ライフサイエンスコーパス: acute kidney injury

1 vs no acute kidney injury and mild-moderate acute kidney injury).

2 one (<1%) patient in the chemotherapy group (acute kidney injury).

3 Three out of 6 patients developed acute kidney injury.

4 h as glomerulosclerosis, renal fibrosis, and acute kidney injury.

5 g Global Outcomes urine output criterion for acute kidney injury.

6 sion, withdrawals due to adverse events, and acute kidney injury.

7 often leads to severe and poorly reversible acute kidney injury.

8 nts were included in whom 50 with persistent acute kidney injury.

9 , 3.5; 95% CI, 1.9-6.5) were associated with acute kidney injury.

10 with elevated serum creatinine suggestive of acute kidney injury.

11 ols to distinguish transient from persistent acute kidney injury.

12 ical ventilation were associated with severe acute kidney injury.

13 CL-K1)), initiates complement activation and acute kidney injury.

14 or-binding protein 7 to predict a persistent acute kidney injury.

15 ter survival time and increased incidence of acute kidney injury.

16 GFBP7) have been validated as biomarkers for acute kidney injury.

17 are of critically ill patients with oliguric acute kidney injury.

18 oplasmic recruitment confers protection from acute kidney injury.

19 ed patients with decompensated cirrhosis and acute kidney injury.

20 eloped end-stage kidney disease, and 943 had acute kidney injury.

21 ent therapy for critically ill patients with acute kidney injury.

22 cohol misuse may allow for the prevention of acute kidney injury.

23 e patients died (30%), and 5 (50%) developed acute kidney injury.

24 CD47 limits autophagy to promote acute kidney injury.

25 d establish a causal link between TMEM33 and acute kidney injury.

26 tabolism, thereby protecting kidneys against acute kidney injury.

27 ing continuous renal replacement therapy for acute kidney injury.

28 mia was significantly associated with severe acute kidney injury.

29 ed with 3.0%; p < 0.0001) had higher risk of acute kidney injury.

30 poreal membrane oxygenation may help prevent acute kidney injury.

31 o hemopexin concentration is associated with acute kidney injury.

32 inflammation and cardiac injury, and severe acute kidney injury.

33 ey disease, and ischemia/reperfusion-induced acute kidney injury.

34 3 +/- 11 mL/min/1.73 m2, and 82% had stage 3 acute kidney injury.

35 acute kidney injury was defined as stage 2/3 acute kidney injury.

36 to malaria and develop high plasma heme and acute kidney injury.

37 e to differentiate transient from persistent acute kidney injury.

38 ave severe COVID-19 are at increased risk of acute kidney injury.

39 ney disease (0.65, 0.53-0.81, p<0.0001), and acute kidney injury (0.75, 0.66-0.85, p<0.0001), with co

40 farction/stroke (5.2% versus 7.5%; P<0.001), acute kidney injury (10.5% versus 11.9%; P=0.043), fasci

41 y Disease: Improving Global Outcomes stage 3 acute kidney injury; 14 patients (5.4%) died before the

42 ory failure (8.2% versus 6.2%, P<0.0001) and acute kidney injury (21.8% versus 18.5%, P<0.0001), but

43 cardial infarction (5.0% vs 3.0%, P = 0.03), acute kidney injury (25% vs 16%, P < 0.001), and new dia

44 ction (cDCD: 18% versus DBD: 32%; P = 0.11), acute kidney injury (26% versus 33%; P = 0.49), 90-d gra

45 readmissions (46.2% vs 25.0%; P = .02), and acute kidney injury (31.2% vs 50.0%; P = .03).

46 %, respectively), as was the percentage with acute kidney injury (4.1% and 4.4%, respectively).

47 yponatremia (67.5% versus 22.5%; P < 0.001), acute kidney injury (62.5% versus 30%; P = 0.001), and i

48 Complications during admission included: acute kidney injury (63%), transaminitis (31%), shock (3

49 90% CI, -7.5 to 5.7]; P(equivalence)=0.011); acute kidney injury, 9.0% versus 9.2% (rate difference,

50 om electronic health records(2-17) and using acute kidney injury-a common and potentially life-threat

51 e number of days free from coma or delirium, acute kidney injury according to severity, the number of

52 Further, these studies define acute kidney injury according to thresholds of serum cre

53 Furthermore, these studies define acute kidney injury according to thresholds of serum cre

54 that remote ischemic preconditioning reduces acute kidney injury (acute kidney injury) in high-risk p

55 significantly improve treatment outcomes in acute kidney injury, acute liver injury and wound healin

56 ociated with mortality in patients with both acute kidney injury (adjusted relative risk, 2.38; 95% C

57 ted relative risk, 1.66; 95% CI, 1.39-1.98), acute kidney injury (adjusted relative risk, 2.63; 95% C

58 acute kidney injury (compared with nonsevere acute kidney injury; adjusted odds ratio 1.04; 95% CI, 1

59 nged cold ischemia (CI) is a risk factor for acute kidney injury after kidney transplantation.

60 Acute kidney injury (AKI) after liver transplantation is

61 Acute kidney injury (AKI) after major trauma is associat

62 The incidence of acute kidney injury (AKI) and AKI requiring dialysis (AK

63 rug (NSAID) administration and postoperative acute kidney injury (AKI) and anastomotic leak.

64 Acute kidney injury (AKI) and cardiorenal syndrome (CRS)

65 ports a protective role for this activity in acute kidney injury (AKI) and chronic kidney disease (CK

66 inalysis in the mouse models of drug-induced acute kidney injury (AKI) and chronic kidney disease (CK

67 sfunction is involved in the pathogenesis of acute kidney injury (AKI) and chronic kidney disease, as

68 s vary in risk for adverse events, including acute kidney injury (AKI) and Clostridium difficile infe

69 to sepsis, the development of sepsis-induced acute kidney injury (AKI) and on survival.

70 traoperative fluid balance and postoperative acute kidney injury (AKI) and other postoperative compli

71 associated with a high risk of postoperative acute kidney injury (AKI) and subsequent loss of kidney

72 Malnutrition is common in patients with acute kidney injury (AKI) and the risk of mortality is h

73 chemic postconditioning (IPo) on IIR-induced acute kidney injury (AKI) and the underling cellular sig

74 Kidneys from deceased donors with acute kidney injury (AKI) are more likely to be discarde

75 nce and our primary outcome was the grade of acute kidney injury (AKI) at 48 hours after surgery.

76 inergic receptor (P2X4) exacerbates ischemic acute kidney injury (AKI) by promoting renal tubular inf

77 Nephrotoxins contribute to 20%-40% of acute kidney injury (AKI) cases in the intensive care un

78 st material (ICM) had a similar frequency of acute kidney injury (AKI) compared with a propensity sco

79 The risk of acute kidney injury (AKI) developing in patients with re

80 s from donation after cardiac death (DCD) or acute kidney injury (AKI) donors may experience delayed

81 ed by whether they developed hypotension and acute kidney injury (AKI) during the index hospitalizati

82 Acute kidney injury (AKI) following cardiac surgery sign

83 ed terminal creatinine likely resulting from acute kidney injury (AKI) had higher odds of kidney nonp

84 While its association with acute kidney injury (AKI) has waxed and waned, recent da

85 eceased donors with serum creatinine-defined acute kidney injury (AKI) have similar allograft surviva

86 kidneys from donors with moderate to severe acute kidney injury (AKI) have similar outcomes to recip

87 Initial reports indicate a high incidence of acute kidney injury (AKI) in Coronavirus Disease 2019 (C

88 This study aimed to investigate the risk of acute kidney injury (AKI) in hospitalized patients based

89 The occurrence of acute kidney injury (AKI) in patients with end-stage liv

90 Acute kidney injury (AKI) initiates a complex pathophysi

91 Acute kidney injury (AKI) is a common clinical condition

92 Acute kidney injury (AKI) is a devastating condition wit

93 Acute kidney injury (AKI) is a frequent complication of

94 In catheter-based procedures, acute kidney injury (AKI) is a frequent, serious complic

95 Acute kidney injury (AKI) is a major clinical concern in

96 Acute kidney injury (AKI) is a major health problem affe

97 Acute kidney injury (AKI) is a serious condition affecti

98 Acute kidney injury (AKI) is associated with prolonged h

99 Acute kidney injury (AKI) is characterized by injury to

100 Acute kidney injury (AKI) is common in hospital patients

101 Acute kidney injury (AKI) is defined by a rapid increase

102 have resulted in a growing appreciation that acute kidney injury (AKI) is increasing in its incidence

103 nic kidney disease (CKD) after an episode of acute kidney injury (AKI) is known in patients without c

104 Recent evidence suggests that acute kidney injury (AKI) is the main predictor of postp

105 potension is associated with new significant acute kidney injury (AKI) or major adverse kidney events

106 n in such settings are at particular risk of acute kidney injury (AKI) owing to preventable and/or re

107 Background Acute kidney injury (AKI) remains a concern in hospitali

108 under the concentration-time curve (AUC) and acute kidney injury (AKI) reported across recent studies

109 he presence of proteinuria and haematuria to acute kidney injury (AKI) requiring renal replacement th

110 ation of a pair of donor kidneys with severe acute kidney injury (AKI) secondary to rhabdomyolysis.

111 more likely to discard deceased donors with acute kidney injury (AKI) versus without AKI (30% versus

112 cutive patients with ACLF diagnosed with HRS acute kidney injury (AKI) were randomized to albumin wit

113 repair process can result in recovery after acute kidney injury (AKI) with adaptive proliferation of

114 splantation recipients to assess the risk of acute kidney injury (AKI) with NSAID use.

115 usted odds ratios (aORs) for community-onset acute kidney injury (AKI) within 3 months and new-onset

116 Patients taking NSBB developed acute kidney injury (AKI) within 90 days more frequently

117 th initial myeloma cast nephropathy (CN) and acute kidney injury (AKI) without need for dialysis.

118 Rationale: Acute kidney injury (AKI), a common complication of seps

119 metabolic waste accumulation- manifesting as acute kidney injury (AKI), a common disorder associated

120 Ischemic acute kidney injury (AKI), a complication that frequentl

121 l-cause 30-day mortality, 7-day incidence of acute kidney injury (AKI), and 30-day incidence of Clost

122 of ceftolozane/tazobactam on clinical cure, acute kidney injury (AKI), and in-hospital mortality.

123 inadvertently omitted from the graph for the acute kidney injury (AKI), double knockout (-/-), S-nitr

124 (AI) has demonstrated promise in predicting acute kidney injury (AKI), however, clinical adoption of

125 In acute kidney injury (AKI), substantial decreases in the

126 edia represents a cause of hospital-acquired acute kidney injury (AKI), targeted preventive strategie

127 n plays a key role in the pathophysiology of acute kidney injury (AKI), the influence of mitochondria

128 Acute kidney injury (AKI), which increases FGF23 levels,

129 the pathogenesis of ischemic and nephrotoxic acute kidney injury (AKI).

130 unnecessary dose reduction in the setting of acute kidney injury (AKI).

131 ted in the pathogenesis of cisplatin-induced acute kidney injury (AKI).

132 as reported to have the potential to lead to acute kidney injury (AKI).

133 Secondary outcomes included acute kidney injury (AKI).

134 d non-burned trauma patients are at risk for acute kidney injury (AKI).

135 d 90; persistent bacteremia at days 2 and 5; acute kidney injury (AKI); microbiological relapse; micr

136 (EAD; 70.8% vs 45.6% and 8.3%; P = .02), and acute kidney injury (AKI; 39.1% vs 19.4%; P = .02) than

137 r and histologic features reflecting injury (acute kidney injury [AKI] and atrophy-fibrosis [chronic

138 .73 m(2) prior to and after LT (irreversible acute kidney injury [AKI]), (2) eGFR < 30 mL/minute/1.73

139 cutoff levels seem reliable in patients with acute kidney injury and "acute on chronic" renal dysfunc

140 confidence interval [CI], 1.77 to 3.99) for acute kidney injury and 2.29 (95% CI, 1.71 to 3.06) for

141 sociated with a 53% reduction in the odds of acute kidney injury and a 2.6-fold higher odds of pharma

142 lting high incidence of diarrhea can lead to acute kidney injury and death, particularly in the young

143 with lower rates of complications, including acute kidney injury and death.

144 vels were associated with the development of acute kidney injury and decreased survival.

145 d protein S-nitrosylation, protected against acute kidney injury and improved survival, whereas this

146 severe acute kidney injury (p <= 0.001 vs no acute kidney injury and mild-moderate acute kidney injur

147 ecipients with COVID-19 have higher rates of acute kidney injury and mortality.

148 e relatively scarce data among patients with acute kidney injury and those with risk factors for chro

149 ey injury, to incomplete kidney repair after acute kidney injury and to chronic kidney disease of var

150 e analysis may help quantify the severity of acute kidney injury and to gauge the efficacy of dialysi

151 t nephropathy who required haemodialysis for acute kidney injury and who received a bortezomib-based

152 ular loss, and renal fibrosis after ischemic acute kidney injury and, thus, can prevent progression t

153 derate acute kidney injury (p <= 0.001 vs no acute kidney injury) and 58% in severe acute kidney inju

154 disease severity (coma, number of seizures, acute kidney injury) and sociodemographic factors.

155 ntestinal hemorrhage, anaphylactic reaction, acute kidney injury, and acute myocardial infarction.

156 allograft dysfunction (EAD), L-GrAFT score, acute kidney injury, and comprehensive complication inde

157 vascular and bleeding complications, stroke, acute kidney injury, and mortality) were evaluated and d

158 tients with de novo multiple myeloma, severe acute kidney injury, and myeloma cast nephropathy relati

159 oglobin concentrations, malaria retinopathy, acute kidney injury, and prolonged coma duration, all P

160 f bleeding (>2.5-fold variation), and death, acute kidney injury, and stroke (all ~1.5-fold variation

161 ns, including myocardial infarction, stroke, acute kidney injury, and transplantation.

162 ering dialysate temperature in patients with acute kidney injury are scarce.

163 , cerebrovascular accident, and stage 2 to 3 acute kidney injury at 30 days were secondary end points

164 nfection requiring antibiotic treatment, and acute kidney injury at 30 days.

165 We assessed the risk of acute kidney injury at 7 days as the primary outcome and

166 All children were diagnosed and staged for acute kidney injury based on the level of serum creatini

167 ion of constitutive hypouricemia may prevent acute kidney injury by avoidance of dehydration and exce

168 g of AMPK protects against cisplatin-induced acute kidney injury by enhancing autophagy in renal prox

169 Contrast-associated acute kidney injury (CA-AKI) associates with an increase

170 nts at increased risk of contrast-associated acute kidney injury (CA-AKI) can help target risk mitiga

171 oncern over associations between PPI use and acute kidney injury, chronic kidney disease, end-stage r

172 echnology-based drug delivery approaches for acute kidney injury, chronic kidney disease, renal fibro

173 hin day 5 or discharge were used to classify acute kidney injury classification into stages.

174 ) of 42 patients and were pneumonitis (n=2), acute kidney injury, colitis, hypokalaemia, and adrenal

175 decreased mortality, and decreased rates of acute kidney injury compared with colistin-based regimen

176 nificant higher intensities in patients with acute kidney injury compared with control patients with

177 nding protein 7] and significantly decreased acute kidney injury compared with controls.

178 hyperferritinemia was associated with severe acute kidney injury (compared with nonsevere acute kidne

179 iagnostic value for the prediction of septic acute kidney injury courses requiring renal replacement

180 Secondarily, we considered acute kidney injury (creatinine concentration >= 0.3 mg/

181 brane oxygenation implantation, of a stage 3 acute kidney injury defined by the Kidney Disease: Impro

182 Acute kidney injury developed in 318 patients (8%) who h

183 In multiple myeloma, severe acute kidney injury due to myeloma cast nephropathy is c

184 cute ischemic stroke patients are at risk of acute kidney injury due to volume depletion, contrast ex

185 namic status of critically ill patients with acute kidney injury during prolonged intermittent renal

186 sion correlates with increased mortality and acute kidney injury early after transcatheter aortic val

187 The development of acute kidney injury, even when mild-moderate in severity

188 In early experimental septic acute kidney injury, fluid bolus therapy transiently imp

189 Acute kidney injury-free data was not pooled, since the

190 therapy, acute kidney injury incidence, and acute kidney injury-free days.

191 on and arrhythmia, acute coronary syndromes, acute kidney injury, gastrointestinal symptoms, hepatoce

192 nal resistive index was higher in persistent acute kidney injury group.

193 ed with higher rates of hospitalization with acute kidney injury (hazard ratio, 1.66 [95% CI, 1.10-2.

194 atio, 2.07 [95% CI, 1.06-4.05]; P=0.034) and acute kidney injury (hazard ratio, 4.35 [95% CI, 2.21-8.

195 k ratio, 0.90; 95% CI, 0.74-1.10; p = 0.31), acute kidney injury, ICU or hospital length of stay comp

196 , cerebrovascular accident in 38 (1.5%), and acute kidney injury in 125 (4.8%) cases.

197 red in 48 of 116 patients (41.4%) and severe acute kidney injury in 32 of 116 (27.6%) patients, which

198 The occurrence rate of acute kidney injury in acute ischemic stroke patients wa

199 te and identified predictors associated with acute kidney injury in acute ischemic stroke patients.

200 tomography in the prevention of postcontrast acute kidney injury in adults with chronic kidney diseas

201 infusion was associated with a reduction in acute kidney injury in critically ill adults (odds ratio

202 he impact of vancomycin infusion strategy on acute kidney injury in critically ill adults.

203 sistive index in predicting reversibility of acute kidney injury in critically ill patients.

204 formance for predicting the reversibility of acute kidney injury in critically ill patients.

205 Acute kidney injury in decompensated cirrhosis has limit

206 high level of suPAR predisposed patients to acute kidney injury in multiple clinical contexts, and w

207 Renal presentation was acute kidney injury in patients with LCCD and CN, and ch

208 Although short-term outcomes for acute kidney injury in pediatric inflammatory multisyste

209 available evidence for and against increased acute kidney injury in the setting of vancomycin and pip

210 uPAR) as a therapeutic strategy to attenuate acute kidney injury in transgenic mice receiving contras

211 High suPAR levels were associated with acute kidney injury in various clinical and experimental

212 preconditioning reduces acute kidney injury (acute kidney injury) in high-risk patients undergoing ca

213 [0.37-0.92]; p = 0.02; I = 49%) and a lower acute kidney injury incidence (odds ratio, 0.58 [0.37-0.

214 zed: the need for renal replacement therapy, acute kidney injury incidence, and acute kidney injury-f

215 To examine secondary objectives including acute kidney injury incidence, we included an observatio

216 Occurrence of acute kidney injury increased the risk of death within 3

217 Acute kidney injury is a frequent complication in this p

218 Acute kidney injury is a severe disease with high morbid

219 Acute kidney injury is common, with a major effect on mo

220 ough the recognition and prompt treatment of acute kidney injury is known to be challenging, our appr

221 c injury during renal transplantation, where acute kidney injury is known to correlate with poor graf

222 itions such as sepsis, diabetes, chronic and acute kidney injury, ischemia/reperfusion, atheroscleros

223 ng Global Outcomes urine output criteria for acute kidney injury lack specificity for identifying pat

224 farction/stroke, any amputation, fasciotomy, acute kidney injury, major bleeding, transfusion, vascul

225 However, employing data science to predict acute kidney injury might be more challenging than it se

226 Acute kidney injury must be carefully monitored when ATM

227 l ventilation, major bleeding, occurrence of acute kidney injury, need for renal-replacement therapy,

228 cutoff levels were applied in patients with acute kidney injury (negative predictive value, 98.8%; s

229 AKI was defined by using Acute Kidney Injury Network SCr-related criteria.

230 e 15.2 [9.8, 23.0] ng/mL; P < 0.001), higher Acute Kidney Injury Network stage (stage I 13.4 [9.8, 20

231 Any-stage acute kidney injury occurred in 48 of 116 patients (41.4

232 llow-up period of 52 days (IQR: 16-66 days), acute kidney injury occurred in 52% cases, with respirat

233 Severe acute kidney injury occurred in just over a quarter of c

234 was significantly higher among patients with acute kidney injury (odds ratio, 2.7; 95% CI, 1.4-4.9) a

235 y Disease: Improving Global Outcomes stage 3 acute kidney injury (odds ratio, 2.81 [95% CI, 1.31-6.07

236 ilar, nonsignificant result was observed for acute kidney injury: odds ratio, 1.08 (95% CI, 1.00-1.17

237 The impact of acute kidney injury on the ventilatory management of pat

238 ration (one [2%]), hyperkalaemia (one [2%]), acute kidney injury (one [2%]), and pulmonary oedema (on

239 Acute kidney injury only occurred in the CI+Txp group, w

240 fter 596 critically ill patients with severe acute kidney injury or clinical indications for initiati

241 injury at 7 days as the primary outcome and acute kidney injury or death at 90 days as a secondary o

242 y injury and 2.29 (95% CI, 1.71 to 3.06) for acute kidney injury or death at 90 days.

243 primary endpoint being development of severe acute kidney injury or death within 1 week.

244 group III GBCM for an MRI in a patient with acute kidney injury or eGFR less than 30 mL/min per 1.73

245 all-cause mortality and hospitalization with acute kidney injury or hyperkalemia using Cox regression

246 rum creatinine may herald the development of acute kidney injury or reflect normal physiology.

247 Data were scant for patients with acute kidney injury or those at risk for chronic kidney

248 In addition to predicting future acute kidney injury, our model provides confidence asses

249 acute kidney injury to 50% in mild-moderate acute kidney injury (p <= 0.001 vs no acute kidney injur

250 vs no acute kidney injury) and 58% in severe acute kidney injury (p <= 0.001 vs no acute kidney injur

251 idates for the risk stratification of septic acute kidney injury patients with the need for renal rep

252 delines for prophylaxis against postcontrast acute kidney injury (PC-AKI) in 2018 (ESUR 10.0).

253 , ketoacidosis, bone fractures, amputations, acute kidney injury, perineal necrotizing fasciitis, and

254 When kidney CD4+ cells of post-acute kidney injury (post-AKI) rats were stimulated with

255 prehensive complication index and grades 2-3 acute kidney injury rate.

256 Kidney Disease: Improving Global Outcomes 3 acute kidney injury received renal replacement therapy,

257 Among critically ill patients with acute kidney injury receiving continuous kidney replacem

258 -threatening bleeding requiring transfusion, acute kidney injury requiring dialysis, or major vascula

259 There was a trend toward higher risk of acute kidney injury requiring renal replacement therapy

260 cell-associated neurotoxicity syndrome, and acute kidney injury requiring renal replacement therapy

261 Acute kidney injury requiring renal replacement therapy

262 k study evaluated 1,124 patients with severe acute kidney injury requiring renal replacement therapy.

263 Organ failure was categorized as acute kidney injury, respiratory failure, hepatic failur

264 t between 0.3 and 0.5mL/kg/hr), or 3) severe acute kidney injury (serum creatinine > 354 umol/L or re

265 serum creatinine or urine output into: 1) no acute kidney injury (serum creatinine < 132 umol/L or ur

266 ne output >= 0.5 mL/kg/hr), 2) mild-moderate acute kidney injury (serum creatinine 132-354 umol/L or

267 renal resistive index to predict persistent acute kidney injury showed contradictory results.

268 EI/ARB use was independently associated with acute kidney injury stage >=1 (OR, 3.28, 95% CI, 2.17-4.

269 In the presence of acute kidney injury (stage 1), [TIMP-2]*[IGFBP7] greater

270 months even in the absence of progression of acute kidney injury (stage 2-3) within 7 days.

271 l mortality, bleeding requiring transfusion, acute kidney injury, stroke, length of stay, and hospita

272 Rationale: Subclinical acute kidney injury (sub-AKI) refers to patients with lo

273 reater functional and histologic evidence of acute kidney injury than wild-type mice.

274 spiratory distress syndrome patients with no acute kidney injury to 50% in mild-moderate acute kidney

275 autophagy contributes to the pathogenesis of acute kidney injury, to incomplete kidney repair after a

276 sfemoral: 3.1%, transradial: 1.6%; P=0.043), acute kidney injury (transfemoral: 9.9%, transradial: 5.

277 Based on this cohort of ICU patients with acute kidney injury, transvenous renal biopsy was safe a

278 %]), urinary tract infection (two [3%]), and acute kidney injury (two [3%]); in group B, diarrhoea (t

279 red only in the capivasertib group, and were acute kidney injury (two), diarrhoea (three), rash (two)

280 Patients with acute kidney injury undergoing prolonged intermittent re

281 ectronic health records promises to forecast acute kidney injury up to 48 hours before it can be diag

282 f common critical care diseases like sepsis, acute kidney injury, urinary tract infections, and HIV/A

283 Severe acute kidney injury was associated with increased durati

284 Severe acute kidney injury was associated with longer PICU stay

285 Severe acute kidney injury was defined as stage 2/3 acute kidne

286 No contrast-induced acute kidney injury was diagnosed in this study.

287 Severity of acute kidney injury was grade I, II, and III in 3.1%, 0.

288 In the direct postoperative period, acute kidney injury was identified in 8.4% of cases.

289 Acute kidney injury was independently associated with ch

290 The risk of acute kidney injury was lower between those who either u

291 Conclusion Acute kidney injury was more common after cardiac cathet

292 serum creatinine was seen in 697 (36.1%) and acute kidney injury was seen in 68 (3.5%) of 1,931 patie

293 s ratio, 2.13; 95% CI, 1.55-2.94; p < 0.001) acute kidney injury were independently associated with m

294 y Disease: Improving Global Outcomes stage 3 acute kidney injury were preoperative left ventricular e

295 Autophagy has been implicated in acute kidney injury, which can arise in response to neph

296 ge: 68.6; males: 113 [58.2%]); 163 (84%) had acute kidney injury, which was associated variously with

297 than or equal to 0.685 predicting persistent acute kidney injury with 78% (95% CI, 64-88%) sensitivit

298 imary endpoint was the development of septic acute kidney injury with the need for renal replacement

299 ng remote ischemic preconditioning developed acute kidney injury within 72 hours after surgery as def

300 emic inflammatory response syndrome, sepsis, acute kidney injury, wound infection (superficial and de