ライフサイエンスコーパス: AKI

1 AKI after cardiac surgery is associated with mortality,

2 AKI after cardiac surgery remains strongly associated wi

3 AKI and CKD are important clinical problems because they

4 AKI associated with an 86% and a 38% increased risk of c

5 AKI associates with increased long-term risk of mortalit

6 AKI carries a significant mortality and morbidity risk.

7 AKI is a frequent complication in hospitalized patients.

8 AKI is a frequent condition that involves renal microcir

9 AKI is associated with a profound and severe increase in

10 AKI is associated with high morbidity and mortality, and

11 AKI is histologically characterized by necrotic cell dea

12 AKI leads to tubular injury and interstitial inflammatio

13 AKI occurred in 2854 (82.5%) patients when they fulfille

14 AKI occurred in 634 patients (15.4%) with RA and 712 pat

15 AKI rates were significantly higher in the VPT group tha

16 AKI was defined as rise in serum creatinine concentratio

17 AKI was defined using a standardized definition -i.e., s

18 AKI was diagnosed in 64,512 patients (12.2%).

19 0% increased mortality compared with stage 1 AKI-SC (14.6% versus 9%; P < 0.001).

20 -fold increase in the odds of mild (stage 1) AKI (aOR, 3.29; 95% CI, 1.25-8.66).

21 et the primary outcome in the early (stage 2 AKI) and delayed (stage 3 AKI) initiation groups, respec

22 Stage 2-3 AKI-UO has a high negative impact on hospital mortality.

23 atients (60.8%) were classified as stage 2-3 AKI.

24 sease Improving Global Outcomes stage 2 or 3 AKI, using an electronic database.

25 % CI: 0.70 to 1.03; p = 0.090), with stage 3 AKI occurring in 28 patients (0.68%) with RA versus 46 p

26 the early (stage 2 AKI) and delayed (stage 3 AKI) initiation groups, respectively (odds ratio [OR] wi

27 ncrease in the odds of severe (stage 2 or 3) AKI (adjusted odds ratio [aOR], 5.22; 95% CI, 1.35-20.22

28 li1(+) pericytes and endothelial cells after AKI (mean+/-SEM: 3.3+/-0.1 microm before injury versus 1

29 s can proliferate to repair the damage after AKI.

30 er protein and mRNA expression 14 days after AKI revealed that wild-type (WT) and Sphk1(-/-) mice exh

31 Mortality after AKI is high, but the causes of death are not well descri

32 Maladaptive repair after AKI may lead to progressive fibrosis and decline in kidn

33 phages contribute to injury and repair after AKI.

34 ole of BRP-39 in profibrotic responses after AKI.

35 he clinical course over the first week after AKI manifestation.

36 mpella 2.5 (pLVAD) support protected against AKI during high-risk PCI.

37 pLVAD during high-risk PCI protected against AKI.

38 c deletion of Rac1 in SMCs protected against AKI.

39 n fraction, pLVAD support protection against AKI persisted (adjusted odds ratio, 0.63; 95% confidence

40 a meeting the urine output criteria for AKI (AKI-UO) and examined its association with clinical outco

41 : 0.62; 95% CI: 0.40 to 0.95; p = 0.03), and AKI (HR: 0.68; 95% CI: 0.58 to 0.81; p < 0.001) compared

42 .76; AKIN 2/3: HR, 2.22; CI, 2.04-2.41), and AKI requiring dialysis (AKIN 1: HR, 2.59; CI, 2.29-2.92;

43 e in eGFR, doubling of serum creatinine, and AKI; however, apixaban did not have a statistically sign

44 th lower risks of >/=30% decline in eGFR and AKI; rivaroxaban was associated with lower risks of >/=3

45 " and "piperacillin" and "tazobactam"] and ["AKI" or "acute renal failure" or "nephrotoxicity"] and r

46 mortality compared with patients without any AKI (14.6% versus 5%; P < 0.001) and more than a 50% inc

47 Acute graft failure was defined as AKI stages 1 to 3 (Acute Kidney Injury Network criteria)

48 57 patients (8.2%) had antibiotic-associated AKI.

49 Ultrasound alone can attenuate AKI and prevent CKD by stimulating the splenic cholinerg

50 lative risk (RR) for the association between AKI and cardiovascular mortality, major cardiovascular e

51 ailure model to test the association between AKI and receipt of IV vancomycin plus piperacillin/tazob

52 %, p = 0.04) Analysis of association between AKI and recipient eGFR suggests a risk of inferior eGFR

53 erval, 1% to 97%) of the association between AKI and the primary outcome.

54 poorly defined, and the relationship between AKI and outcomes after hospital discharge remains unders

55 te immune system has been implicated in both AKI and CKD.

56 diagnosis, monitoring, and treatment of both AKI and CKD, especially considering recent advances in t

57 Expanding our understanding of the burden AKI has on the clinical course of burn patients would hi

58 ata suggest that neonates may be impacted by AKI in a manner similar to pediatric and adult patients.

59 Clinical AKI, measured by serum creatinine elevation, is associat

60 These results suggest that clinical AKI at the time of cardiac surgery is indicative of conc

61 In conclusion, AKI associates with an elevated risk of cardiovascular m

62 cline in eGFR, doubling of serum creatinine, AKI, and kidney failure, respectively.

63 lassified with AKI according to UO criteria (AKI-UO) had nearly a 3-fold increased rate of hospital m

64 Disease Improving Global Outcomes criteria, AKI was 3-fold less prevalent and trended lower with RA

65 eath within 48 hours, inability to determine AKI status or severe congenital kidney abnormalities.

66 ion of children hospitalized for DKA develop AKI.

67 s who received radiocontrast did not develop AKI at a clinically significant higher rate.

68 of children hospitalized for DKA who develop AKI and to identify the associated clinical and biochemi

69 ly patients undergoing PCI, 39 850 developed AKI (8.8% overall; AKIN stage 1, 85.8%; AKIN 2/3, 14.2%)

70 trast was and was not administered developed AKI at rates of 5.5% and 5.6%, respectively.

71 2) of unsupported control patients developed AKI (P<0.001).

72 iver transplantation patients that developed AKI.

73 was the proportion of patients who developed AKI according to Kidney Disease Improving Global Outcome

74 The proportion of patients who developed AKI within 7 days of surgery was similar in THR-184 trea

75 Among patients who developed AKI, the median onset was more rapid in the VPT group co

76 ssociation with patients' risk of developing AKI after PCI.

77 of hypertension, polycystic kidney disease, AKI, and CKD.

78 DGF rates increase with donor AKI stage (p < 0.005), and PNF rates are significantly h

79 During AKI, plasmatic villin 1 levels corresponded with the sev

80 , which occurs in renal tubular cells during AKI.

81 signals to mitochondrial dysfunction during AKI partly via PPARGC1A signaling.

82 ry T cells (Tregs) protect the kidney during AKI.

83 e early gene expressed in the kidneys during AKI.

84 Villin 1 is released in plasma during AKI and shows potential as an early marker for proximal

85 plain the protection conferred by THP during AKI.

86 going cardiac surgery with evidence of early AKI to receive intra-aortic MSCs (AC607; n=67) or placeb

87 When conducted after established AKI, 24 hours after I/R injury, HIFD produced substantia

88 For disease-specific events, AKI associated with a 58% increased risk of heart failur

89 counsel patients with cancer who experience AKI.

90 1 was confirmed in patients who experienced AKI after liver transplantation.

91 t postsurgical AKI, patients who experienced AKI Network stage 2 or 3 had an adjusted hazard ratio fo

92 FA-AKI in mice associates with lipid peroxidation and downr

93 nhibitor zVAD-fmk did not protect against FA-AKI.

94 Additionally, although FA-AKI resulted in increased protein expression of the necr

95 that ferroptosis is the primary cause of FA-AKI and that immunogenicity secondary to ferroptosis may

96 Finally, AKI was associated with a 15% increased risk of stroke (

97 uld be used; however, caution is advised for AKI stage 3 donors.

98 iguria meeting the urine output criteria for AKI (AKI-UO) and examined its association with clinical

99 ed CT was not an independent risk factor for AKI, dialysis, or mortality.

100 y bypass and had recognized risk factors for AKI.

101 that the major sources of heterogeneity for AKI stage I were age (coefficient = 0.06; P = 0.01; adju

102 We sought to examine different patterns for AKI reversal that are found in patients and assess how t

103 py with VPT was an independent predictor for AKI (hazard ratio = 4.27; 95% confidence interval, 2.73-

104 nistration associated with an odds ratio for AKI of 0.93 (95% confidence interval, 0.88 to 0.97).

105 tein-7 agonist, in patients at high risk for AKI after cardiac surgery.

106 ss contrast in patients with higher risk for AKI.

107 tion as a promising therapeutic strategy for AKI.

108 t DRP1 may serve as a therapeutic target for AKI.

109 ance Treg- and ILC2-mediated protection from AKI, bears strong therapeutic potential.

110 (MSCs) in reducing the time to recovery from AKI after cardiac surgery.

111 e immune tolerance, accelerate recovery from AKI, and promote functional improvement in chronic nephr

112 YKL-40 concentration in 1301 donors (111 had AKI, defined as doubling of serum creatinine) and ascert

113 data, 92% had a nephrotic syndrome, 64% had AKI, and 67% had a documented infection.

114 primary outcome was incidence of in-hospital AKI according to AKI network criteria.

115 ermined the relationship between in-hospital AKI and risk of post-discharge adverse events by AKIN st

116 Compared with no AKI, in-hospital AKI was associated with higher post-discharge hazard of

117 During initial hospitalization, AKI was associated with increased pulmonary failure, mec

118 cells in acute folate nephropathy and human AKI.

119 AKI in the Large White pig, a model of human AKI.

120 -1beta) in regulating PPARGC1A expression in AKI.

121 Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show significant poly

122 To examine its function in AKI, we utilized a specific function-blocking antibody t

123 o corroborate the presence of macrophages in AKI and their persistence in progressive chronic kidney

124 oved understanding of pathogenic pathways in AKI may identify novel therapeutic approaches.

125 y associated with a significant reduction in AKI (adjusted odds ratio, 0.13; 95% confidence intervals

126 elated proteins may have additional roles in AKI.

127 To examine the national variation in AKI incidence and contrast use among US physicians and t

128 A large variation in AKI rates was observed among individual physicians rangi

129 I risk was used to identify the variation in AKI rates, the variation in contrast use, and the associ

130 cases showed that the physician variation in AKI remained unchanged.

131 Increased AKI with concomitant vancomycin and piperacillin/tazobac

132 nation was associated with both an increased AKI risk and a more rapid onset of AKI compared to the V

133 In mice, endotoxin injection to induce AKI also induced early and transient inflammation and PP

134 a lower mortality rate in cisplatin-induced AKI.

135 sruption protects against, cisplatin-induced AKI.

136 s and necroptosis to folic acid (FA)-induced AKI in mice.

137 ective effect of MR antagonism in IR-induced AKI in the Large White pig, a model of human AKI.

138 educed the incidence of acute kidney injury (AKI) [odds ratio (OR) = 0.79; P = 0.02; I(2) = 38%], and

139 mine the development of acute kidney injury (AKI) after burn injury as an independent risk factor for

140 oning could also reduce acute kidney injury (AKI) after HIR is unknown.

141 dies comparing rates of acute kidney injury (AKI) among patients receiving vancomycin + piperacillin-

142 ion regimens, including acute kidney injury (AKI) and Clostridium difficile infection (CDI), were als

143 sociated with increased acute kidney injury (AKI) compared to vancomycin without piperacillin/tazobac

144 d with a higher risk of acute kidney injury (AKI) compared with vancomycin plus 1 other beta-lactam a

145 s of donor kidneys with acute kidney injury (AKI) in a large UK cohort.

146 Acute kidney injury (AKI) in children is associated with poor short-term and

147 s and classification of acute kidney injury (AKI) in patients with chronic liver disease (CLD).

148 Acute kidney injury (AKI) is a growing global health concern, yet no treatmen

149 s suggest that neonatal acute kidney injury (AKI) is associated with poor outcomes.

150 RATIONALE: Acute kidney injury (AKI) is common during high-risk percutaneous coronary in

151 Postinterventional acute kidney injury (AKI) occurred in four kidney transplant recipients (KDIG

152 Acute kidney injury (AKI) remains a common complication after percutaneous co

153 Acute kidney injury (AKI) remains a major clinical event with high mortality

154 ttle is known about how acute kidney injury (AKI) resolves, and whether patterns of reversal of renal

155 Ischaemic acute kidney injury (AKI), an inflammatory disease process, often progresses

156 serum creatinine level, acute kidney injury (AKI), and kidney failure.

157 To compare the rates of acute kidney injury (AKI), emergent dialysis, and short-term mortality betwee

158 aminotransferase (ALT), acute kidney injury (AKI), model for end stage liver disease (MELD) and septi

159 , mitigates the risk of acute kidney injury (AKI).

160 One year after injury, AKI was associated with development of chronic kidney di

161 alprotectin was 36 times higher in intrinsic AKI (1955 ng/mL) than in prerenal AKI (P < 0.001).

162 phosphatase, in the development of ischemic AKI in mice.

163 ng the kidney highly susceptible to ischemic AKI.

164 f this approach in patients with IR-mediated AKI.

165 he specific role of vascular MR in mediating AKI induced by IR.

166 Novel strategies that minimize AKI and halt the progression of CKD are urgently needed.

167 e end point of AKI or in-hospital mortality (AKI/death).

168 Interpretation: Neonatal AKI is a common and independent risk factor for mortalit

169 In order to determine whether neonatal AKI is independently associated with increased mortality

170 Donors were classified as no AKI, or AKI stage 1-3 according to Acute Kidney Injury N

171 s a risk of inferior eGFR with AKI versus no AKI (p < 0.005; OR 1.25 [95% CI: 1.08-1.31]).

172 Compared with no AKI, in-hospital AKI was associated with higher post-dis

173 lowest YKL-40 tertile) and recipients of non-AKI donor kidneys (adjusted relative risk, 0.79 [95% CI,

174 dds (95% confidence interval, 1.6 to 9.5) of AKI/death.

175 plasma may be a promising novel biomarker of AKI, death, and other adverse outcomes in critically ill

176 uffer from misclassification of the cause of AKI and confounding.

177 perfusion injury (IRI) is a leading cause of AKI.

178 re universally involved in diverse causes of AKI and CKD.

179 ent are crucial to avoid the consequences of AKI after burn injury.

180 mmation, a key process in the development of AKI and CKD.

181 AKI stage (P=0.53) or the total duration of AKI (P=0.44).

182 duce the incidence, severity, or duration of AKI after cardiac surgery in high-risk patients.

183 e that HIFD performed after establishment of AKI rapidly restores microvascular perfusion and small m

184 sed, 604 patients (17.5%) had no evidence of AKI and had the lowest hospital mortality rate (5%).

185 d T cell transcripts, but less expression of AKI transcripts compared with preexisting DSA ABMR.

186 m health outcomes; however, the frequency of AKI in children hospitalized for diabetic ketoacidosis (

187 thPCI registry, we assessed the incidence of AKI among Medicare beneficiaries after PCI from 2004 to

188 In this study we compared the incidence of AKI among patients receiving combination therapy with VP

189 The authors assessed the incidence of AKI in patients with acute coronary syndrome (ACS) enrol

190 CLD patients have a high incidence of AKI.

191 The primary outcome was the incidence of AKI.

192 criteria increased the measured incidence of AKI.

193 ith a mean adjusted 43% excess likelihood of AKI (median odds ratio, 1.43; 95% CI, 1.41-1.44) for sta

194 sociated clinical and biochemical markers of AKI.

195 ondrial dynamics as an important mediator of AKI and progression to fibrosis and suggest that DRP1 ma

196 that have been evaluated in animal models of AKI and CKD.

197 n therapy was associated with higher odds of AKI each hospital day compared with vancomycin plus 1 ot

198 increased AKI risk and a more rapid onset of AKI compared to the VC combination.

199 our understanding of the pathophysiology of AKI and CKD.

200 ls associate with the composite end point of AKI or in-hospital mortality (AKI/death).

201 ession analysis determined the predictors of AKI.

202 >20% total body surface area, by presence of AKI.

203 ical diagnosis, management, and prognosis of AKI through the combined use of available clinical marke

204 improve the detection and prognostication of AKI are therefore required.

205 receptor CD11b/CD18 prevents progression of AKI to CKD in cynomolgus monkeys.

206 ssociated with AKI and evaluated the rate of AKI between strata.

207 After propensity score adjustment, rates of AKI, dialysis, and mortality were not significantly high

208 Rates of AKI, emergent dialysis, and mortality were compared betw

209 th reduced risk of DGF in both recipients of AKI donor kidneys (adjusted relative risk, 0.51 [95% con

210 Relationship of AKI with delayed graft function/primary nonfunction (DGF

211 ificant association between absolute risk of AKI and receipt of combination regimens across all types

212 d acuity of illness, to estimate the risk of AKI associated with radiocontrast administration within

213 nt, RA was associated with a reduced risk of AKI compared with FA.

214 To assess the risk of AKI in children during concomitant therapy with vancomyc

215 racillin/tazobactam may increase the risk of AKI in hospitalized children.

216 erences regarding risk of SSI versus risk of AKI is needed to improve clinical decision-making.

217 ss all types of surgical procedures, risk of AKI was increased in the combination antimicrobial proph

218 w significant differences in the severity of AKI stage (P=0.53) or the total duration of AKI (P=0.44)

219 ortality, but the prognostic significance of AKI in terms of long-term cardiovascular disease remains

220 eperfusion injury mitigated the worsening of AKI.

221 Patients with transient oliguria (AKI-UO stage 1) had increased mortality rates compared w

222 Donors were classified as no AKI, or AKI stage 1-3 according to Acute Kidney Injury Network (

223 9; P = 0.02; I(2) = 38%], and in particular, AKI stage I (OR = 0.65; P = 0.01; I(2) = 55%).

224 rrelation between contrast use and patients' AKI risk (r = -0.054).

225 cal regression with adjustment for patients' AKI risk was used to identify the variation in AKI rates

226 Post-PCI AKI is associated with increased risk of death, myocardi

227 spital discharge in patients having post-PCI AKI is poorly defined, and the relationship between AKI

228 Post-PCI AKI should be recognized as a significant risk factor no

229 t the highest perceived risk of postcontrast AKI, intravenous administration of iodixanol for contras

230 Postinterventional AKI in these patients is often mild and does not impact

231 edures) and harms (increase in postoperative AKI).

232 Compared with patients without postsurgical AKI, patients who experienced AKI Network stage 2 or 3 h

233 of contrast volume with patients' predicted AKI risk.

234 intrinsic AKI (1955 ng/mL) than in prerenal AKI (P < 0.001).

235 differentiation of intrinsic versus prerenal AKI.

236 harmacologic inhibition of MR also prevented AKI induced by IR in the Large White pig.

237 acologic approach for treating or preventing AKI.

238 arly sepsis are major barriers to preventing AKI after burn injury.

239 ocorticoid receptor (MR) antagonism prevents AKI induced by ischemia-reperfusion (IR).

240 The primary AKI-MATRIX endpoint was AKI, defined as an absolute (>0.

241 After multivariate adjustment, r-AKI associated with increased risk for preeclampsia (adj

242 The effect of clinically recovered AKI (r-AKI) on future pregnancy outcomes is unknown.

243 al to assess whether a previous episode of r-AKI associated with subsequent adverse maternal and feta

244 diastolic BP, parity, and diabetes status, r-AKI remained associated with preeclampsia (OR, 4.7; 95%

245 The r-AKI and control groups had similar prepregnancy serum cr

246 When women with r-AKI and controls were matched 1:2 by age, race, body mas

247 However, women with r-AKI had increased rates of preeclampsia compared with co

248 Infants of women with r-AKI were born earlier than infants of controls (37.6+/-3

249 compared pregnancy outcomes in women with r-AKI without history of CKD (eGFR>90 ml/min per 1.73 m(2)

250 In 45 rats AKI was induced by right nephrectomy and contralateral c

251 in high-iron conditions did not reconstitute AKI after ischemia-reperfusion, whereas macrophages cult

252 The effect of clinically recovered AKI (r-AKI) on future pregnancy outcomes is unknown.

253 KIN 2/3: HR, 2.13; CI, 2.01-2.26), recurrent AKI (AKIN 1: HR, 1.70; CI, 1.64-1.76; AKIN 2/3: HR, 2.22

254 s suggest an important opportunity to reduce AKI by reducing the variation in contrast volumes across

255 ey, we used a bilateral ischemia-reperfusion AKI mouse model, in which gallein attenuated renal dysfu

256 causal, the number needed to harm for severe AKI following cardiac surgery would be 167.

257 ce, MLKL knockout mice displayed more severe AKI.

258 ed with a 22% increase in the odds of severe AKI (aOR, 1.22; 95% CI, 1.07-1.39).

259 In our study, AKI induced Bpifa2 expression in the kidneys of mice wit

260 the noncontrast group for all CKD subgroups (AKI odds ratios [ORs], 0.74-0.91, P = .16-0.69; dialysis

261 We conclude that AKI stage 1 or 2 kidneys should be used; however, cautio

262 This analysis provides direct evidence that AKI causes pericyte detachment from capillaries, and tha

263 as incidence of in-hospital AKI according to AKI network criteria.

264 ) axis and instrumental to the adaptation to AKI associated with endoplasmic reticulum stress.

265 necrosis have been reported to contribute to AKI, but the molecular regulators involved remain unclea

266 igh susceptibility of the aged population to AKI and their increased propensity to develop subsequent

267 contributor to the inflammatory response to AKI.

268 2 as the main driver of post-transplantation AKI.

269 he role of MIOX in cisplatin-induced tubular AKI, we generated conditional MIOX-overexpressing transg

270 Using AKI-UO criteria alone, 2103 patients (60.8%) were classi

271 The primary AKI-MATRIX endpoint was AKI, defined as an absolute (>0.5 mg/dl) or a relative (

272 The primary outcome was AKI on hospital days 3 to 7 and within 2 days of receivi

273 c review and meta-analysis to assess whether AKI associates with long-term cardiovascular disease.

274 tudies involving 254,408 adults (55,150 with AKI) were included.

275 There were 11 219 kidneys (1869 [17%] with AKI) included.

276 F23 levels are prospectively associated with AKI and death in critically ill patients is unknown.

277 relatively common diagnoses associated with AKI and evaluated the rate of AKI between strata.

278 o identify potential factors associated with AKI.

279 Donors with AKI had higher urinary YKL-40 concentration (P<0.001) an

280 failure at 1 year is greater for donors with AKI than for those without (graft survival 89% vs. 91%,

281 r graft-survival of kidneys from donors with AKI.

282 t eGFR suggests a risk of inferior eGFR with AKI versus no AKI (p < 0.005; OR 1.25 [95% CI: 1.08-1.31

283 potential confounding factors, infants with AKI had higher mortality compared to those without AKI [

284 Deceased donor kidneys with AKI are often discarded for fear of poor transplant outc

285 However, RIPK3 knockout mice with AKI had less inflammation than their wild-type counterpa

286 ation of RRT in Critically Ill Patients with AKI (ELAIN) Trial from 90 days to 1 year after randomiza

287 In these patients with AKI after cardiac surgery, administration of allogeneic

288 I], 0.86 to 0.96; P=0.001) for patients with AKI but did not change in patients without AKI (from 1.5

289 ation of RRT in critically ill patients with AKI can improve outcomes remains debated.

290 Notably, patients with AKI had higher blood and urine levels of BPIFA2 than did

291 of RRT in these critically ill patients with AKI significantly reduced the occurrence of major advers

292 9.3 to 9.0 days (P<0.001) for patients with AKI, with no change for patients without AKI.

293 asing from 7.2 to 6.0 days for patients with AKI.

294 and in-hospital mortality for patients with AKI.

295 ABBA disease were elderly and presented with AKI and subnephrotic proteinuria.

296 Patients reclassified with AKI according to UO criteria (AKI-UO) had nearly a 3-fol

297 tudies that examined adults with and without AKI and reported a multivariable-adjusted relative risk

298 ses of mortality in patients with or without AKI.

299 h AKI but did not change in patients without AKI (from 1.5% to 1.4%).

300 ith AKI, with no change for patients without AKI.

301 d higher mortality compared to those without AKI [(59/605 (9.7%) vs. 20/1417 (1.4%); p< 0.001; adjust