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1 jections of glycerol (rhabdomyolysis-induced acute kidney injury).
2 nal ischemia/reperfusion is a major cause of acute kidney injury.
3 and can be complicated by the development of acute kidney injury.
4 ry outcomes were end-stage renal disease and acute kidney injury.
5 initiation of renal replacement therapy for acute kidney injury.
6 I was not associated with the development of acute kidney injury.
7 t and attenuate the risk of contrast-induced acute kidney injury.
8 sodium, were associated with development of acute kidney injury.
9 ferences in the rates of contrast-associated acute kidney injury.
10 .2) mg/dL and more than 20% had stage 2 or 3 acute kidney injury.
11 Forty-three percent of patients developed acute kidney injury.
12 or for the prevention of contrast-associated acute kidney injury.
13 ath and complications associated with severe acute kidney injury.
14 k of cardiogenic shock, severe bleeding, and acute kidney injury.
15 tional outcomes of children suffering septic acute kidney injury.
16 voke adaptive responses that protect against acute kidney injury.
17 Safety was assessed by the rate of acute kidney injury.
18 idney disease following hospitalization with acute kidney injury.
19 rior allowing more accurate qualification of acute kidney injury.
20 ctive strategy available to prevent or treat acute kidney injury.
21 , which is a key response in the recovery of acute kidney injury.
22 d with genetic susceptibility to in-hospital acute kidney injury.
23 urve had an area under the curve of 0.73 for acute kidney injury.
24 was associated with lower mortality and less acute kidney injury.
25 myocardial infarction, ischemic stroke, and acute kidney injury.
26 tes a strong trend toward the development of acute kidney injury.
27 95% CI, 1.06-1.24; p < 0.001) of more severe acute kidney injury.
28 8%] patients) were the most common causes of acute kidney injury.
29 d non-hospital settings who met criteria for acute kidney injury.
30 urve for plasma angiopoietin-2 levels versus acute kidney injury.
31 hrotoxic drugs are the most common causes of acute kidney injury.
32 logic role in heart ischemia-reperfusion and acute kidney injury.
33 lications, type 4a myocardial infarction, or acute kidney injury.
34 roach for early recognition and treatment of acute kidney injury.
35 and dedifferentiated proximal tubules after acute kidney injury.
36 ther common genetic variants contributing to acute kidney injury.
37 al two genetic loci that are associated with acute kidney injury.
38 injury, 2) pneumonia, and 3) pneumonia with acute kidney injury.
39 events obesity, hepatocellular carcinoma and acute kidney injury.
40 Improving Global Outcomes criteria to define acute kidney injury.
41 could be a potential therapeutic target for acute kidney injury.
42 emia-reperfusion-injury and glycerol-induced acute kidney-injury.
43 rates of procedural complications (5.8%) and acute kidney injury (1.6%) were identical in each group
44 eatening bleeding (8.3% vs. 2.3%; p = 0.03), acute kidney injury (11.1% vs. 4.0%; p = 0.03), and subs
45 .76; 95% CI, 0.62-0.93), lower prevalence of acute kidney injury (16.0% vs 19.2%; p = 0.028; odds rat
46 ex admission and serum creatinine values: 1) acute kidney injury, 2) pneumonia, and 3) pneumonia with
47 001) as well as secondary outcomes of 30-day acute kidney injury (20.8% vs 13.8%, P < .001), 30-day b
48 s also significantly higher in patients with acute kidney injury (28.3% vs 6.1% in the non-acute kidn
49 e 30-day all-cause readmission rates, 30-day acute kidney injury, 30-day blood transfusion, and 1-yea
50 e cardiac injury; 5) The role of exosomes in acute kidney injury; 6) The role of exosomes in sepsis;
52 r 1000 patient-years), including the rate of acute kidney injury (7.1 and 6.2 events per 1000 patient
53 ) availability was limited, particularly for acute kidney injury (8 countries [7%]) and nondialysis C
54 e; tackle major risk factors for CKD; reduce acute kidney injury-a special risk factor for CKD; enhan
57 orter ICU length of stay, lower incidence of acute kidney injury, acute respiratory distress syndrome
59 r associated with hyperchloremic acidosis or acute kidney injury after controlling for total fluids,
60 cuses on the risk factors for posttransplant acute kidney injury after liver and heart transplantatio
61 RIPC significantly reduced the incidence of acute kidney injury (AKI) [odds ratio (OR) = 0.79; P = 0
64 urin inhibitors, data on the consequences of acute kidney injury (AKI) after cardiac transplantation
67 dequately powered studies comparing rates of acute kidney injury (AKI) among patients receiving vanco
68 ociated with combination regimens, including acute kidney injury (AKI) and Clostridium difficile infe
71 f renal replacement therapy (RRT) for severe acute kidney injury (AKI) but without life-threatening i
72 /tazobactam may be associated with increased acute kidney injury (AKI) compared to vancomycin without
73 m sodium is associated with a higher risk of acute kidney injury (AKI) compared with vancomycin plus
76 eria for the diagnosis and classification of acute kidney injury (AKI) in patients with chronic liver
77 abigatran is associated with a lower risk of acute kidney injury (AKI) in patients with nonvalvular a
78 fferentiation between prerenal and intrinsic acute kidney injury (AKI) in the nontransplant populatio
82 Single-center studies suggest that neonatal acute kidney injury (AKI) is associated with poor outcom
96 transferase, alanine aminotransferase (ALT), acute kidney injury (AKI), model for end stage liver dis
97 Urinary biomarkers augment the diagnosis of acute kidney injury (AKI), with AKI after cardiovascular
101 e heart failure, renal failure, hypotension, acute kidney injury, altered gas exchange, or emergency
104 otein 7 results in patients with and without acute kidney injury and across nonrenal Sequential Organ
106 al acetylcysteine are widely used to prevent acute kidney injury and associated adverse outcomes afte
107 There was a significant interaction between acute kidney injury and chronic kidney disease on cumula
110 r shock, we examined the association between acute kidney injury and daily mental status using multin
111 apy modified the association between stage 3 acute kidney injury and daily peak serum creatinine and
113 reatments, therapeutic advances to attenuate acute kidney injury and expedite recovery have largely f
117 indices of urinary GAG fragmentation predict acute kidney injury and in-hospital mortality in patient
118 in postischemic tissue is a potent source of acute kidney injury and is amenable to sugar-specific bl
120 out the associations of obesity with risk of acute kidney injury and post acute kidney injury mortali
121 p inhibitors (PPI) have been associated with acute kidney injury and recent studies suggest that they
123 Innate immune activation contributes to both acute kidney injury and tissue remodeling that is associ
125 filter group and 5 in the control group had acute kidney injury, and 3 patients in the filter group
127 gical conditions, including viral infection, acute kidney injury, and cardiac ischemia/reperfusion.
128 nine value, albuminuria, greater severity of acute kidney injury, and higher serum creatinine value a
129 Crude rates of hyperchloremic acidosis, acute kidney injury, and hospital mortality all increase
130 ven after controlling for the development of acute kidney injury, and its addition to clinical models
131 dural myocardial infarction, major bleeding, acute kidney injury, and new-onset atrial fibrillation w
132 h improved survival, decreased prevalence of acute kidney injury, and shorter duration of vasoactive
134 the development of hyperchloremic acidosis, acute kidney injury, and survival among those with highe
136 vive a pneumonia hospitalization and develop acute kidney injury are at high risk for major adverse k
139 stopathologic changes associated with septic acute kidney injury are poorly understood, in part, beca
141 ected to be study drug-related (eltrombopag: acute kidney injury, arterial thrombosis, bone pain, dia
142 trong association between hyperchloremia and acute kidney injury as well as acute kidney injury and m
143 nts included in this cohort, 16.7% developed acute kidney injury, as defined by Kidney Disease Improv
144 t was the development of contrast-associated acute kidney injury, as defined by the Acute Kidney Inju
148 Surgery was associated with higher rates of acute kidney injury, atrial fibrillation, and transfusio
149 95% CI, 1.1-2.6; OR, 1.8; 95% CI, 1.4-2.4), acute kidney injury (beta coefficient, 5.0; 95% CI, 3.9-
151 e of the resulted phenotypes are sepsis with acute kidney injury, cardiac surgery, anemia, respirator
153 functional, potentially reversible, form of acute kidney injury characterized by rapid (<2 wk) and p
155 p (adjusted odds ratio, 1.06 [1.03-1.09] for acute kidney injury+/chronic kidney disease+; 1.09 [1.05
156 ospital mortality were identified: 5.9 L for acute kidney injury+/chronic kidney disease+; 3.8 L for
157 hronic kidney disease+; 1.05 [1.03-1.08] for acute kidney injury+/chronic kidney disease-; and 1.07 [
158 y injury-/chronic kidney disease+; 4.3 L for acute kidney injury+/chronic kidney disease-; and 1.5 L
159 hronic kidney disease+; 1.09 [1.05-1.13] for acute kidney injury-/chronic kidney disease+; 1.05 [1.03
160 y injury+/chronic kidney disease+; 3.8 L for acute kidney injury-/chronic kidney disease+; 4.3 L for
163 associated with hospital mortality based on acute kidney injury/chronic kidney disease status, under
164 [95% CI] 1.04-1.08; p < 0.001), and in each acute kidney injury/chronic kidney disease subgroup (adj
165 continues to pose a risk of contrast-induced acute kidney injury (CI-AKI) for a subgroup of patients
167 asure of readmission for the same infection, acute kidney injury, Clostridium difficile infection, or
168 ly higher in patients with septic shock with acute kidney injury compared with patients with septic s
169 d by inflammation, we hypothesized that when acute kidney injury complicates pneumonia, major adverse
171 ury analysis, we excluded patients achieving acute kidney injury criteria in the first 2 days of ICU
172 nal six events each occurred in two (3%) for acute kidney injury, decreased lymphocyte count, fatigue
175 m2 and who had survived hospitalization with acute kidney injury (defined by a serum creatinine incre
176 A total of 4683 patients were evaluated; acute kidney injury developed in 1261 patients (26.9%; 9
177 nce interval [CI], 25.6 to 28.2), and severe acute kidney injury developed in 543 patients (11.6%; 95
178 More than twice as many patients with severe acute kidney injury died or developed new moderate disab
179 ratio [HR]: 20.6; P = 0.01), development of acute kidney injury during hospitalization (HR: 23.2; P
181 nd 1-year survival rates associated with the acute kidney injury episodes were similar across body ma
182 The primary endpoint was moderate-severe acute kidney injury (equivalent to Kidney Disease Improv
183 control group experienced significantly more acute kidney injury events (14 vs 4, respectively; P = .
186 ith reduced hospital mortality and with less acute kidney injury from days 3-7 after ICU admission.
187 ischarge were most common in the pneumonia + acute kidney injury group (51% died and 62% reached majo
189 s without acute kidney injury, patients with acute kidney injury had a higher prevalence of diabetes
190 cteristics of children and young adults with acute kidney injury have been described in single-center
191 emonstrated a strong trend toward developing acute kidney injury (hazard ratio, 1.39; 95% CI, 0.99-1.
192 ing for the aforementioned confounders, both acute kidney injury (hazard ratio, 3.73; 95% CI, 2.39-5.
194 kidney disease after a hospitalization with acute kidney injury; however, no risk-prediction tools h
195 7; 95% confidence interval [CI], 1.24-1.73), acute kidney injury (HR, 1.23; 95% CI, 1.05-1.44), >4 El
199 ma creatinine level alone failed to identify acute kidney injury in 67.2% of the patients with low ur
200 s that showed the strongest association with acute kidney injury in a replication patient population
203 paediatric and adult patients with confirmed acute kidney injury in hospital and non-hospital setting
204 roduction of cell-free plasma hemoglobin and acute kidney injury in infants and children undergoing c
205 Dehydration was the most frequent cause of acute kidney injury in LLMICs (526 [46%] of 1153 vs 518
207 unctional and potentially reversible form of acute kidney injury in patients with advanced cirrhosis,
210 id a systematic review to assess outcomes of acute kidney injury in sub-Saharan Africa and identify b
216 , plasma from patients with septic shock and acute kidney injury inhibited neutrophilic-differentiate
228 nd development of hyperchloremic acidosis or acute kidney injury is less clear, and further research
231 ized trial, we assigned patients with severe acute kidney injury (Kidney Disease: Improving Global Ou
235 netic loci associated with increased risk of acute kidney injury may reveal novel pathways for therap
238 erload, hepatic and coagulation dysfunction, acute kidney injury, mortality, and plasma cytokines in
239 grade 4 hyperkalemia (n=1 [6%]), and grade 2 acute kidney injury (n=1 [6%]) in the NSCLC cohort.
242 risk/injury/failure/loss/end stage (RIFLE), acute kidney injury network (AKIN), or kidney disease: i
243 ry outcome was AKI, defined according to the Acute Kidney Injury Network criteria as an absolute incr
244 ft failure was defined as AKI stages 1 to 3 (Acute Kidney Injury Network criteria), exclusion criteri
246 iated acute kidney injury, as defined by the Acute Kidney Injury Network criteria, 72 hours after con
249 ale gender were found to be risk factors for acute kidney injury (odds ratio, 1.02 and 3.78, respecti
250 xception of a higher rate of adjusted 30-day acute kidney injury (odds ratio, 1.22; 95% CI, 1.10-1.36
251 ts with septic shock (with or without severe acute kidney injury) on neutrophilic-differentiated NB4
252 ciated with hospital mortality regardless of acute kidney injury or chronic kidney disease presence.
253 al Classification of Diseases-9 code 584.xx (acute kidney injury) or 486.xx (pneumonia) between Octob
254 toneal injections of folic acid (nephrotoxic acute kidney injury) or by IM injections of glycerol (rh
264 te kidney injury was defined as stage 2 or 3 acute kidney injury (plasma creatinine level >/=2 times
266 We aimed to assess regional differences in acute kidney injury recognition, management, and outcome
267 g/dL; glomerular filtration rate <15 mL/min; acute kidney injury requiring dialysis; and renal transp
269 toperative complications with a preoperative acute kidney injury risk index of class III or higher (i
270 ransaminase, international normalized ratio, acute kidney injury, septic shock, hepatic encephalopath
271 surgery and also resulted in lower rates of acute kidney injury, severe bleeding, and new-onset atri
273 5% CI, 1.9%-25.1%) or included age, sex, and acute kidney injury stage alone (integrated discriminati
275 plasma from patients with septic shock plus acute kidney injury still showed elevated resistin level
276 fusion injury (IRI) is an important cause of acute kidney injury that can lead to end-stage renal fai
277 crucial role in the pathogenesis of ischemic acute kidney injury through regulating tubular cell apop
278 alidate predictive models for progression of acute kidney injury to advanced chronic kidney disease.
279 atients without significant risk factors for acute kidney injury undergoing elective colectomy to a m
280 n 60 of the 543 patients (11.0%) with severe acute kidney injury versus 105 of the 4140 patients (2.5
281 ession model showed the hazard ratio (HR) of acute kidney injury was 2.212 (95% CI: 1.334-3.667), sep
294 nvolving critically ill patients with severe acute kidney injury, we found no significant difference
295 thic hemolytic anemia, thrombocytopenia, and acute kidney injury were found in a group of 3 patients
296 to event analyses, patients with pneumonia + acute kidney injury were most likely to die or reach maj
297 I, 0.56 to 0.95; P=0.02), but admissions for acute kidney injury were not (101.9 and 86.0 admissions
300 of mortality, clinical ischemic stroke, and acute kidney injury within 30 days after surgery; deliri
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