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1 in patients with either C3 glomerulopathy or thrombotic microangiopathy).
2 ning, chronic disease of complement-mediated thrombotic microangiopathy.
3 ocytopenic purpura (TTP), a life-threatening thrombotic microangiopathy.
4 se resulted in the development of glomerular thrombotic microangiopathy.
5 en with TAMOF syndrome can have VWF-mediated thrombotic microangiopathy.
6 had been diagnosed with posttransplantation thrombotic microangiopathy.
7 was predominantly from the development of a thrombotic microangiopathy.
8 There were no episodes of thrombotic microangiopathy.
9 dered in patients with transplant-associated thrombotic microangiopathy.
10 hrombocytopenia, hemolytic anemia, and renal thrombotic microangiopathy.
11 typical hemolytic uremic syndrome, a form of thrombotic microangiopathy.
12 l hemolytic uremic syndrome (aHUS) is a rare thrombotic microangiopathy.
13 g investigated in transplantation-associated thrombotic microangiopathy.
14 on, 3 relapsed, 5 died of infection and 2 of thrombotic microangiopathy.
15 neralocorticoid excess may also present with thrombotic microangiopathy.
16 g clinical disease, but mice still developed thrombotic microangiopathy.
17 Renal biopsy showed signs of chronic thrombotic microangiopathy.
18 osis, arterial cerebral thromboembolism, and thrombotic microangiopathy.
19 ad features of collapsing glomerulopathy and thrombotic microangiopathy.
20 ytes preceded and potentially contributed to thrombotic microangiopathy.
21 luminal deposits, which are classic signs of thrombotic microangiopathy.
22 essing the diagnostic challenge presented by thrombotic microangiopathy.
23 rted quality of life, and increased risk for thrombotic microangiopathy.
24 ypertension, proteinuria, renal failure, and thrombotic microangiopathy.
25 a, hemolytic anemia, and AKI with glomerular thrombotic microangiopathy.
26 helium, which may contribute to formation of thrombotic microangiopathy.
27 lytic-uremic syndrome (DHUS), a severe renal thrombotic microangiopathy.
28 the diagnosis and treatment of TTP and other thrombotic microangiopathies.
29 o events during pathogenesis of Stx-mediated thrombotic microangiopathies.
30 interest including thromboembolic events and thrombotic microangiopathies.
31 There were no deaths or thrombotic microangiopathies.
33 of these 4 grafts revealed focal glomerular thrombotic microangiopathy (4/4), transplant glomerulopa
34 may present in pregnancy or postpartum as a thrombotic microangiopathy, a life-threatening condition
35 -the PLASMIC score-to stratify patients with thrombotic microangiopathy according to their risk of ha
36 s factor response to endotoxin < 200 pg/mL), thrombotic microangiopathy (ADAMTS13 activity <57%), and
37 In group 2 (n = 10), grafts also developed thrombotic microangiopathy affecting mainly the glomerul
39 icient animals developed severe C5-dependent thrombotic microangiopathy after induction of complement
40 emolytic uremic syndrome/complement-mediated thrombotic microangiopathy (aHUS/CM-TMA), which has seve
41 mic medical centres in Boston, MA, USA, with thrombotic microangiopathy and a possible diagnosis of t
42 ssion alone, without TPE, rapidly controlled thrombotic microangiopathy and achieved a sustained clin
44 rienced xenograft rejection with evidence of thrombotic microangiopathy and antibody-mediated rejecti
45 rsus 49 +/- 3 mg/d; P < 0.01); and abrogated thrombotic microangiopathy and decreased plasma aldoster
46 k of TLR2/4 attenuated histone-induced renal thrombotic microangiopathy and glomerular necrosis in mi
47 ation is not required for the development of thrombotic microangiopathy and HUS induced by EHEC Shiga
48 creatinine at presentation, acute arteriolar thrombotic microangiopathy and onion skinning in small a
50 II infusion, proteinuria (17 +/- 9 mg/d) and thrombotic microangiopathy and plasma aldosterone (18 +/
51 ily characterized by vascular lesions (e.g., thrombotic microangiopathy and vasculitis) is a hallmark
52 Eculizumab inhibited complement-mediated thrombotic microangiopathy and was associated with signi
53 ith transplant glomerulopathy and glomerular thrombotic microangiopathy and was localized to glomerul
54 stitial oedema, red cell extravasation, rare thrombotic microangiopathy, and complement deposition.
55 t-versus-host disease, transplant-associated thrombotic microangiopathy, and eculizumab treatment cor
57 rrow transplantation/chemotherapy-associated thrombotic microangiopathy, and in the hemolytic-uremic
58 s including tubular swelling, vacuolization, thrombotic microangiopathy, and increased expression of
59 se, is decreased in adults with VWF-mediated thrombotic microangiopathy, and intensive plasma exchang
60 underlying matrix and platelet aggregation, thrombotic microangiopathy, and neutrophilic infiltratio
62 tic events manifested with acute and chronic thrombotic microangiopathy; and (c) EC proinflammatory c
63 thies, HELLP syndrome, transplant-associated thrombotic microangiopathy, antiphospholipid antibody sy
65 tologists alike, classically associated with thrombotic microangiopathy are the hemolytic-uremic synd
66 sufficient to establish posttransplantation thrombotic microangiopathy as a discrete clinical or pat
67 Notably, we identify complement-mediated thrombotic microangiopathy as a key pathophysiologic mec
68 tself and with LDL may improve the course of thrombotic microangiopathies, atherosclerosis, and other
69 , who are frequently called upon to diagnose thrombotic microangiopathy, be aware of its association
70 ation (atypical hemolytic uremic syndrome as thrombotic microangiopathy), biopsy appearance (dense de
71 in patients with TTP during acute attacks of thrombotic microangiopathy but not in those in remission
72 (C, 6%; C3, 1%), associated mainly with late thrombotic microangiopathy (C: 78%; C3: 11% of cases).
74 lytic uremic syndrome (aHUS), a rare form of thrombotic microangiopathy caused by complement pathogen
75 c purpura (TTP) is a rare, potentially fatal thrombotic microangiopathy caused by severe ADAMTS13 (a
76 tic uremic syndrome is a complement-mediated thrombotic microangiopathy caused by uncontrolled activa
77 ypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy caused by uncontrolled activa
78 P) is characterized by recurring episodes of thrombotic microangiopathy, causing ischemic organ impai
79 ediated thrombocytopenic purpura (iTTP) is a thrombotic microangiopathy characterized by an acquired
80 VID-19 autopsy reports have shown widespread thrombotic microangiopathy characterized by extensive di
82 purpura (TTP) is a rare and life-threatening thrombotic microangiopathy characterized by microangiopa
83 sanguineous family with patients affected by thrombotic microangiopathy characterized by significant
84 hemolytic uremic syndrome (aHUS) is a severe thrombotic microangiopathy characterized by uncontrolled
88 lytic uremic syndrome (aHUS) is a rare renal thrombotic microangiopathy commonly associated with rare
90 For 19 months, the patient had relapsing thrombotic microangiopathy despite plasma exchange; sple
92 ns or by autoantibodies is associated with a thrombotic microangiopathy disease, atypical hemolytic u
93 ring system also more consistently diagnosed thrombotic microangiopathy due to severe ADAMTS13 defici
95 hange in the platelet count (in trial 1) and thrombotic microangiopathy event-free status (no decreas
97 can cause hemolytic-uremic syndrome (HUS), a thrombotic microangiopathy, following infections by Shig
98 ndrome during pregnancy, and implications of thrombotic microangiopathies for subsequent pregnancies
99 S, and their frequency is six-fold higher in thrombotic microangiopathy forms associated with bone ma
100 registry of the French Reference Center for Thrombotic Microangiopathies from 2000-2010 to identify
101 alternative pathway that are associated with thrombotic microangiopathies, glomerulonephritides, and
103 patients with bone marrow transplant-related thrombotic microangiopathy had anti-factor H IgM autoant
105 elated complication, including preeclampsia, thrombotic microangiopathy, heart failure, sepsis, or po
106 pered by the inability to reproduce HUS with thrombotic microangiopathy, hemolytic anemia, and acute
107 arks of hemolytic uremic syndrome, including thrombotic microangiopathy, hemolytic anemia, thrombocyt
108 nsider this newly established mouse model of thrombotic microangiopathy highly predictive for investi
109 nt mediated, untreated transplant-associated thrombotic microangiopathy (hrTMA) has dismal outcomes d
110 alysis of case series of posttransplantation thrombotic microangiopathy illustrates uncertainties reg
111 pact of rapid genomic screening for managing thrombotic microangiopathies in 18 prospective cases, ac
116 liorate malignant nephrosclerotic lesions of thrombotic microangiopathy in salt-loaded, stroke-prone,
117 ecome more prominent, such as development of thrombotic microangiopathy in the graft or systemic cons
118 sometimes complicated by a potentially fatal thrombotic microangiopathy in the recipient baboons.
119 erized by marked interstitial hemorrhage and thrombotic microangiopathy in the renal vasculature.
120 enes have been demonstrated to predispose to thrombotic microangiopathies including atypical hemolyti
121 l role for aldosterone in the development of thrombotic microangiopathy, independent of hypertension.
126 nitoring of such pregnancies for episodes of thrombotic microangiopathy is essential but, the best st
127 recise spectrum of complement-mediated renal thrombotic microangiopathy is still a matter of debate.
128 l hemolytic uremic syndrome (aHUS), a severe thrombotic microangiopathy, is often related to compleme
129 the development of T3SS-dependent intestinal thrombotic microangiopathy (iTMA) and ischemic enteritis
130 F multimers, as are present in patients with thrombotic microangiopathy, lack an inhibitory effect on
131 a life-threatening disease characterized by thrombotic microangiopathy leading to end-organ damage.
132 proteinuria (78 +/- 7 mg/d) were greater and thrombotic microangiopathy lesions were comparable to SH
133 rious condition, characterized by multiorgan thrombotic microangiopathy, mainly affecting children.
134 ombocytopenic purpura (cTTP) is an ultrarare thrombotic microangiopathy mediated through inherited de
136 x glomerulonephritis (n = 3), HIV-associated thrombotic microangiopathy (n = 1), and HIV-negative pat
137 of necroinflammation to AKI is discussed in thrombotic microangiopathies, necrotizing and crescentic
139 disease) and paraneoplastic manifestations, thrombotic microangiopathy, obstructive nephropathy due
142 genetic and therapeutic studies showed that thrombotic microangiopathy of the kidney can still devel
145 In addition, two patients had findings of thrombotic microangiopathy, one had pauci-immune crescen
146 ity might prove useful in the future care of thrombotic microangiopathy patients and might be a ratio
148 e in understanding the pathogenesis of other thrombotic microangiopathies, post-HSCT TMA remains poor
151 y appears to be an important risk factor for thrombotic microangiopathy rather than a specific diagno
152 enrolled in the French Reference Center for Thrombotic Microangiopathies registry between 2000 and 2
157 ek 26, 77.8% of patients achieved a complete thrombotic microangiopathy response; 94.4%, 88.9% and 83
158 ggest that in DGKE-associated aHUS patients, thrombotic microangiopathy results from impaired EC prol
159 s presented with biopsy-proven de novo renal thrombotic microangiopathy (RTMA), occurring 5 to 120 d
160 or modestly reduced (>20%) in other forms of thrombotic microangiopathy secondary to hematopoietic pr
161 All patients with transplant-associated thrombotic microangiopathy should be screened for the ca
162 their relative roles in the pathogenesis of thrombotic microangiopathy, SHRSP were adrenalectomized
163 to overlapping clinical features with other thrombotic microangiopathy syndromes including hypertens
164 uated the incidence of transplant-associated thrombotic microangiopathy (TA-TMA) in adult allogeneic
167 stem cell transplantation (HSCT)-associated thrombotic microangiopathy (TA-TMA) is not completely un
169 (HSCT) recipients with transplant-associated thrombotic microangiopathy (TA-TMA), and untreated patie
170 sporadic hemolytic-uremic syndrome (HUS) are thrombotic microangiopathies that occur in the absence o
171 These findings could be a consequence of a thrombotic microangiopathy that affected retinal structu
172 l role in creating the hyperinflammation and thrombotic microangiopathy that appear to contribute to
173 d related to a hyper-inflammatory status and thrombotic microangiopathy that are observed in severe C
174 uremic syndrome (aHUS) is a life-threatening thrombotic microangiopathy that can progress, when untre
176 tibody-mediated rejection (AMR) with C4d and thrombotic microangiopathy that eventually led to graft
177 otheliosis" represents a specific variant of thrombotic microangiopathy that is characterized by glom
179 nties about the evaluation and management of thrombotic microangiopathy that occurs following allogen
180 topenic purpura (iTTP) is a life-threatening thrombotic microangiopathy that presents with microangio
181 lthough there was no evidence of spontaneous thrombotic microangiopathy, the hepatocyte-specific FH-d
182 ne response that fuels hyperinflammation and thrombotic microangiopathy, thereby increasing coronavir
183 ication of patients with posttransplantation thrombotic microangiopathy; these criteria may result in
185 e innate immune system in the development of thrombotic microangiopathy (TM) after alpha1,3-galactosy
186 and marrow transplantation (BMT)-associated thrombotic microangiopathy (TM) contributes to transplan
188 cell chimerism, however, results in a severe thrombotic microangiopathy (TM) that includes pronounced
189 cell chimerism, however, results in a severe thrombotic microangiopathy (TM) that includes pronounced
190 cell chimerism, however, results in a severe thrombotic microangiopathy (TM) that includes vascular i
193 regulation contributes to the development of thrombotic microangiopathy (TMA) after hematopoietic ste
194 emonstration of impaired C regulation in the thrombotic microangiopathy (TMA) atypical hemolytic urem
195 purpura (TTP) is an acute, life-threatening thrombotic microangiopathy (TMA) caused by acquired or c
196 ypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy (TMA) characterized by excess
199 ase reports have described the occurrence of thrombotic microangiopathy (TMA) following IV abuse of e
206 ietic stem cell transplant (HSCT)-associated thrombotic microangiopathy (TMA) is a complication that
215 the numerous adverse side effects of FK506, thrombotic microangiopathy (TMA) stands out as an infreq
216 typical hemolytic uremic syndrome, a type of thrombotic microangiopathy (TMA) that causes renal failu
217 l hemolytic uremic syndrome (aHUS) develop a thrombotic microangiopathy (TMA) that in most cases is a
218 glomerular proliferative lesions, glomerular thrombotic microangiopathy (TMA) was found as a common g
219 Rates of veno-occlusive disease (VOD) and thrombotic microangiopathy (TMA) were lower in the nonsi
220 Complement activation has a major role in thrombotic microangiopathy (TMA), a disorder that can oc
221 hreatening inflammatory responses, including thrombotic microangiopathy (TMA), acute kidney injury du
222 uncontrolled complement activation, systemic thrombotic microangiopathy (TMA), and vital organ damage
223 ed complement activity, the development of a thrombotic microangiopathy (TMA), and widespread end org
225 ons in fH are associated with a rare form of thrombotic microangiopathy (TMA), known as atypical hemo
226 mia (MAHA) with thrombocytopenia, suggests a thrombotic microangiopathy (TMA), linked with thrombus f
227 s developed hemolytic uremic syndrome (HUS), thrombotic microangiopathy (TMA), or HUS-like events, ex
228 These all result in pathologic features of thrombotic microangiopathy (TMA), which cause endothelia
229 iciency virus-2 (HIV-2) strain develop renal thrombotic microangiopathy (TMA), which morphologically
242 istinguishes TTP from HUS and other types of thrombotic microangiopathy (TMA); therefore, the term TT
245 accurately define the specific etiologies of thrombotic microangiopathies (TMAs) based on objective,
247 , would be the second hit for development of thrombotic microangiopathies (TMAs), a group of life-thr
248 e events (AEs), thromboembolic events (TEs), thrombotic microangiopathies (TMAs), and immunogenicity
250 5N (C3KI) mice developed spontaneous chronic thrombotic microangiopathy together with hematuria, thro
253 g group of specialty-specific experts in the thrombotic microangiopathies was convened to review the
256 endothelial growth factor (VEGF) results in thrombotic microangiopathy, we addressed the possibility
258 t is one of a group of conditions termed the thrombotic microangiopathies, which are characterized by
259 croangiopathic hemolytic anemia characterize thrombotic microangiopathy, which includes two major dis
260 diseases that result in a common pathology, thrombotic microangiopathy, which is classically charact
261 The emerging data on the risk of developing thrombotic microangiopathy while on Ticlopidine and the
264 ypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy with severe renal injury seco
265 r renal injury and in particular developed a thrombotic microangiopathy, with mesangiolysis, endothel
266 t lesion associated with graft failure was a thrombotic microangiopathy, with resulting ischemic inju