ライフサイエンスコーパス: calcineurin inhibitor

1 herapy (steroids, mycophenolate mofetil, and calcineurin inhibitor).

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

3 c anti-inflammatory drug Tacrolimus (TAC), a calcineurin inhibitor.

4 ression included mycophenolate mofetil and a calcineurin inhibitor.

5 uppression toward lower doses especially for calcineurin inhibitors.

6 ications for immunosuppressive therapy using calcineurin inhibitors.

7 cations, especially glucocorticosteroids and calcineurin inhibitors.

8 immunosuppression compared to patients given calcineurin inhibitors.

9 in in organ transplant recipients treated by calcineurin inhibitors.

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

11 e treatment with topical glucocorticoids and calcineurin inhibitors.

12 in SCC development following treatment with calcineurin inhibitors.

13 s and azathioprine without administration of calcineurin inhibitors.

14 vation and reduce the nephrotoxic effects of calcineurin inhibitors.

15 ew-onset diabetes after transplantation with calcineurin inhibitors.

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

17 ars) from transplantation were maintained on calcineurin inhibitors.

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

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

20 nteract with immunosuppressive drugs such as calcineurin inhibitors.

21 nosuppressive agents were antimetabolites or calcineurin inhibitors.

22 ors probably reduced skin cancer compared to calcineurin inhibitors (12 trials, 2225 participants, RR

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

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

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

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

27 ) and graft-versus-host disease prophylaxis (calcineurin inhibitor and mycophenolate).

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

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

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

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

32 mplementation of this strategy to avoid both calcineurin inhibitors and corticosteroids at this time.

33 mitigate early rejection risk while limiting calcineurin inhibitors and corticosteroids.

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

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

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

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

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

39 rity and responsiveness to topical steroids, calcineurin inhibitors and step-up treatment.

40 es are limited by toxicities associated with calcineurin inhibitors and steroids.

41 Nephrotoxicity of calcineurin inhibitors and uncontrolled effector functio

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

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

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

45 r monoclonal antibodies, 28% did not receive calcineurin inhibitors, and 36% did not receive steroids

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

47 opical corticosteroids, vitamin D analogues, calcineurin inhibitors, and keratolytics.

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

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

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

53 Calcineurin inhibitors are associated with adverse cardi

54 The antitumor effects of calcineurin inhibitors are associated with the reduced e

55 e development of CIPS.SIGNIFICANCE STATEMENT Calcineurin inhibitors are immunosuppressants used to pr

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

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

64 an HEart transplant De-novo stUdy with earLy calcineurin inhibitors avoidancE trial was a prospective

65 an HEart transplant De-novo stUdy with earLy calcineurin inhibitors avoidancE trial was the first ran

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 Until measurement of unbound fraction of calcineurin inhibitors becomes clinically available, we

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

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

76 Calcineurin inhibitors cause vascular and renal injury a

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

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

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

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

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

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

83 d the association of optimal-dose mTORi with calcineurin inhibitor (CNI) have excluded hypersensitize

84 d the association of optimal-dose mTORi with Calcineurin Inhibitor (CNI) have excluded hypersensitize

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

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

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 ipients with renal dysfunction attributed to calcineurin inhibitor (CNI) nephrotoxicity.

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

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

93 As conversion from calcineurin inhibitor (CNI) to sirolimus (SRL), an mTOR-

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

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

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

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

98 Early calcineurin inhibitor (CNI) withdrawal with mycophenolat

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

100 -1a) cells, which were highly sensitive to a calcineurin inhibitor (CNI), while co-stimulation of TLR

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

102 kidney (SPK) recipients were randomized to a calcineurin inhibitor (CNI)-based immunosuppressive regi

103 Calcineurin inhibitor (CNI)-based therapy is associated

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

105 dy sought to examine whether conversion from calcineurin inhibitor (CNI)-based to SRL-based IS was as

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

107 A calcineurin inhibitor (CNI)-free immunosuppressive regim

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

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

110 Calcineurin inhibitor (CNI)-related acute nephrotoxicity

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

112 mbination of mycophenolates (MMF/MPA) with a calcineurin inhibitor (CNI).

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

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

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

116 and safety of belatacept when converted from calcineurin inhibitors (CNI) in HLA-sensitized (HS) kidn

117 and safety of belatacept when converted from calcineurin inhibitors (CNI) in HLA-sensitized kidney tr

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

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

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

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

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

123 0 with our usual triple immunosuppression of calcineurin inhibitors (CNI), mycofenolate sodium (MMF),

124 The long-term use of calcineurin inhibitors (CNIs) after liver transplantatio

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

126 Calcineurin inhibitors (CNIs) are among the most effecti

127 Calcineurin inhibitors (CNIs) are essential immunosuppre

128 Calcineurin inhibitors (CNIs) are immunosuppressive drug

129 Maintenance steroids and calcineurin inhibitors (CNIs) at discharge were associat

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

131 Calcineurin inhibitors (CNIs) have an unfavorable cardio

132 Calcineurin inhibitors (CNIs) have failed to improve lon

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

134 Calcineurin inhibitors (CNIs) in combination with predni

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

136 pressive regimen mostly relies on converting calcineurin inhibitors (CNIs) into EVL.

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

138 Calcineurin inhibitors (CNIs) revolutionized the field o

139 Calcineurin inhibitors (CNIs) target NFAT activation.

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

141 been partially attributed to treatment with calcineurin inhibitors (CNIs).

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

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

144 tics and concurrent graft function and blood calcineurin inhibitor concentration.

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

146 Calcineurin inhibitor cyclosporin A (CsA) and calcineuri

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

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

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

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

154 For decades, GVHD prophylaxis has included calcineurin inhibitors, despite their incomplete efficac

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 clinically available, we recommend to adjust calcineurin inhibitor dose according to whole blood trou

158 If nephrotoxicity is suspected, the calcineurin inhibitor dose should be reduced.

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

160 cipients consecutively converted to EVL with calcineurin inhibitor elimination.

161 strategy of transplant immunosuppression is calcineurin inhibitor elimination.

162 llograft rejection without using steroids or calcineurin inhibitors, enriches for naive cells suscept

163 Calcineurin inhibitors exacerbate renal dysfunction and

164 understanding the association between early calcineurin inhibitors exposure post-liver transplantati

165 The calcineurin inhibitor FK506 (tacrolimus) reduced cell de

166 nsistently, AMPA receptor antagonist CNQX or calcineurin inhibitor FK506 abolished the S-SCAM overexp

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

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

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

170 The calcineurin inhibitor FK506 prevented contrast-induced a

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

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

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

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

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

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

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

181 28-CD80/86 costimulatory pathway, allows for calcineurin-inhibitor free immunosuppressive therapy in

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

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

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

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

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

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

188 Likewise, alternatives to calcineurin inhibitors have been investigated as a strat

189 Calcineurin inhibitors have shown evidence to promote ca

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

191 Cyclosporine and tacrolimus are calcineurin inhibitor immunosuppressants used to prevent

192 To reduce calcineurin inhibitor immunosuppression and preserve kid

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

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

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

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

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

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

199 Calcineurin inhibitors induce detrimental vascular remod

200 Calcineurin inhibitors induce nephrotoxicity through poo

201 Calcineurin inhibitors induce production of renin in the

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

203 alpha2delta-1 is essential for calcineurin inhibitor-induced aberrant activation of pre

204 Calcineurin inhibitor-induced neurotoxicity (CIIN) is a

205 ting alpha2delta-1-NMDAR interaction reduces calcineurin inhibitor-induced pain hypersensitivity.

206 neurons or alpha2delta-1 KO also attenuates calcineurin inhibitor-induced pain hypersensitivity.

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

208 re pain in patients, commonly referred to as calcineurin inhibitor-induced pain syndrome (CIPS).

209 cate that alpha2delta-1-bound NMDARs mediate calcineurin inhibitor-induced tonic activation of presyn

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

211 The use of calcineurin inhibitors is associated with chronic nephro

212 Use of calcineurin inhibitors is associated with HTN.

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

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

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

216 to analyze this association exploring median calcineurin inhibitor levels and intrapatient variabilit

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

218 egimes (azathioprine, mycophenolate mofetil, calcineurin inhibitors, mammalian target of rapamycin [m

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

220 Topical calcineurin inhibitors may be used in steroid-dependent/

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

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

223 Calcineurin inhibitors might be developed to prevent pos

224 Strategies allowing calcineurin inhibitor minimization while maintaining eff

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

226 115 days posttransplant to convert from CNI (calcineurin inhibitor)/MMF to sirolimus (SRL)/MMF had a

227 ment of dnDSA in 69 LT patients who received calcineurin inhibitor monotherapy and were enrolled in t

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

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

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

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

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

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

234 Enhancement of calcineurin inhibitor nephrotoxicity by sirolimus (SRL)

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

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

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

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

239 atacept, induction agents, and withdrawal of calcineurin inhibitors or corticosteroids).

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

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

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

243 The calcineurin inhibitors reduced the intra-acinar activati

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

245 4s with the immunosuppressant cyclosporin, a calcineurin inhibitor, robustly inhibited HIV-1 reactiva

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

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

248 Calcineurin inhibitor-sparing or reduction regimens usin

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

250 Calcineurin inhibitors successfully control rejection of

251 Calcineurin inhibitors such as cyclosporine A (CsA) were

252 Calcineurin inhibitors such as cyclosporine A and FK506

253 Calcineurin inhibitors, such as cyclosporin A and tacrol

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

255 Calcineurin inhibitors, such as tacrolimus (FK506) and c

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

257 Calcineurin inhibitors, such as tacrolimus, used for hum

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

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

260 Treatment with sirolimus, but not the calcineurin inhibitor tacrolimus, at levels routinely ac

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

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

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

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

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

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

267 interstitial fibrosis/tubular atrophy versus calcineurin inhibitor therapy.

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

269 Calcineurin-inhibitor therapy is a contributing factor t

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

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

272 ive patients were treated with conversion of calcineurin inhibitor to mammalian target of rapamycin i

273 As conversion from calcineurin inhibitor to sirolimus (SRL), a mechanistic

274 Although conversion from calcineurin inhibitors to mammalian target of rapamycin

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

276 Switching from calcineurin inhibitors to sirolimus had an antitumoral e

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

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

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

280 CKD was related to calcineurin inhibitors toxicity in 38 (84.4%) cases.

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

285 , HLA mismatches, donor type, donor age, 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 Antimetabolites +/- calcineurin inhibitors were held or reduced.

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 nt included antimetabolite withdrawal (68%), calcineurin inhibitor withdrawal (23%), hydroxychloroqui

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

298 .2, 4.0) after transplantation with complete 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