induced nephrotoxicity (35%) appeared to be prevalent in subject
91 The administration of KBrO(3) resulted in nephrotoxicity, a decline in the specific activities of
93 bilities for new methods to prevent or treat nephrotoxicity after contrast medium administration.
94 ent amifostine protected rats from long-term nephrotoxicity after PRRT with (177)Lu-DOTA,Tyr(3)-octre
96 dromes were classified including accelerated nephrotoxicity (Amanita proxima, Amanita smithiana), rha
98 usly shown to be a predictor of drug-induced nephrotoxicity and compared its response to Stx2 exposur
99 anisms underlying cisplatin-induced oto- and nephrotoxicity and compelling preclinical evidence for t
100 role in both the development of CNI-induced nephrotoxicity and endothelial vasculopathy in chronic a
101 superior to the CSA era, with less early CNI nephrotoxicity and fewer rejection episodes, but compara
105 ociated with immunosuppression, specifically nephrotoxicity and infection risk, significantly affect
107 In this article we assess the evidence for nephrotoxicity and its possible mechanisms, provide reco
109 neurin inhibitors is associated with chronic nephrotoxicity and lower glomerular filtration rate (GFR
110 ological changes like haemorrhage, necrosis, nephrotoxicity and often develop hypersensitive reaction
111 arios, especially in light of posttransplant nephrotoxicity and other adverse events associated with
112 ease cisplatin and aspirin to ameliorate the nephrotoxicity and ototoxicity caused by cisplatin.
115 their utility is compromised by significant nephrotoxicity and polymyxin-resistant bacterial strains
117 ific effects of RAS stimulation on cisplatin nephrotoxicity and raise the concern that inflammatory m
118 expression of APOL1 may not be the driver of nephrotoxicity and specifically, of podocyte injury.
120 demonstrate a role of PKCdelta in cisplatin nephrotoxicity and support targeting PKCdelta as an effe
122 opment of novel strategies to ameliorate its nephrotoxicity and to develop safer, new polymyxins.
123 mplication for the prevention of IFO-induced nephrotoxicity and/or mitochondrial diseases secondary t
124 am"] and ["AKI" or "acute renal failure" or "nephrotoxicity"] and registered meta-analysis (PROSPERO:
125 am"] and ["AKI" or "acute renal failure" or "nephrotoxicity"] and registered meta-analysis with relev
126 , glycerol-induced rhabdomyolysis, cisplatin nephrotoxicity, and bilateral ureteral obstruction.
127 IV infection, antiretroviral therapy-related nephrotoxicity, and developments in kidney transplantati
128 F-alpha is a fundamental driver of cisplatin nephrotoxicity, and generation of TNF-alpha is suppresse
129 d transplant ischemia, calcineurin inhibitor nephrotoxicity, and inflammatory response within the all
130 , a metabolite of IFO, is the chief cause of nephrotoxicity, and that agmatine (AGM), which we found
131 r antibacterial effect overlap those causing nephrotoxicity, and there is large inter-patient variabi
132 r antibacterial effect overlap those causing nephrotoxicity, and there is large inter-patient variabi
133 lso associated with adverse effects, such as nephrotoxicity, anemia, leukopenia, and new-onset diabet
135 h and without SRI, including hepatotoxicity, nephrotoxicity, any reported AE, mortality and length of
136 of kidney injury associated with ischemia or nephrotoxicity, are the site of oligonucleotide reabsorp
137 which VEGFA-VEGFR2 inhibitors contribute to nephrotoxicity, as well as the wide range of clinical ma
138 eadout for ototoxicity and kidney cell-based nephrotoxicity assay, we screened 1280 compounds and ide
140 tal and clinical evidence behind the diverse nephrotoxicities associated with the inhibition of this
141 inhibitors (CNIs) in transplant recipients, nephrotoxicity associated with long-term CNI use remains
142 tion to overcome calcineurin inhibitor (CNI) nephrotoxicity but the evidence base for this approach i
143 or an inflammatory pathogenesis of cisplatin nephrotoxicity, but immune cell-mediated mechanisms in t
144 re significantly protected against cisplatin nephrotoxicity, but it is unknown whether the DNA fragme
145 luated the impact of reduced nephron mass on nephrotoxicity by cyclosporine A (CsA) and/or sirolimus
146 ts of dimethyl fumarate (DMF) on CsA-induced nephrotoxicity by enhancing the antioxidant defense syst
147 sEH inhibition attenuates cisplatin-induced nephrotoxicity by modulating nuclear factor-kappaB signa
148 luating the Val effect in alleviation of CsA nephrotoxicity by probable increase in renal Klotho expr
149 ion of Val might lead to amelioration of CsA nephrotoxicity by probably diminishing CsA-induced renal
150 that EET analogs attenuate cisplatin-induced nephrotoxicity by reducing oxidative stress, inflammatio
151 gs (10 mg/kg/d) attenuated cisplatin-induced nephrotoxicity by reducing these renal injury markers by
155 negative 'superbugs'; however, dose-limiting nephrotoxicity can occur in up to 60% of patients after
156 o the role of miRNAs in cyclosporine-induced nephrotoxicity (CIN) and the gene pathways they regulate
157 l SCr criteria for contrast material-induced nephrotoxicity (CIN; SCr increase >/=0.5 mg/dL [44.20 mu
159 is associated with a decreased likelihood of nephrotoxicity compared with intermittent infusion.
160 therapy had approximately twice the odds of nephrotoxicity compared with those receiving monotherapy
161 oreover, we demonstrated that the attenuated nephrotoxicity correlated with decreased apoptosis that
163 ated, without any signs of acute or subacute nephrotoxicity during a mean follow-up of nearly 2 y (an
164 adiolabeled somatostatin analogs may lead to nephrotoxicity during peptide receptor radionuclide ther
167 2011 that contained search terms related to nephrotoxicity following intravenous contrast medium adm
168 ntation include chronic allograft rejection, nephrotoxicity from calcineurin inhibitors (CNIs), and s
171 study evaluated histological evidence of CNI nephrotoxicity from normal donor kidneys of successful k
173 sed that chronic calcineurin inhibitor (CNI) nephrotoxicity has a central role in chronic kidney dise
175 in renal proximal tubules resulting in late nephrotoxicity, highlighting the importance of long-term
176 and elevated CNI levels are associated with nephrotoxicity; however, they do not fully explain the r
178 in administration, including ototoxicity and nephrotoxicity, impact the clinical utility of this effe
179 drug-related deaths), and treatment-emergent nephrotoxicity in 10% and 56% (P = .002), respectively.
180 studied the regulation of TauT in cisplatin nephrotoxicity in a human embryonic kidney cell line and
181 histopathology remains the gold standard for nephrotoxicity in animal systems, serum creatinine (SCr)
182 uvastatin can inhibit aminoglycoside-induced nephrotoxicity in children with Cystic Fibrosis (CF).
183 demonstrated that the worsening of cisplatin nephrotoxicity in DC-depleted mice was not a result of t
184 it will be used to help assess the origin of nephrotoxicity in desferrithiocin analogues: is toxicity
189 acid containing MMP-13 inhibitors; however, nephrotoxicity in preclinical toxicology species preclud
193 ay treatment with cyclosporine (CsA)-induced nephrotoxicity in syngeneic kidney transplants correlate
194 long-term lithium therapy is associated with nephrotoxicity in the absence of episodes of acute intox
196 een SNPs and time to early CNI-related acute nephrotoxicity in the first 6 months posttransplant.
199 However, its therapeutic use is limited by nephrotoxicity, in part mediated by oxidative stress.
200 istological features common with cyclosporin nephrotoxicity including matrix expansion, arteriole hya
201 Calcineurin inhibitor (CNI)-related acute nephrotoxicity is a common complication of transplantati
209 Our data demonstrate that cisplatin-induced nephrotoxicity is mitigated by DR3 signaling, suggesting
213 ugh the exact mechanism of cisplatin-induced nephrotoxicity is not understood, several studies showed
216 ut the exact nature of vancomycin-associated nephrotoxicity is unclear, in particular when considerin
219 hat glomerular NPY-NPY2R signaling predicted nephrotoxicity, modulated RNA processing, and inhibited
220 e rejection (n=17), or calcineurin inhibitor nephrotoxicity (n=9) based on clinical presentation and
221 iocontrast" and any of the words or phrases "nephrotoxicity," "nephropathy," kidney failure," or "ren
222 to treat several cancers, is associated with nephrotoxicity, neurotoxicity, and ototoxicity, which ha
223 ong-term effects include pulmonary toxicity, nephrotoxicity, neurotoxicity, decreased fertility, hypo
224 include cardiac toxicity, acute and chronic nephrotoxicity, neurotoxicity, hearing loss, infertility
225 o elucidate the reason for the difference in nephrotoxicity observed between the groups and to assess
229 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 =
230 ng precision-cut tissue slices suggested the nephrotoxicities of 3a-c to be clinically manageable.
231 s in cell culture raise the possibility that nephrotoxicity of APOL1 risk variants may be mediated by
233 Mrp2-null mice reduced the accumulation and nephrotoxicity of cisplatin to levels observed in wild-t
235 which had previously been shown to block the nephrotoxicity of cisplatin, decreased the binding of Pt
240 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
243 role in protecting against cisplatin-induced nephrotoxicity, possibly by attenuating a p53-dependent
246 dered for prevention of cisplatin-associated nephrotoxicity, reduction of grade 3 to 4 neutropenia (a
248 research, the mechanism of cisplatin-induced nephrotoxicity remains unclear, and renoprotective appro
250 human kidney diseases, provide platforms for nephrotoxicity screening, enable cellular therapy, and p
253 liver transplant recipients with chronic CsA nephrotoxicity showed significantly greater Nox2, alpha-
255 l neuropathy, high-dose methotrexate-related nephrotoxicity, sinusoidal obstructive syndrome, thrombo
258 Here we describe a long term repeat dose nephrotoxicity study conducted on the human renal proxim
259 ociated with a significantly greater risk of nephrotoxicity than continuous infusion (odds ratio = 8.
260 rophylactic ABLC in HSCT was associated with nephrotoxicity that could be aggravated by the concomita
261 tic use of cyclosporin A (CsA) is limited by nephrotoxicity that is manifested by reduced GFR, fibros
262 hanges that are characteristic of gentamicin nephrotoxicity that is seen with the native compound.
264 ential antibacterial benefit against risk of nephrotoxicity the algorithms were designed to achieve t
267 pared lipid emulsion or in liposomes reduced nephrotoxicity to a similar degree, by 18.4% (relative r
269 contribution of calcineurin inhibitors (CNI) nephrotoxicity to progressive kidney transplant injury r
270 us mouse models of ARF were studied: Maleate nephrotoxicity, unilateral ureteral obstruction, and LPS
271 of dendritic cell-derived IL-10 in cisplatin nephrotoxicity using a conditional cell ablation approac
273 e treatment resulted in reduced systemic and nephrotoxicity, validated by decreased biodistribution o
275 ling against P. aeruginosa ATCC 27853 and no nephrotoxicity was found after systemic administration,
280 Local diagnosis of calcineurin inhibitor nephrotoxicity was spread across all four subgroups and
282 rrent study, using mouse models of cisplatin nephrotoxicity, we show that the G1/S-regulating cyclin-
283 ily dose and trough concentration at time of nephrotoxicity were 400 mg (400-500 mg) and 228 ng/mL (1
284 teria, and independent factors predictive of nephrotoxicity were identified using logistic regression
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
293 earch to elucidate mechanisms for minimizing nephrotoxicity while maintaining therapeutic efficacy.
295 rains, poor clinical outcomes, and increased nephrotoxicity with high-dose therapy are challenging it
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