ライフサイエンスコーパス: AKI

1 AKI after MitraClip occurred in 106 patients (14.7%).

2 AKI commonly occurs in patients with coronavirus disease

3 AKI is a common sequela of coronavirus disease 2019 (COV

4 AKI is common among hospitalized patients with coronavir

5 AKI is common among patients hospitalized with COVID-19

6 AKI is common but mostly self-limiting after esophageal

7 AKI is defined using changes in creatinine from baseline

8 AKI measured using injury biomarkers was not associated

9 AKI was defined according to the AKI Network criteria.

10 AKI was defined as an absolute or a relative increase in

11 AKI-RRT is common among critically ill patients with COV

12 rporating the PERSEVERE biomarkers and Day 1 AKI status predicted severe D(3) SA-AKI with an area und

13 Mortality was higher in COVID-19 AKI versus COVID-19 patients without AKI (60.5% versus 2

14 Compared with AKI controls, COVID-19 AKI was observed in a higher proportion of men (58.9% ve

15 mproving outcomes for patients with COVID-19 AKI.

16 ut the prevention and management of COVID-19 AKI.

17 anting more donor kidneys with stage 1 and 2 AKI, and cautious utilization of stage 3 AKI donors, may

18 Factors that were predictive of stage 2 or 3 AKI included initial respiratory rate, white blood cell

19 The proportions with stages 1, 2, or 3 AKI were 39%, 19%, and 42%, respectively.

20 d 2 AKI, and cautious utilization of stage 3 AKI donors, may increase the pool of viable kidneys.

21 AKI stage 2 (OR 1.74, 95% CI 1.05 to 2.90), AKI stage 3 (OR 2.01, 95% CI 1.13 to 3.57), and COVID-19

22 of AKI at days 1, 2, 4, 7, 11, and 14 after AKI onset.

23 enhancer and super-enhancer landscape after AKI by ChIP-seq in uninjured and repairing kidneys on da

24 of mechanisms controlling renal repair after AKI.

25 transcription factor in tubular repair after AKI.

26 th colchicine or metformin protected against AKI, with lower serum creatinine, improved histological

27 rval [CI], 1.31-5.30) and protective against AKI (aOR, 0.08; 95% CI, 0.03-0.22).

28 The incidence of AKI (AKI stage >=2) within 48 h after transplant was lower in

29 New significant AKI was defined as an AKI-stage increase of two or more (Kidney Disease: Impro

30 verage the US PCORnet platform to develop an AKI prediction model and assess its transportability acr

31 In multivariable analysis, AKI patients aged 65 to 84 years, (OR 3.08, 95% CI 1.77

32 out AKI (60.5% versus 27.4%, p < 0.001), and AKI was an independent predictor of mortality (OR 3.27,

33 of previous AKI (SHR, 1.26; 1.02-1.56), and AKI stage at enrollment (no AKI [SHR, 1] vs. stage 1 [SH

34 Thus, recipients of LD, DCD, and AKI kidneys were studied to provide a more complete unde

35 Treatment failure and AKI occurred in 18% and 26% of patients, respectively.

36 is associated with markers of hemolysis and AKI in both humans and mice with SCD.

37 nued NSBB, most commonly for hypotension and AKI, had increased subsequent MELD and mortality.

38 ho developed nephrotic-range proteinuria and AKI early in the course of disease.

39 k factor for AKI and how COVID-19-associated AKI may differ from AKI due to other causes.

40 They developed COVID-19-associated AKI with podocytopathy, collapsing glomerulopathy, or bo

41 dia administration) from contrast-associated AKI (CA-AKI; ie, AKI coincident to contrast media admini

42 after immune checkpoint inhibitor-associated AKI was independently associated with higher mortality.

43 sk of immune checkpoint inhibitor-associated AKI.

44 with immune checkpoint inhibitor-associated AKI.

45 itigates nephrotoxic and ischemia-associated AKI.

46 , of whom 23% developed recurrent associated AKI.

47 -, cisplatin-, and rhabdomyolysis-associated AKI in vivo and cisplatin-induced RTEC cell death in vit

48 ing patients receiving dialysis at baseline, AKI occurred in 34 of 145 (23%) vs 9 of 145 (6%) (differ

49 CA-AKI does not mediate the association of the pre-angiogra

50 CA-AKI was associated with an increased relative risk for 9

51 CA-AKI was not a mediator of the association of pre-angiogr

52 nistration) from contrast-associated AKI (CA-AKI; ie, AKI coincident to contrast media administration

53 .e., proportion of patients who developed CA-AKI and the 90-day outcome) and examined whether CA-AKI

54 rse outcomes following the development of CA-AKI and to explore whether CA-AKI mediates the associati

55 d the incidence of clinically significant CA-AKI (i.e., proportion of patients who developed CA-AKI a

56 , the incidence of clinically significant CA-AKI is very low.

57 Whereas CA-AKI is associated with an increased relative risk of ser

58 elopment of CA-AKI and to explore whether CA-AKI mediates the association of pre-angiography estimate

59 the 90-day outcome) and examined whether CA-AKI was a mediator of the association of baseline kidney

60 ine and outcome data, we assessed whether CA-AKI was associated with the 90-day outcome comprising de

61 ys in SCD in a process involving A1M causing AKI, whereas excess heme in controls is transported to t

62 ficient to separate contrast-induced AKI (CI-AKI; ie, AKI caused by contrast media administration) fr

63 In patients with decompensated cirrhosis, AKI is associated with both hypocoagulable and hypercoag

64 Among participants with CKD, AKI rate in people with diabetes was more than twice tha

65 Conclusion: AKI in ACLF carries a high mortality.

66 Among patients with available data, AKI developed in 31 of 33 patients (94%), including 6 wi

67 f fluid balance on either 48-hour AKI, 7-day AKI, or on the need for postoperative renal replacement

68 The results fully define AKI-associated dedifferentiation programs, potential pat

69 evated biomarkers without creatinine-defined AKI) and GF.

70 noted that such patients frequently develop AKI.

71 es were more likely than controls to develop AKI (48.6% versus 17.2%, respectively) and have preexist

72 ith diabetes are much more likely to develop AKI than people without diabetes.

73 ite, 20% Black, 5% other race), 9% developed AKI overall (14% of Black, 8% of White, 10% of others).

74 wo percent of the study population developed AKI.

75 lack patients had greater odds of developing AKI after PCI compared with White patients.

76 e examined if serum creatinine-defined donor AKI modified this association to assess the relationship

77 s the relationship between subclinical donor AKI (elevated biomarkers without creatinine-defined AKI)

78 D(3) SA-AKI and identify patients with early AKI who are likely to recover.

79 rapies to reduce mortality related to either AKI or CRS, apart from supportive care and volume status

80 our objective was to simultaneously evaluate AKI and CDI risks with AP-BL in the same patient cohort.

81 r repair in GSK3beta knockout mice following AKI.

82 ant for renal tubular regeneration following AKI and that GSK3beta suppresses tubular repair by inhib

83 , particularly a B220(low) subset, following AKI.

84 confidence interval (CI), 0.72 to 0.79] for AKI, 0.79 (95% CI, 0.74 to 0.83) for severe AKI, and 0.8

85 n in the kidney limits their application for AKI detection.

86 KL5 antagonism as a therapeutic approach for AKI.

87 from low-resource areas to provide care for AKI, including acute PD, have already saved hundreds of

88 The mean 12-month eGFR for AKI kidney recipients was lower, but differences were no

89 f COVID-19 is an independent risk factor for AKI and how COVID-19-associated AKI may differ from AKI

90 ing that diabetes is a major risk factor for AKI and we review the causes of this increased risk.

91 nary intervention (PCI) is a risk factor for AKI development, but few studies have quantified racial

92 1) and in patients with <=2 risk factors for AKI (DR: n = 27; Deltacreatinine -0.01(-0.18,0.07)mg/dL

93 patient-and hospital-level risk factors for AKI-RRT and to examine risk factors for 28-day mortality

94 Patient-level risk factors for AKI-RRT included CKD, men, non-White race, hypertension,

95 urposes and to provide further resources for AKI management.

96 tegies to better identify people at risk for AKI and to develop new approaches to improve AKI outcome

97 ds regression was used to contrast risks for AKI and CDI across individual target antimicrobials and

98 There is no effective treatment for AKI and new therapies are urgently needed.

99 how COVID-19-associated AKI may differ from AKI due to other causes.

100 ggested that estrogens may protect mice from AKI.

101 of Sult1e1 protected mice of both sexes from AKI, independent of the presence of sex hormones.

102 rgoing transcatheter mitral valve repair had AKI, linked to device failure or other severe conditions

103 d for COVID-19 are predictive of in-hospital AKI and the need for dialysis.

104 and in-hospital AKI, with nadir in-hospital AKI was in serum ionized calcium of 5.00-5.19 mg/dL.

105 ission serum ionized calcium and in-hospital AKI, with nadir in-hospital AKI was in serum ionized cal

106 etween suPAR levels and incident in-hospital AKI.

107 no effect of fluid balance on either 48-hour AKI, 7-day AKI, or on the need for postoperative renal r

108 However, AKI among hospitalized patients with COVID-19 in the Uni

109 improved survival in ACLF patients with HRS-AKI.

110 o separate contrast-induced AKI (CI-AKI; ie, AKI caused by contrast media administration) from contra

111 n) from contrast-associated AKI (CA-AKI; ie, AKI coincident to contrast media administration).

112 ord variables to accurately predict imminent AKI in hospitalized children.

113 AKI and to develop new approaches to improve AKI outcomes.

114 refore, uNGAL is a useful tool for improving AKI risk stratification.

115 e similar between recipient groups (15.5% in AKI vs 15.1% ideal comparator allografts, p = 0.2).

116 Advancing age in AKI onset was associated with maladaptive response and k

117 activity and effects in normal kidney and in AKI.

118 tudies have quantified racial differences in AKI incidence after this procedure.

119 In contrast, factor XIII was lower in AKI (increased bleeding tendency).

120 ate AKI and extend the importance of NGAL in AKI beyond diagnostics.

121 discovered a protective role of periostin in AKI.

122 However, its role in AKI is unknown.

123 ogens, but studies on the role of SULT1E1 in AKI are lacking.

124 factors responsible for bleeding tendency in AKI, we performed a prospective study comparing all thre

125 ced SCr elevations, 3 (75%) patients were in AKI prior to RDV.

126 race and baseline eGFR on odds for incident AKI (P value for interaction = 0.75).

127 Compared with Whites, odds for incident AKI were not significantly higher in other patients (OR,

128 Piperacillin/tazobactam increased AKI risk, which was exacerbated by concurrent vancomycin

129 oups sufficient to separate contrast-induced AKI (CI-AKI; ie, AKI caused by contrast media administra

130 clinical diagnostic methods in drug-induced AKI and CKD mice models, but also possesses a higher dia

131 ter renal ischemia/reperfusion (I/R)-induced AKI in mouse kidneys.

132 Acute kidney injury (AKI) after liver transplantation is associated with incr

133 Acute kidney injury (AKI) after major trauma is associated with increased mor

134 ation and postoperative acute kidney injury (AKI) and anastomotic leak.

135 models of drug-induced acute kidney injury (AKI) and chronic kidney disease (CKD).

136 verse events, including acute kidney injury (AKI) and Clostridium difficile infection (CDI).

137 common in patients with acute kidney injury (AKI) and the risk of mortality is high, especially if re

138 cardiac death (DCD) or acute kidney injury (AKI) donors may experience delayed function with eventua

139 veloped hypotension and acute kidney injury (AKI) during the index hospitalization.

140 e likely resulting from acute kidney injury (AKI) had higher odds of kidney nonprocurement.

141 le its association with acute kidney injury (AKI) has waxed and waned, recent data suggest nephrotoxi

142 erum creatinine-defined acute kidney injury (AKI) have similar allograft survival as non-AKI kidneys

143 with moderate to severe acute kidney injury (AKI) have similar outcomes to recipients who receive kid

144 ate a high incidence of acute kidney injury (AKI) in Coronavirus Disease 2019 (COVID-19), but more da

145 investigate the risk of acute kidney injury (AKI) in hospitalized patients based on admission serum i

146 Acute kidney injury (AKI) is a frequent complication of traumatic injury; how

147 heter-based procedures, acute kidney injury (AKI) is a frequent, serious complication ranging from 10

148 Acute kidney injury (AKI) is a major health problem affecting millions of pat

149 owing appreciation that acute kidney injury (AKI) is increasing in its incidence rapidly and that peo

150 KD) after an episode of acute kidney injury (AKI) is known in patients without cirrhosis.

151 evidence suggests that acute kidney injury (AKI) is the main predictor of postparacentesis bleeding

152 ed with new significant acute kidney injury (AKI) or major adverse kidney events (MAKE) within 14 day

153 rd deceased donors with acute kidney injury (AKI) versus without AKI (30% versus 18%).

154 ACLF diagnosed with HRS acute kidney injury (AKI) were randomized to albumin with infusion of terlipr

155 esult in recovery after acute kidney injury (AKI) with adaptive proliferation of tubular epithelial c

156 Rationale: Acute kidney injury (AKI), a common complication of sepsis, is associated wit

157 ulation- manifesting as acute kidney injury (AKI), a common disorder associated with adverse long-ter

158 Ischemic acute kidney injury (AKI), a complication that frequently occurs in hospital

159 actam on clinical cure, acute kidney injury (AKI), and in-hospital mortality.

160 d promise in predicting acute kidney injury (AKI), however, clinical adoption of these models require

161 In acute kidney injury (AKI), substantial decreases in the levels of NAD(+) impa

162 Acute kidney injury (AKI), which increases FGF23 levels, rapidly increased ci

163 ndary outcomes included acute kidney injury (AKI).

164 atients are at risk for acute kidney injury (AKI).

165 eremia at days 2 and 5; acute kidney injury (AKI); microbiological relapse; microbiological treatment

166 and 8.3%; P = .02), and acute kidney injury (AKI; 39.1% vs 19.4%; P = .02) than patients with no stea

167 ems promising to non-intrusively interrogate AKI-related biomarkers, the low kidney contrast of many

168 and even fewer simultaneously investigating AKI and CKD in this population.

169 nt (KO) mice were protected against ischemic AKI with significantly attenuated renal tubular necrosis

170 ist (5-BDBD) were protected against ischemic AKI.

171 tubular P2X4 activation exacerbates ischemic AKI and promotes NLRP3 inflammasome signaling.

172 a mechanism by which CD4(+) T cells mediate AKI and extend the importance of NGAL in AKI beyond diag

173 eceive kidneys from donors with none to mild AKI.

174 nalysis confirmed the dominance of molecular AKI, CKD, and eGFR.

175 dneys and in ABMR, were related to molecular AKI and CKD and to eGFR, not rejection activity, presuma

176 Moreover, AKI caused the formation of "mixed-identity cells" (expr

177 mmatory and profibrotic phenotype; moreover, AKI dramatically modified ligand-receptor crosstalk, wit

178 anging gene expression patterns for multiple AKI stages and all renal cell types.

179 and 0.81 (95% CI, 0.77 to 0.86) for neonatal AKI.

180 enced the best global outcomes (no TF and no AKI).

181 1.02-1.56), and AKI stage at enrollment (no AKI [SHR, 1] vs. stage 1 [SHR, 3.28; 1.30-8.25] vs. stag

182 (AKI) have similar allograft survival as non-AKI kidneys but are discarded at a higher rate.

183 at would reveal whether there are aspects of AKI risk, course, and outcomes unique to this infection.

184 inine but elevated alternative biomarkers of AKI.

185 Gene expression in peripheral blood of AKI/DCD recipients offers a novel platform to understand

186 on and signalling pathways characteristic of AKI, and tested them in models of acute and chronic kidn

187 Combination of AKI with significant residual MR after the procedure con

188 er, there have been no direct comparisons of AKI in hospitalized patients with and without COVID-19 t

189 L) in patients not meeting the definition of AKI.

190 less severe than predicted for the degree of AKI, suggesting a role for hemodynamic factors, such as

191 tential biomarker for the early detection of AKI and has multiple potential biological functions.

192 UDP-Glc concentration and the development of AKI in cardiac surgery patients.

193 tors, might contribute to the development of AKI in patients with cirrhosis.

194 and older age associated with development of AKI, these associations were not unique to COVID-19.

195 ts as potential risks for the development of AKI.

196 iterion of KDIGO definition for diagnosis of AKI.

197 G-3-P in humans and mice, and the effect of AKI on FGF23 was abrogated by GPAT inhibition or Lpar1 d

198 on who had COVID-19 and clinical features of AKI, including proteinuria with or without hematuria.

199 Adult studies have shown frequencies of AKI after CT with intravenous ICM to be similar to prope

200 We describe the frequency of AKI and dialysis requirement, AKI recovery, and adjusted

201 Frequency of AKI with eGFR greater than or equal to 60 mL/min/1.73 m(

202 Our secondary outcomes were the grade of AKI at 7 days, the need for postoperative renal replacem

203 The incidence of AKI (AKI stage >=2) within 48 h after transplant was low

204 , was associated with a reduced incidence of AKI after liver transplantation.

205 , LOS, all-cause mortality, and incidence of AKI and CDI.

206 Further analyses included incidence of AKI and safety evaluation.

207 Current management of AKI, a potentially fatal disorder that can also initiate

208 ated leukocyte responses in a mouse model of AKI and observed an increase in circulating and kidney B

209 lateral ischemia-reperfusion murine model of AKI at days 1, 2, 4, 7, 11, and 14 after AKI onset.

210 ysis, MELD (SHR, 1.01; 1.00-1.03), number of AKI episodes (SHR, 1.25; 1.15-1.37), and CysC (SHR, 1.38

211 The occurrence of AKI was associated with worse outcomes, highlighting the

212 ted with a 9.15-fold increase in the odds of AKI (95% confidence interval [95% CI], 3.64 to 22.93) an

213 R was associated with graded, higher odds of AKI incidence (P value for trend <0.001); however, there

214 , which is upregulated at the early onset of AKI.

215 have a novel function in the pathogenesis of AKI.

216 Timely prediction of AKI in children can allow for targeted interventions, bu

217 perative factors independently predictive of AKI were age [P = 0.027, odds ratio (OR) 1.02 (1.00-1.04

218 Significant multivariable predictors of AKI included eGFR before imaging (OR: 0.99; 95% CI: 0.98

219 7; p < 0.001) were independent predictors of AKI.

220 ients with differing risk for progression of AKI.

221 onic healthcare records to evaluate rates of AKI and various statistical methods to determine their r

222 ACGF was slightly higher among recipients of AKI kidneys (aHR 1.05, 95%CI:1.01-1.09).

223 r study aimed to evaluate the 2-week risk of AKI after at least 3 days of intravenous vancomycin mono

224 limited by concerns around increased risk of AKI and anastomotic leak.

225 n mono-therapy does not increase the risk of AKI compared to other intravenous antibiotics used for s

226 observational studies evaluating the risk of AKI in people with type 2 diabetes, and even fewer simul

227 Patients with cirrhosis are at risk of AKI owing to a wide range of factors.

228 Delayed diagnosis and treatment of AKI due to the lack of efficient early diagnosis is an i

229 le mice, indicating that Sult1e1's effect on AKI was also tissue-specific and sex-specific.

230 ct of pharmacologic inhibition of SULT1E1 on AKI.

231 patients who had end-stage kidney disease or AKI at admission.

232 against postcontrast acute kidney injury (PC-AKI) in 2018 (ESUR 10.0).

233 of age (OR 3.54, 95% CI 1.87 to 6.70), peak AKI stage 2 (OR 1.74, 95% CI 1.05 to 2.90), AKI stage 3

234 an association between uNGAL and persistent AKI, MAKE30, and MAKE365.

235 lly ill surgical sepsis patients, persistent AKI and the absence of renal recovery are associated wit

236 idney allografts from donors with persistent AKI are often discarded, yet those that were transplante

237 Postoperative AKI did not impact survival outcomes.

238 Postoperative AKI was observed in 208 (18.3%) patients, with AKI Netwo

239 traoperative fluid balance and postoperative AKI.

240 primary outcome was the 7-day postoperative AKI rate.

241 f developing a higher stage of postoperative AKI (odds ratio, 0.49; 95% confidence interval, 0.37-0.6

242 ruction technique and stage of postoperative AKI was assessed using multivariable ordinal logistic re

243 Postoperatively, AKI was associated with atrial fibrillation (P = 0.013)

244 The AI/ML algorithm helped predict AKI 61.8 (32.5) hours faster than the Kidney Disease and

245 SHR], 1.58; 1.07-2.33), episodes of previous AKI (SHR, 1.26; 1.02-1.56), and AKI stage at enrollment

246 th cirrhosis, more so in those with previous AKI episodes and a high CysC level and MELD score.

247 cteristics allowed us to develop a proactive AKI clinical tool, which grouped patients into four risk

248 Recognizing AKI as a bona fide complication of diabetes should open

249 manage complications of medically refractory AKI and CRS and may restore normal electrolyte, acid-bas

250 e frequency of AKI and dialysis requirement, AKI recovery, and adjusted odds ratios (aORs) with morta

251 PERSEVERE biomarkers predict severe D(3) SA-AKI and identify patients with early AKI who are likely

252 nd Day 1 AKI status predicted severe D(3) SA-AKI with an area under the received operating characteri

253 AKI, 0.79 (95% CI, 0.74 to 0.83) for severe AKI, and 0.81 (95% CI, 0.77 to 0.86) for neonatal AKI.

254 Eight patients had severe AKI, necessitating RRT.

255 th COVID-19 had a higher incidence of severe AKI compared with controls.

256 of accepting kidneys with moderate to severe AKI in pediatric kidney transplant recipients.

257 ent status is common in patients with severe AKI regardless of treatment with CRRT.

258 -adjusted odds of developing new significant AKI and MAKE increased by 1.2% (0.3-2.2; P = 0.008) and

259 New significant AKI was defined as an AKI-stage increase of two or more

260 Among 8473 encounters studied, AKI occurred in 516 (10.2%), 207 (9%), and 27 (2.5%) enc

261 Sub-AKI was defined by an admission penKid concentration abo

262 ionale: Subclinical acute kidney injury (sub-AKI) refers to patients with low serum creatinine but el

263 AdrenOSS-1 cohorts met the definition of sub-AKI (11.6% and 17.5% of patients without AKI).

264 we explored the incidence and outcome of sub-AKI based on penKid.Methods: A prospective observational

265 Here, I propose that AKI should be considered a complication of diabetes alon

266 In the AKI/DCD groups, elevations in gene expression were maint

267 AKI was defined according to the AKI Network criteria.

268 tic AKI requiring renal replacement therapy (AKI-RRT).

269 tcome of vehicle-traumatic and non-traumatic AKI requiring renal replacement therapy (AKI-RRT).

270 After propensity matching with non-traumatic AKI-RRT cases with similar demographic and clinical char

271 better long-term survival than non-traumatic AKI-RRT patients, but a similar risk of ESKD.

272 CI, 0.894-1.438; p = 0.301) as non-traumatic AKI-RRT patients.

273 , 0.325-0.937; p = 0.028) than non-traumatic AKI-RRT patients.

274 Compared to non-traumatic AKI-RRT, vehicle-traumatic AKI-RRT patients had longer l

275 Despite severe injuries, vehicle-traumatic AKI-RRT patients had better long-term survival than non-

276 to non-traumatic AKI-RRT, vehicle-traumatic AKI-RRT patients had longer length of stay in hospital [

277 Vehicle-traumatic AKI-RRT patients had lower rates of long-term mortality

278 dels that focused on ESKD, vehicle-traumatic AKI-RRT patients were associated with lower ESKD rates (

279 546 vehicle-traumatic AKI-RRT patients, median age 47.6 years (interquartile r

280 f long-term outcomes after vehicle-traumatic AKI-RRT.

281 olecule in situ hybridizations, we validated AKI signatures in multiple experiments.

282 The primary outcome was AKI, and secondary outcomes included in-hospital mortali

283 in 31 of 33 patients (94%), including 6 with AKI stage 1, 9 with stage 2, and 16 with stage 3.

284 Compared with AKI controls, COVID-19 AKI was observed in a higher prop

285 The predominant finding correlating with AKI was acute tubular injury.

286 Donors with AKI are more likely to undergo delayed graft function bu

287 ack, White, or other) and baseline eGFR with AKI incidence among patients who underwent PCI at Duke U

288 am was 5, and the number needed to harm with AKI with a polymyxin/aminoglycoside was 4.

289 when available to differentiate kidneys with AKI from those with chronic injury.

290 Of the 435 patients with AKI and urine studies, 84% had proteinuria, 81% had hema

291 Patients with AKI had worse outcomes compared to those without AKI, in

292 Of all patients with AKI, only 30% survived with recovery of kidney function

293 I was observed in 208 (18.3%) patients, with AKI Network 1, 2, and 3 in 173 (15.2%), 28 (2.5%), and 7

294 Fifteen patients (88%) presented with AKI; nine had nephrotic-range proteinuria.

295 ith decompensated cirrhosis with and without AKI.

296 similar long-term outcomes as donors without AKI.

297 OVID-19 AKI versus COVID-19 patients without AKI (60.5% versus 27.4%, p < 0.001), and AKI was an inde

298 sub-AKI (11.6% and 17.5% of patients without AKI).

299 had worse outcomes compared to those without AKI, including a higher proportion of in-hospital bleedi

300 ith acute kidney injury (AKI) versus without AKI (30% versus 18%).