ライフサイエンスコーパス: calcineurin inhibitor

1 single extra copy of Dscr1, an Hsa21-encoded calcineurin inhibitor.

2 ression included mycophenolate mofetil and a calcineurin inhibitor.

3 e immunosuppression including prednisone and calcineurin inhibitor.

4 R 0.62, P=0.102) compared with SRL without a calcineurin inhibitor.

5 rapidly released Gal-3, which was blocked by calcineurin inhibitors.

6 nosuppressive agents were antimetabolites or calcineurin inhibitors.

7 e treatment with topical glucocorticoids and calcineurin inhibitors.

8 in SCC development following treatment with calcineurin inhibitors.

9 s and azathioprine without administration of calcineurin inhibitors.

10 vation and reduce the nephrotoxic effects of calcineurin inhibitors.

11 ew-onset diabetes after transplantation with calcineurin inhibitors.

12 for the diabetogenicity seen with the use of calcineurin inhibitors.

13 ars) from transplantation were maintained on calcineurin inhibitors.

14 ude infections, chemotherapy, radiation, and calcineurin inhibitors.

15 contribute to the antiproteinuric effects of calcineurin inhibitors.

16 oblasts, and these effects were abolished by calcineurin inhibitors.

17 vels is needed to prevent adverse effects of calcineurin inhibitors.

18 use of immunosuppressive agents, especially calcineurin inhibitors.

19 uppression toward lower doses especially for calcineurin inhibitors.

20 ications for immunosuppressive therapy using calcineurin inhibitors.

21 cations, especially glucocorticosteroids and calcineurin inhibitors.

22 immunosuppression compared to patients given calcineurin inhibitors.

23 in in organ transplant recipients treated by calcineurin inhibitors.

24 T cells (NFAT) control and is upregulated by calcineurin inhibitors.

25 ncipal treatment regimens were SRL without a calcineurin inhibitor (33%), SRL+cyclosporine A (CsA) (3

26 HRS2 patients had lower initial exposure to calcineurin inhibitors, a greater proportion of HRS2 pat

27 include the use of steroids together with a calcineurin inhibitor after transplantation.

28 healthy volunteers or RTX patients receiving calcineurin inhibitors (all P<0.001) but did not correla

29 Finally, beta cell cytotoxicity of the calcineurin inhibitor and immunosuppressant tacrolimus (

30 A calcineurin inhibitor and mycophenolate mofetil were use

31 HD) prophylaxis with PT-Cy with or without a calcineurin inhibitor and mycophenolate.

32 f the 4,110 participants (61.4%) were taking calcineurin inhibitor and statin, 378 (9.2%) were taking

33 s to show the efficacy and safety of topical calcineurin inhibitors and atopiclair.

34 cascade, and highlight the potential use of calcineurin inhibitors and caspofungin for emerging drug

35 cation of effort in trials assessing topical calcineurin inhibitors and corticosteroids as treatment

36 at least partly related to administration of calcineurin inhibitors and diminution of NETs production

37 signed transplant recipients who were taking calcineurin inhibitors and had at least one cutaneous sq

38 d T-plastin expression was down-regulated by calcineurin inhibitors and involved nuclear factor of ac

39 al existing immunosuppressive drugs, such as calcineurin inhibitors and mammalian target of rapamycin

40 Calcineurin inhibitors and mycophenolate mofetil are pot

41 ectrum anti-inflammatory treatments, such as calcineurin inhibitors and other immunomodulators, or no

42 syndrome unresponsive to the combination of calcineurin inhibitors and prednisone.

43 found in transplant recipients treated with calcineurin inhibitors and with high expression of phosp

44 ng withdrawal of the carcinogenic effects of calcineurin inhibitors and/or their impact on chronic (o

45 essive drugs (especially corticosteroids and calcineurin inhibitors) and physiologic challenges can p

46 not complete, was seen with only one dose of calcineurin inhibitor, and the effect was sustained for

47 o 100% with regimens using dose increases of calcineurin inhibitors, and 55% with IL-2 antagonists.

48 rly, potentially related to corticosteroids, calcineurin inhibitors, and mechanistic target of rapamy

49 sted of plasma exchanges (PE), high doses of calcineurin inhibitors, and steroids.

50 al controls treated with antibody induction, calcineurin inhibitor, antimetabolite, and maintenance p

51 recipients treated with antibody induction, calcineurin inhibitor, antimetabolite, and RDP versus hi

52 transplantation, immunosuppressive therapy (calcineurin inhibitors, antitumor necrosis factor-alpha

53 [AOR], 6.23; P = .03) and discontinuation of calcineurin inhibitor (AOR, 5.11; P = .02) were independ

54 The administration of calcineurin inhibitors appeared to play an important rol

55 Calcineurin inhibitors are associated with adverse cardi

56 Calcineurin inhibitors are imperfect long-term maintenan

57 High-dose steroids and calcineurin inhibitors are ineffective in the treatment

58 Calcineurin inhibitors are known to be nephrotoxic.

59 Calcineurin inhibitors are standard immunosuppression dr

60 Topical corticosteroids and calcineurin inhibitors are well-known treatments of atop

61 SR including an antiproliferative drug and a calcineurin inhibitor as follows: mycophenolate mofetil

62 Despite the administration of a calcineurin inhibitor as prophylaxis against GVHD, vacci

63 All children continued prednisone and calcineurin inhibitors at the doses prescribed before en

64 A de novo calcineurin inhibitor avoidance regimen based on sirolim

65 ansplant Everolimus De Novo Study With Early Calcineurin Inhibitor Avoidance trial, where de novo HTx

66 esponses to an everolimus-based arm versus a calcineurin inhibitor-based arm in de novo kidney transp

67 The MSD group received calcineurin inhibitor-based GVHD prophylaxis.

68 Calcineurin inhibitor-based immunosuppressants were give

69 prophylaxis, whereas URD recipients received calcineurin inhibitor-based prophylaxis.

70 th the highest remission rates achieved with calcineurin inhibitor-based protocols.

71 wer risk of CMV disease than a standard-dose calcineurin inhibitor-based regimen.

72 CI, 1.20-3.86; P=0.01) than those receiving calcineurin inhibitor-based regimens.

73 Calcineurin inhibitors benefit axonal damage, cellular d

74 This has functional implications because calcineurin inhibitors blunted the enhanced osteoblast r

75 n and reversed the antitolerogenic effect of calcineurin inhibitors by boosting the critical role of

76 ibitors (FK506, cyclosporin A, and a peptide calcineurin inhibitor [CAIN]) abolished glucose-induced

77 Calcineurin inhibitors cause vascular and renal injury a

78 treated with tofacitinib/basiliximab (n=5), calcineurin inhibitor (CNI) (cyclosporine A)/basiliximab

79 At diagnosis, we either reduced calcineurin inhibitor (CNI) and mycophenolate mofetil by

80 ntly associated with longer exposure to high calcineurin inhibitor (CNI) concentrations (hazard ratio

81 Interestingly, the calcineurin inhibitor (CNI) cyclosporine A (CsA), an imm

82 Strategies to reduce calcineurin inhibitor (CNI) dose or conversion to either

83 aracterization of the HNF1B expression after calcineurin inhibitor (CNI) exposure.

84 T, with particular emphasis on the choice of calcineurin inhibitor (CNI) immunosuppressive therapy.

85 ion has increased, yet little is known about calcineurin inhibitor (CNI) metabolism in this group.

86 study evaluated a corticosteroid (CS)-free, calcineurin inhibitor (CNI) minimization immunosuppressi

87 en used in liver transplantation to overcome calcineurin inhibitor (CNI) nephrotoxicity but the evide

88 It is proposed that chronic calcineurin inhibitor (CNI) nephrotoxicity has a central

89 ion in liver transplant (LT) recipients with calcineurin inhibitor (CNI) nephrotoxicity is unclear.

90 ross-sectional study, we assessed effects of calcineurin inhibitor (CNI) or rapamycin on T-regulatory

91 to 14 weeks after transplant to convert from calcineurin inhibitor (CNI) to everolimus or remain on s

92 new immunosuppression strategies to minimize calcineurin inhibitor (CNI) toxicity while effectively p

93 ered the histopathologic hallmark of chronic calcineurin inhibitor (CNI) toxicity.

94 r transplantation (LT) and may worsen due to calcineurin inhibitor (CNI) use.

95 fludarabine, and GVHD prophylaxis involved a calcineurin inhibitor (CNI) with either methotrexate (MT

96 Early calcineurin inhibitor (CNI) withdrawal with mycophenolat

97 Haploidentical recipients received calcineurin inhibitor (CNI), mycophenolate, and posttran

98 , randomized trial evaluated conversion from calcineurin inhibitor (CNI)- to sirolimus (SRL)-based im

99 plantation (LT) and especially in those with calcineurin inhibitor (CNI)-associated nephrotoxicity.

100 Calcineurin inhibitor (CNI)-based therapy is associated

101 the setting of solid-organ transplantation, calcineurin inhibitor (CNI)-based therapy remains the co

102 e-arm, 2-step prospective trial of bottom-up calcineurin inhibitor (CNI)-free de novo immunosuppressi

103 A prednisone and calcineurin inhibitor (CNI)-free protocol was compared w

104 ic NADPH oxidase, plays an important role in calcineurin inhibitor (CNI)-induced renal fibrosis.

105 with poor renal response when switching to a calcineurin inhibitor (CNI)-lowered or CNI-free immunosu

106 Calcineurin inhibitor (CNI)-related acute nephrotoxicity

107 ) had a different effect on weight gain than calcineurin inhibitor (CNI).

108 Calcineurin inhibitors (CNI) and steroids are known to p

109 graft function and/or renal side effects of calcineurin inhibitors (CNI) at each stage of treatment

110 nt of tumor-specific T cell responses due to calcineurin inhibitors (CNI) could contribute to SCC dev

111 inical outcomes among users of mTORIs versus calcineurin inhibitors (CNI) in their primary immunosupp

112 The contribution of calcineurin inhibitors (CNI) nephrotoxicity to progressi

113 studies have suggested that conversion from calcineurin inhibitors (CNI) to sirolimus (SRL) can impr

114 We have recently shown that calcineurin inhibitors (CNI) used to treat transplant pa

115 plantation (LT) is presently based on use of calcineurin inhibitors (CNI), although they are associat

116 such as polyomavirus-associated nephropathy, calcineurin inhibitors (CNI), and genetic factors.

117 esized that conventional immunosuppressives, calcineurin inhibitors (CNi), and mammalian target of ra

118 0 with our usual triple immunosuppression of calcineurin inhibitors (CNI), mycofenolate sodium (MMF),

119 /-3.90 years after transplant, with complete calcineurin-inhibitor (CNI) withdrawal.

120 Tacrolimus (Tac) and Cyclosporine A (CyA) calcineurin inhibitors (CNIs) are 2 effective immunosupp

121 Calcineurin inhibitors (CNIs) are among the most effecti

122 Calcineurin inhibitors (CNIs) are essential immunosuppre

123 Calcineurin inhibitors (CNIs) are immunosuppressive drug

124 ir effect on renal function in comparison to calcineurin inhibitors (CNIs) defined by measured GFR.

125 exposure of kidney transplant recipients to calcineurin inhibitors (CNIs) has potential merit, but t

126 Calcineurin inhibitors (CNIs) have an unfavorable cardio

127 Calcineurin inhibitors (CNIs) have failed to improve lon

128 Concerns about adverse effects of calcineurin inhibitors (CNIs) have prompted development

129 Calcineurin inhibitors (CNIs) in combination with predni

130 ection and early renal allograft loss due to calcineurin inhibitors (CNIs) in transplant recipients,

131 The calcineurin inhibitors (CNIs) may have protumorigenic ef

132 nsible for the disposition and metabolism of calcineurin inhibitors (CNIs) on clinical outcomes in ki

133 Calcineurin inhibitors (CNIs) revolutionized the field o

134 Calcineurin inhibitors (CNIs) target NFAT activation.

135 nic allograft rejection, nephrotoxicity from calcineurin inhibitors (CNIs), and systemic hypertension

136 us) are best placed to determine how topical calcineurin inhibitors compare with established clinical

137 and that only a combination of both PI3K and calcineurin inhibitors completely blocked the suppressiv

138 pients with GI symptoms receiving MMF plus a calcineurin inhibitor +/- corticosteroids were randomize

139 Calcineurin inhibitor cyclosporin A (CsA) and calcineuri

140 ibited mTOR signaling; pretreatment with the calcineurin inhibitor cyclosporin A (CsA), an antagonist

141 we examined wild-type mice treated with the calcineurin inhibitor cyclosporin A and transgenic mice

142 nuclear translocation were inhibited by the calcineurin inhibitor cyclosporin A.

143 s, an effect that was fully abrogated by the calcineurin inhibitors cyclosporin A or FK506, confirmin

144 ucleus, an event that is blocked by specific calcineurin inhibitors cyclosporin A or FK520.

145 e-filling solution or preincubation with the calcineurin inhibitors, cyclosporin A or ascomycin, sign

146 gan transplant patients are administered the calcineurin inhibitor cyclosporine A (CsA) chronically a

147 + B cell depletion therapy combined with the calcineurin inhibitor cyclosporine A (CsA) prolonged med

148 The immunosuppressive action of the calcineurin inhibitor cyclosporine A (CsA) stems from th

149 Cell treatment with the calcineurin inhibitor cyclosporine A or a NFAT-specific

150 gene regulation in a manner superior to the calcineurin inhibitor cyclosporine and the FKBP12 ligand

151 blocked by MK-801, by scavenging ROS, by the calcineurin inhibitor cyclosporine, and by the TRPC chan

152 d FHL2 knockdown cells, was abolished by the calcineurin inhibitor cyclosporine, confirming the calci

153 ro-1H-3-benzazepine) plus haloperidol] nor a calcineurin inhibitor (cyclosporine), prevents the nicot

154 ion, which is partly explained by the use of calcineurin inhibitors, data on the consequences of acut

155 the effectiveness of the recently recognized calcineurin inhibitor dipyridamole in limiting SLE-relat

156 of rapamycin inhibitor and reduced-exposure calcineurin inhibitor does not appear to alter the risk.

157 For such recipients, the initial use of a calcineurin inhibitor drug for 2 to 4 months is preferre

158 of preemptive conversion to everolimus from calcineurin inhibitors early after liver transplantation

159 cipients consecutively converted to EVL with calcineurin inhibitor elimination.

160 strategy of transplant immunosuppression is calcineurin inhibitor elimination.

161 Calcineurin inhibitors exacerbate renal dysfunction and

162 The calcineurin inhibitor FK506 (tacrolimus) reduced cell de

163 glucan synthase inhibitor caspofungin or the calcineurin inhibitor FK506 against the human fungal pat

164 n is abolished by in vivo treatment with the calcineurin inhibitor FK506 and the specific NFAT-inhibi

165 were given intraperitoneal injections of the calcineurin inhibitor FK506 before and after infusion of

166 g development, we examined the activity of a calcineurin inhibitor FK506 in combination with caspofun

167 The calcineurin inhibitor FK506 prevented contrast-induced a

168 tor, was suppressed by coincubation with the calcineurin inhibitor FK506, suggesting involvement of D

169 nts being treated with the immunosuppressive calcineurin inhibitor FK506.

170 duced by miR-30 reduction but blocked by the calcineurin inhibitor FK506.

171 enoxy)ethane-N,N,N',N'-tetraacetic acid, the calcineurin inhibitors FK506 and cyclosporine A, or use

172 Treatment of neurons with the calcineurin inhibitors FK506 or cyclosporin A resulted i

173 thyl ester) (BAPTA-AM) or the three specific calcineurin inhibitors FK506, cyclosporine A, or calcine

174 nt transcription of ncs1 is abolished by the calcineurin inhibitor (FK506) and by knocking out the ca

175 ct of a corticosteroid (dexamethasone) and a calcineurin inhibitor (FK506).

176 Calcineurin inhibitors (FK506 and cyclosporine A) and th

177 cotransport activity was inhibited 20-30% by calcineurin inhibitors (FK506 and cyclosporine A).

178 Calcineurin inhibitors (FK506, cyclosporin A, and a pept

179 alcineurin, based on the observations that a calcineurin inhibitor, FK506, completely abrogated the d

180 urin sensitive, we assessed the effects of a calcineurin inhibitor, FK506.

181 ght to explore the architecture of trials of calcineurin inhibitors for atopic eczema to document the

182 28-CD80/86 costimulatory pathway, allows for calcineurin-inhibitor free immunosuppressive therapy in

183 NHPs, and offers a potentially translatable calcineurin inhibitor-free protocol inclusive of a singl

184 antigen (HLA)-compatible donors and standard calcineurin inhibitor graft-versus-host disease prophyla

185 roup, as compared with 14 such events in the calcineurin-inhibitor group (average, 0.938 vs. 0.250).

186 hdrawal of sirolimus) and in 22 (39%) in the calcineurin-inhibitor group (median time until onset, 15

187 ly longer in the sirolimus group than in the calcineurin-inhibitor group.

188 Calcineurin inhibitors had no effect on Ca(2+) release o

189 who are not candidates for antimetabolite or calcineurin inhibitor immunomodulation.

190 Cyclosporine and tacrolimus are calcineurin inhibitor immunosuppressants used to prevent

191 To reduce calcineurin inhibitor immunosuppression and preserve kid

192 he activity of calcineurin was elevated, and calcineurin inhibitors improved contractility and amelio

193 therapeutic target and supports the study of calcineurin inhibitors in acute KD.

194 the addition of rituximab to prednisone and calcineurin inhibitors in children with resistant idiopa

195 Further investigation of the role of calcineurin inhibitors in the treatment for Aspergillus

196 her to receive sirolimus as a substitute for calcineurin inhibitors (in 64 patients) or to maintain t

197 th either topical corticosteroids or topical calcineurin inhibitors) in mild AD cases or the preventi

198 Calcineurin inhibitors induce detrimental vascular remod

199 Calcineurin inhibitors induce nephrotoxicity through poo

200 Calcineurin inhibitors induce production of renin in the

201 These findings have implications in calcineurin-inhibitor induced carcinoma, a complication

202 evere pain in patients, often referred to as calcineurin inhibitor-induced pain syndrome (CIPS).

203 Altogether, these results might suggest that calcineurin inhibitor-induced tubular SNAI1 protein cyto

204 ese results suggest that corticosteroids and calcineurin inhibitors inhibit expression of distinct su

205 The use of calcineurin inhibitors is associated with chronic nephro

206 Immunosuppression (IS) withdrawal from calcineurin inhibitors is only possible in approximately

207 Conversion to EVL and elimination of calcineurin inhibitors is safe.

208 The mechanism of action of the calcineurin inhibitors is to bind in a complex with a bi

209 losporine (as opposed to tacrolimus) and low calcineurin inhibitor levels increased the risk of de no

210 Calcineurin inhibitor levels should be closely monitored

211 that a combination of a corticosteroid and a calcineurin inhibitor may be more effective than each si

212 loration of EVL in combination with low dose calcineurin inhibitors may be of potential benefit.

213 is dependent on calcineurin activation, and calcineurin inhibitors may provide an adjunctive therapy

214 scue to adulthood a valuable animal model of calcineurin inhibitor-mediated neuronal and renal toxici

215 Calcineurin inhibitors might be developed to prevent pos

216 Strategies allowing calcineurin inhibitor minimization while maintaining eff

217 ated with early posttransplant CKD3, despite calcineurin-inhibitor minimization.

218 115 days posttransplant to convert from CNI (calcineurin inhibitor)/MMF to sirolimus (SRL)/MMF had a

219 re prescribed rabbit antithymocyte globulin, calcineurin inhibitor, mycophenolate mofetil, and steroi

220 2) receptor blocker and were discharged on a calcineurin inhibitor/mycophenolate mofetil/steroid-free

221 r kidney transplant recipients maintained on calcineurin inhibitor/mycophenolate mofetil/steroid-free

222 tubules from kidney transplant recipients on calcineurin inhibitors, mycophenolic acid (MPA), and pre

223 ction followed by mycophenolate mofetil plus calcineurin inhibitors (n=28, with 7 also receiving ster

224 steroids) or sirolimus with (n=3) or without calcineurin inhibitors (n=4).

225 linical (n=10) or acute rejection (n=17), or calcineurin inhibitor nephrotoxicity (n=9) based on clin

226 Enhancement of calcineurin inhibitor nephrotoxicity by sirolimus (SRL)

227 Calcineurin inhibitor nephrotoxicity in nonrenal allogra

228 Local diagnosis of calcineurin inhibitor nephrotoxicity was spread across a

229 s from size- mismatched transplant ischemia, calcineurin inhibitor nephrotoxicity, and inflammatory r

230 for the diagnosis and monitoring of chronic calcineurin inhibitor nephrotoxicity.

231 pical agents for vitiligo, including topical calcineurin inhibitors; new topical combinations such as

232 ence of pharmacologic preconditioning with a calcineurin inhibitor on IRI in a syngeneic F344 rat kid

233 After bortezomib therapy, the addition of a calcineurin inhibitor or mycophenolate mofetil was predi

234 ical anti-inflammatory treatments (steroids, calcineurin inhibitors, or lithium salts) and placebo or

235 equired the use of topical steroids, topical calcineurin inhibitors, or other medications within the

236 Both AMPA receptor and calcineurin inhibitors prevent oligomer-induced surface

237 A targeted the ubiquitin ligase Itch and the calcineurin inhibitor RCAN1 for degradation to maintain

238 The calcineurin inhibitors reduced the intra-acinar activati

239 y subunit expression may alter the effect of calcineurin inhibitors regionally following a traumatic

240 inhibition of cathepsin K, or treatment with calcineurin inhibitor rescued cells from high-glucose tr

241 4s with the immunosuppressant cyclosporin, a calcineurin inhibitor, robustly inhibited HIV-1 reactiva

242 sus-host disease (GVHD) prophylaxis included calcineurin inhibitor, short-course methotrexate, and me

243 In addition to calcineurin inhibitors, sirolimus may also be associated

244 Calcineurin inhibitor-sparing or reduction regimens usin

245 are effective, well tolerated, and the first calcineurin inhibitor/steroid-sparing islet protocols re

246 on of allograft rejection without the use of calcineurin inhibitors, steroids or pan-T cell depletion

247 renal transplant recipients (RTRs) receiving calcineurin inhibitors, steroids, and mycophenolate mofe

248 Calcineurin inhibitors such as cyclosporin A (CsA) are t

249 Calcineurin inhibitors such as cyclosporine A (CsA) were

250 Calcineurin inhibitors such as cyclosporine A and FK506

251 erations in calcineurin signaling as current calcineurin inhibitors, such as cyclosporin A and FK-506

252 Calcineurin inhibitors, such as cyclosporin A and tacrol

253 Immunosuppressive therapies using calcineurin inhibitors, such as cyclosporine A, are asso

254 These results suggest that NF-AT/calcineurin inhibitors, such as tacrolimus and cyclospor

255 Calcineurin inhibitors, such as tacrolimus, used for hum

256 bicans during exposure to fluconazole plus a calcineurin inhibitor, suggesting that TORC1 broadly pro

257 this methodology, EBV-CTLs resistant to the calcineurin inhibitor Tacrolimus (TAC) can be produced i

258 Following treatment with the calcineurin inhibitor tacrolimus, human beta-cell apopto

259 To determine the ability of the calcineurin inhibitors tacrolimus (FK506) and cyclospori

260 olimus), via a dual mechanism of action as a calcineurin inhibitor that also binds FK-binding protein

261 Tacrolimus, a calcineurin inhibitor that inhibits dephosphorylation of

262 tivated T cells (NFAT), and cyclosporin A, a calcineurin inhibitor that reduces NFAT activity, reduce

263 tients who maintained immunosuppression with calcineurin inhibitor therapy after failure (P<0.001).

264 ation, has been assessed as a substitute for calcineurin inhibitor therapy after low-to-moderate risk

265 Patients were transitioned onto calcineurin inhibitor therapy when they reached chronic

266 regimen can serve as an effective bridge to calcineurin inhibitor therapy.

267 interstitial fibrosis/tubular atrophy versus calcineurin inhibitor therapy.

268 Calcineurin-inhibitor therapy is a contributing factor t

269 g all patients that had discontinued topical calcineurin inhibitors, those with the rs1898671 single-

270 with A. fumigatus, as well as the impact of calcineurin inhibitors, through a combination of single-

271 Although conversion from calcineurin inhibitors to mammalian target of rapamycin

272 immunosuppressive therapy or the switch from calcineurin inhibitors to mTOR inhibitors, as alternativ

273 Switching from calcineurin inhibitors to sirolimus had an antitumoral e

274 chronic T-cell rejection (C, 67%; C3, 29%), calcineurin inhibitor toxicity (C, 36%; C3, 18%), or C4d

275 due to humoral rejection (HR-TMA) or due to calcineurin inhibitor toxicity (CNI-TMA).

276 There is little calcineurin inhibitor toxicity in this group.

277 ctors being ischemia, immune burden, and the calcineurin inhibitor toxicity score.

278 y, increased creatinine, overdose (primarily calcineurin inhibitor toxicity), acne, urinary tract dis

279 rular diseases, and only 16% had evidence of calcineurin inhibitor toxicity.

280 l cellular or humoral rejection, and chronic calcineurin inhibitor toxicity.

281 ly evident in biopsy specimens obtained from calcineurin inhibitor-treated patients, which might be b

282 ecause of renal function decline and in whom calcineurin inhibitor treatment was subsequently reduced

283 tive antibodies, transplant year, donor age, calcineurin inhibitor treatment, and donor type were fou

284 , HLA mismatches, donor type, donor age, and calcineurin inhibitor treatment.

285 pe (living or deceased), age and gender, and calcineurin inhibitor treatment.

286 In multivariable analysis, high calcineurin inhibitor trough levels in the month before

287 mozygotes were less likely to report topical calcineurin inhibitor use (OR, 0.16; 95% CI, 0.06-0.42),

288 cy for improving renal function and reducing calcineurin inhibitor use, attenuating cardiac allograft

289 nt complication and has been associated with calcineurin inhibitors use.

290 pic dermatitis due to its similarity to oral calcineurin inhibitors used in solid-organ transplantati

291 r IRS and have shown that discontinuation of calcineurin inhibitors was independently associated with

292 relates with the nephron segments injured by calcineurin inhibitors, we hypothesized that NFATc1 play

293 Blood levels of calcineurin inhibitors were monitored, and dosages were

294 ical corticosteroids with or without topical calcineurin inhibitors where inadvisable for topical cor

295 Substituting calcineurin inhibitor with sirolimus as primary immunosu

296 essive weaning protocols, particularly early calcineurin inhibitor withdrawal without lymphocyte-depl

297 .2, 4.0) after transplantation with complete calcineurin inhibitor withdrawal.

298 e primary and secondary prevention trials in calcineurin inhibitor withdrawal.

299 uzumab induction therapy and a steroid-free, calcineurin-inhibitor-withdrawal maintenance regimen.

300 o 4 ng/mL and sirolimus, 4 to 6 ng/mL or, if calcineurin inhibitor-withdrawn, sirolimus 8 to 12 ng/mL