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1 al anesthesia (Cr, 2.8 +/- 0.3 mg/dl; severe tubular necrosis).
2 site of vascular leak and the kidneys suffer tubular necrosis.
3 ccidental overdose of OP can result in acute tubular necrosis.
4 may play a role in the pathogenesis of acute tubular necrosis.
5 o estimate risk early in the course of acute tubular necrosis.
6 rvival in critically ill patients with acute tubular necrosis.
7 ced scores of acute tubular injury and acute tubular necrosis.
8 de in 504 critically ill patients with acute tubular necrosis.
9  in patients without oliguria who have acute tubular necrosis.
10 e was consistent with the diagnosis of acute tubular necrosis.
11 cule-1 (ICAM-1) in the pathogenesis of acute tubular necrosis.
12  ameliorated the histological score of acute tubular necrosis.
13 sulting in a unique morphological pattern of tubular necrosis.
14 g at autopsy in patients with ischemic acute tubular necrosis.
15 emarkable pathologic renal injury, including tubular necrosis.
16 revent recovery from ischemic or toxic acute tubular necrosis.
17  cecal luminal fluid accumulation, and renal tubular necrosis.
18 zed patients with AKI and COVID-19 was acute tubular necrosis.
19  to differentiate acute rejection from acute tubular necrosis.
20 matory response in the pathogenesis of acute tubular necrosis.
21 as significant novel findings in human acute tubular necrosis.
22  previously underappreciated aspect of acute tubular necrosis.
23 ly new approaches for the treatment of acute tubular necrosis.
24                 There were no cases of acute tubular necrosis.
25 d urea nitrogen, serum creatinine, and renal tubular necrosis.
26  kidneys of rats with ischemia-induced acute tubular necrosis.
27 nts who develop delayed graft function/acute tubular necrosis.
28 osporine or tacrolimus toxicity (58%), acute tubular necrosis (12%), and urinary obstruction (12%).
29 tients with acute renal failure due to acute tubular necrosis (12), bilateral renal cortical necrosis
30 f AKI were prerenal azotemia (68.6 %), acute tubular necrosis (25.7 %), hepatorenal syndrome (5.7 %),
31 r degenerative changes consistent with acute tubular necrosis (73%).
32 from mice infected with C227-11 showed acute tubular necrosis, a finding seen in mice infected with t
33 imilar to the human condition known as acute tubular necrosis, a process that resolved by cellular re
34 eatotic rats was associated with renal acute tubular necrosis after 24 hours of reperfusion in the fa
35 lso exacerbated kidney dysfunction and acute tubular necrosis after subthreshold ischemia.
36                           The HLA B49, acute tubular necrosis after transplantation, previous transpl
37 al AKI, 64 (39.5%) HRS-AKI, 27 (16.7%) acute tubular necrosis-AKI (ATN-AKI), and 36 (22.2%) a mixed f
38 in detail, the cell death propagation during tubular necrosis, although described morphologically, re
39 kade during the early injury phase prevented tubular necrosis and AKI, TLR4 blockade during the heali
40 ged CI followed by WI and reperfusion, acute tubular necrosis and apoptosis did not occur in hibernat
41 Ischemic injury to the kidney produces acute tubular necrosis and apoptosis followed by tubular regen
42 corresponding to the morphologic evidence of tubular necrosis and cell detachment; quite surprisingly
43  survival rate, and significantly less acute tubular necrosis and cellular infiltrates.
44 e was associated with higher scores of acute tubular necrosis and chronic allograft nephropathy (P<0.
45 y, shown by the increased incidence of acute tubular necrosis and consequent delayed graft function.
46  into infants has an increased risk of acute tubular necrosis and graft loss from vascular thrombosis
47 th small molecules, affects initial ischemic tubular necrosis and immediate GFR loss upon unilateral
48 d serum creatinine) and histologic criteria (tubular necrosis and in situ DNA fragmentation assessed
49 )C(2)]fumarate allows the detection of early tubular necrosis and its distinction from glomerular inf
50 the kidneys and liver, consistent with acute tubular necrosis and multifocal necrosis, and changes in
51        Histologic examination revealed acute tubular necrosis and neutrophilic infiltration, both of
52 ies in two patients at 70 mg/m(2) were renal tubular necrosis and proteinuria (both grade 3).
53 h" must include the inflammatory response to tubular necrosis and regenerative signals potentially co
54 owed utility in the early detection of acute tubular necrosis and rejection.
55 ical course was further complicated by acute tubular necrosis and renal failure requiring long-term h
56 e shows little correlation between the renal tubular necrosis and the degree of OP-induced acetylchol
57 eys from surviving wild-type mice had severe tubular necrosis and tubular cell apoptosis 24 hours aft
58                           Simultaneous acute tubular necrosis and tubular cell apoptosis was rare (55
59 al injury, as assessed by plasma creatinine, tubular necrosis, and apoptosis.
60 f hepatic steatosis and kidney injury, acute tubular necrosis, and apoptotic cell death by the endopl
61 rial rods, proliferative glomerulonephritis, tubular necrosis, and fibrin thrombi within small vessel
62 emia (volume-responsive prerenal AKI), acute tubular necrosis, and hepatorenal syndrome (HRS), a func
63 athies, necrotizing and crescentic GN, acute tubular necrosis, and infective pyelonephritis or sepsis
64 opsy samples showed varying degrees of acute tubular necrosis, and one patient had associated widespr
65 tects against ischemic AKI by reducing renal tubular necrosis, apoptosis, and inflammation, and that
66 lar and tubular damage consistent with acute tubular necrosis, apoptosis, and renal tubular cell desq
67                                        Acute tubular necrosis, apoptosis, urinary kidney damage marke
68 nction, antibody-mediated rejection or acute tubular necrosis, as compared with normal biopsy results
69                A renal biopsy showed massive tubular necrosis associated with a prominent granulomato
70 BK virus nephropathy (BKVAN) 9.9%; and acute tubular necrosis (ATN with i-INT) in 5.9% of cases.
71           Cases included patients with acute tubular necrosis (ATN) (n = 10), hepatorenal syndrome (H
72 ction due to acute rejection (n = 12), acute tubular necrosis (ATN) (n = 8), chronic rejection (n = 6
73 ighest recovery rates of recovery were acute tubular necrosis (ATN) and acute interstitial nephritis
74 y, lower serum creatinine, and reduced acute tubular necrosis (ATN) and apoptosis.
75  diagnostic groups-SAGN, primary IgAN, acute tubular necrosis (ATN) and normal kidney (baseline trans
76 eful in differential diagnosis between acute tubular necrosis (ATN) and other types of acute kidney i
77                                        Acute tubular necrosis (ATN) is a syndrome of intrinsic renal
78                                        Acute tubular necrosis (ATN) is common in hospitalized patient
79 tained in these recipients demonstrate acute tubular necrosis (ATN) occasionally associated with tubu
80 the influence of donor tissue mass and acute tubular necrosis (ATN) on graft survival and incidence o
81 ics are used successfully to alleviate acute tubular necrosis (ATN) produced by chemotherapeutic agen
82 significant reduction in morphological acute tubular necrosis (ATN) score compared with vehicle-treat
83 welling resulted in varying degrees of acute tubular necrosis (ATN) that slowed the recovery of the d
84 opsies were diagnosed as no rejection, acute tubular necrosis (ATN), acute rejection (AR), chronic re
85 d patient survival rates, incidence of acute tubular necrosis (ATN), acute rejection episodes, and ca
86 s setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal syndrome (HRS).
87   Histologic analysis at 24 h revealed acute tubular necrosis (ATN), and intravital two-photon micros
88 c section of a nephron, referred to as acute tubular necrosis (ATN).
89 MR, acute cellular rejection (ACR), or acute tubular necrosis (ATN).
90 -intoxicated mice revealed multifocal, acute tubular necrosis (ATN).
91      The most frequent cause of AKI is acute tubular necrosis (ATN).
92 sy-proven acute allograft dysfunction (acute tubular necrosis [ATN, n=5] and acute rejection [n=13] i
93 obtained for 77 patients (96.3%), with acute tubular necrosis being the most frequent: 23 (29.9%).
94       In ischemic allografts, eg, with acute tubular necrosis but no cellular rejection, DR3 was indu
95         Kidneys of moribund wt mice revealed tubular necrosis, but no histopathologic changes were ob
96 lar switch and the inflammatory responses to tubular necrosis can inform the discussion of therapeuti
97 enal function, renal inflammation, and acute tubular necrosis compared with mice receiving isotype co
98                     Most patients with acute tubular necrosis-delayed graft function that resolved la
99         Renal transplant biopsies with acute tubular necrosis demonstrated high levels of CtsD in dam
100  argue that a molecular switch downstream of tubular necrosis determines nephron regeneration versus
101 vious acute rejection episode, initial acute tubular necrosis, diastolic blood pressure above 85 mmHg
102                          Three patients with tubular necrosis died after seven, 11 and 26 days of oli
103         The clinical syndrome known as acute tubular necrosis does not actually manifest the morpholo
104  is used primarily for differentiating acute tubular necrosis from interstitial nephritis and as an a
105     Other lesions included progressive renal tubular necrosis, glomerular fibrin thrombosis, and red
106 k, previously thought to contribute to acute tubular necrosis, has now emerged as a potentially benef
107 l models of toxin and ischemia-induced acute tubular necrosis, human studies have not shown any clini
108 m cells ameliorates the acute phase of acute tubular necrosis in animals by promoting proliferation o
109 versed the dexamethasone-induced increase in tubular necrosis in freshly isolated renal tubules.
110        Transplant kidney biopsy showed acute tubular necrosis in patient 2.
111 sted in eight additional patients with acute tubular necrosis in the absence of hypovolemia.
112           Hypoxic injury is a major cause of tubular necrosis in the corticomedullary junction of iso
113 ed with severe COVID-19 in China found acute tubular necrosis in the kidney, a few patient reports ha
114 n was consistent with an area of focal acute tubular necrosis in the newly transplanted kidney.
115 orrelated with the degree of single cell and tubular necrosis in the S(3)-M segment of the proximal t
116 erum creatinine/urea, caspase-3 protein, and tubular necrosis induced by rhabdomyolysis in wild-type
117 emic AKI with significantly attenuated renal tubular necrosis, inflammation, and apoptosis when compa
118                                        Acute tubular necrosis involves dynamic cell death propagation
119 t biopsies, acute CsA toxicity but not acute tubular necrosis is associated with elevated levels of r
120  for recovery of the renal tubule from acute tubular necrosis is that surviving cells from the areas
121 ter cisplatin administration revealed marked tubular necrosis localized to the outer stripe of the ou
122 y attenuated increases in plasma creatinine, tubular necrosis, macrophage infiltration, oxidative str
123        Differential diagnosis with AKI-acute tubular necrosis may be challenging and kidney biomarker
124                                        Acute tubular necrosis mediates acute kidney injury (AKI) and
125 the folic acid nephrotoxicity model of acute tubular necrosis, mice expressing KCP survived high dose
126 il influx in an in vivo renal ischemic acute tubular necrosis model.
127 rfusion, Slit2 significantly inhibited renal tubular necrosis, neutrophil and macrophage infiltration
128       Thus, acute kidney injury is not acute tubular necrosis, nor is it renal failure.
129  reactions, thromboembolic events, and renal tubular necrosis occurred rarely.
130 ice, while histology showed multifocal acute tubular necrosis of the kidney and edema in the lungs of
131 ary YKL-40 concentration (P<0.001) and acute tubular necrosis on procurement biopsies (P=0.05).
132   No differences were seen in rates of acute tubular necrosis or overall acute rejection incidence, a
133 spase-3 activation, tubular apoptosis, acute tubular necrosis, or BBI, and reduced renal function.
134 phase of IRI had no impact on organ atrophy, tubular necrosis, or fibrosis.
135 d clinical rejection (P = 0.0006), and acute tubular necrosis (P < 0.0001).
136  mild renal damage (Cr, 0.9 +/- 0.1, minimal tubular necrosis; P < 0.01).
137 al "prerenal acute kidney injury" and "acute tubular necrosis" paradigm might be of limited interest
138 matching, occurrence of posttransplant acute tubular necrosis, presence versus absence of previous al
139                       There was a 4.2% acute tubular necrosis rate for the kidney.
140      Somewhat worse azotemia, but comparable tubular necrosis, resulted with desflurane use.
141  creatinine levels and a lower morphological tubular necrosis score than did wild-type mice with isch
142 od-perfused kidneys had vastly reduced acute tubular necrosis scores and degrees of terminal deoxynuc
143                           Furthermore, acute tubular necrosis scores were also similar in IL-1Ra-trea
144                                        Acute tubular necrosis secondary to ischemic acute renal failu
145 an biopsy specimens from patients with acute tubular necrosis showed similar increases in Nogo-B in c
146                                     In acute tubular necrosis, there are early transient increases in
147                 All patients developed acute tubular necrosis; two required a brief period of hemodia
148 sic graft failure comprised rejection, acute tubular necrosis, urinary tract infection/pyelonephritis
149 void low-flow states that could induce acute tubular necrosis, vascular thrombosis, or primary nonfun
150 AD organ recipients, the occurrence of acute tubular necrosis was a significnat risk factor for the d
151 any renal histopathologic changes, but acute tubular necrosis was found in 184 (17.4%).
152                      The prevalence of acute tubular necrosis was not related to animal size or model
153 olistically evaluated; minimal-to-mild renal tubular necrosis was observed.
154                                              Tubular necrosis was reduced 69% with nanoparticles trea
155 idney injury in contemporary articles, acute tubular necrosis was relatively uncommon and, when prese
156 e in two patients, with one developing acute tubular necrosis, was dose-limiting at 6.0 mg/m(2).
157 tients with acute renal failure due to acute tubular necrosis, we evaluated 256 patients enrolled in
158 l failure, glomerular capillary collapse and tubular necrosis were observed.
159                 Glomerulonephritis and acute tubular necrosis were present in 28 (68%) and 16 (39%) o
160 eated animals had significant cortical acute tubular necrosis, which was almost completely prevented
161 , patients with delayed graft function/acute tubular necrosis who were treated with tacrolimus+MMF ex
162 response that follows glycerol-induced acute tubular necrosis worsened peak renal injury in vivo.

 
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