1 HUS is responsible for most deaths associated with E. co
2 HUS is similar to TTP, but is associated with acute rena
3 HUS is usually categorized as typical, caused by Shiga t
4 HUS was the primary outcome.
5 oses (n = 11) exceeded the MTCD because of
2 HUS/TMA/HUS-like events.
6 Compared with waitlisted
adult HUS patients on dialysis, 5-year mortality risks were 73
7 We retrospectively studied
adult-
HUS end-stage renal disease patients (n = 559) placed on
8 n the intermediate outcome in children
after HUS due to E. coli O104:H4 have been lacking.
9 overall outcome of pediatric patients
after HUS due to E. coli O104:H4 was equivalent to previous re
10 at provide cost-effective protection
against HUS opens up new therapeutic approaches to managing dise
11 SpHUS accounts for 5-15% of
all HUS cases.
12 ucture revealing that the N-terminal DCB
and HUS regulatory domains of the Arf-GEF Sec7 form a single
13 Bloody diarrhea
and HUS were recorded as the most severe outcome for 44 and
14 ains, including strains isolated from HC
and HUS cases.
15 57:H7 resulted in higher hospitalization
and HUS rates than previous STEC outbreaks.
16 evelopment of thrombotic microangiopathy
and HUS induced by EHEC Shiga toxins in these preclinical mo
17 idence of pediatric HUS, which is defined
as HUS in children <18 years.
18 n dysregulation preceded HUS and worsened
as HUS developed.
19 Diarrhea-
associated HUS accounts for more than 90% of cases and is usually c
20 et and fibrin thrombi in diarrhea-
associated HUS.
21 ly no specific therapies for STEC-
associated HUS, and the mechanism of Stx-induced renal injury is no
22 Atypical HUS (aHUS) can result from genetic or autoimmune factors
23 Atypical HUS (aHUS) is a disorder most commonly caused by inherit
24 Atypical HUS is frequently a diagnosis of exclusion.
25 Atypical HUS recurred after 43 (34.1%) of the transplants; in fou
26 pients among patients with ESKD and
atypical HUS sharply increased between 2012 and 2016, from 46.2%
27 cherichia coli (STEC) infection, as
atypical HUS (aHUS), usually caused by uncontrolled complement ac
28 To assess how
atypical HUS epidemiology in France in the eculizumab era evolved
29 o be at a high and moderate risk of
atypical HUS recurrence, respectively.
30 or protein (MCP;CD46) predispose to
atypical HUS (aHUS), which is not associated with exposure to Shi
31 ent and inflammation, predispose to
atypical HUS, we assessed whether impaired TM function may advers
32 ulizumab to prevent post-transplant
atypical HUS recurrence throughout the country.
33 ess complement activation underlies
atypical HUS and is evident in Shiga toxin-induced HUS (STEC-HUS)
34 at included all adult patients with
atypical HUS (n=397) between 2007 and 2016.
35 , enrolling all adult patients with
atypical HUS who had undergone complement analysis and a kidney t
36 er-increasing number of associations
between HUS and a variety of drugs.
37 clude some of the newer associations
between HUS and a variety of infections, including, but not limi
38 aware that STEC, other than O157, can
cause HUS, and 34% correctly interpreted a positive Shiga toxi
39 equently produced by STEC strains that
cause HUS than is Stx1a.
40 Shiga toxin 2 are much more likely to
cause HUS than are those that produce Shiga toxin 1 alone.
41 t contribute to an enhanced ability to
cause HUS.
42 uman primates (Papio) recapitulated
clinical HUS after Stx challenge and that novel therapeutic inter
43 tric series of Shiga toxin-producing E.
coli HUS.
44 ame disease process, whereas others
consider HUS and TTP to be distinct clinical and pathologic entit
45 at express Stx2 are more likely to cause
D(+)
HUS than are E coli expressing only Stx1.
46 ea-associated hemolytic uremic syndrome (
D(+)
HUS) is caused by the ingestion of Escherichia coli that
47 ible exception of Shiga toxin-mediated HUS(
D+
HUS), long-term outcome information is often limited by
48 Renal damage in
D+
HUS is caused by Shiga toxin (Stx), which is elaborated
49 rhea-associated hemolytic uremic syndrome (
D+
HUS) is the most common cause of acute renal failure amo
50 ic purpura, a disease with similarities to
D+
HUS, in Adamts13(-/-) mice.
51 We find that the
DCB/
HUS domain amplifies the ability of Sec7 to activate Arf
52 he 259 children analyzed, 36 (14%)
developed HUS.
53 of the remaining 886, 126 (14.2%)
developed HUS.
54 men, 22 (92%) were adults, 7 (29%)
developed HUS, 5 (21%) developed bloody diarrhea, and 12 (50%) dev
55 the diarrhea phase more frequently
developed HUS than those who did not (36% vs 12%; P = .001).
56 A case was an attendee who
developed HUS or diarrhea between 8 and 24 June.
57 who received antibiotics, (3) who
developed HUS, and (4) for whom data reported timing of antibiotic
58 diarrhea (odds ratio = 1.81) and
developing HUS (odds ratio = 1.83) than did men.
59 ther established risk factors for
developing HUS, such as Shiga toxin 2 and EHEC serotypes traditiona
60 nd/or individuals at high risk of
developing HUS due to exposure to STEC.
61 lly protected against the risk of
developing HUS.
62 ociated with an increased risk of
developing HUS; however, after excluding studies at high risk of bi
63 nding of the pathogenetic mechanisms
driving HUS has increased.
64 ion is profoundly affected before and
during HUS, reflecting that subclinical endothelial dysfunction
65 ophils and monocytes as the key event
during HUS development.
66 macrophages were evaluated in an
established HUS mouse model.
67 for microvascular thrombosis in
experimental HUS.
68 erve as a marker of a greater propensity
for HUS, similar to the correlation between the absence of s
69 n the absence of stx(1) and a propensity
for HUS.
70 s (Stx1, Stx2) are primarily responsible
for HUS and the kidney and neurologic damage that ensue.
71 ation during STEC infections on the risk
for HUS.
72 Currently, specific therapeutics
for HUS are lacking, and therapy for patients is primarily s
73 argets and development of new treatments
for HUS is described.
74 t produce only Stx1 are rarely isolated
from HUS cases.
75 Of 927 STEC-infected children, 41 (4.4%)
had HUS at presentation; of the remaining 886, 126 (14.2%) d
76 However, SNPs from the
IL12A,
HUS, CYP2C8 genes were associated with time to anemia, a
77 of p38 MAPK may be of therapeutic benefit
in HUS.
78 Differences
in HUS frequency among E. coli O157:H7 outbreaks have been
79 /Ang-1 ratio were significantly different
in HUS vs the pre-HUS phase of illness or uncomplicated inf
80 ed RBC-derived microvesicles are elevated
in HUS patients and induced in vitro by incubation of RBCs
81 ar transplantation probability was higher
in HUS than in DM and HTN patients.
82 neutrophil/platelet aggregates) involved
in HUS pathogenesis.
83 associated with podocyte damage and loss
in HUS mice generated by the coinjection of Stx2 and LPS.
84 Activated neutrophils are observed
in HUS patients, yet it is unclear whether Stx exerts a dir
85 Shiga toxins (Stx) play a pivotal role
in HUS by triggering endothelial damage in kidney and brain
86 al HUS and is evident in Shiga toxin-
induced HUS (STEC-HUS).
87 E. coli O104:H4 caused the
largest HUS outbreak in children reported in detail to date and
88 Complement
mediated HUS (aHUS) has a worse prognosis compared with shiga tox
89 prognosis compared with shiga toxin
mediated HUS, often resulting in end stage renal disease.
90 e possible exception of Shiga toxin-
mediated HUS(D+HUS), long-term outcome information is often limit
91 ed to E. coli 0157:H7 (Shiga toxin-
mediated)
HUS, as well as the ever-increasing number of associatio
92 Diarrhea-
negative HUS is associated with complement dysregulation in up to
93 ic syndrome (HUS; n = 49), or glomerular-
non-
HUS (heterogeneous childhood onset; n = 216).
94 99% of the nonglomerular and glomerular-
non-
HUS groups were 42.5 years (95% confidence interval (CI)
95 uration (median, 13-14 days) compared to
non-
HUS patients (median, 33-34 days).
96 STEC O111 accounted for most cases
of HUS and was also the cause of 3 of 7 non-O157 STEC outbr
97 oli O157:H7 remains the predominant cause
of HUS in our institution.
98 o [OR] with 95% confidence interval [CI])
of HUS included younger age (0.77 [.69-.85] per year), leuk
99 ases platelet aggregation, in the context
of HUS.
100 In addition, a time course
of HUS disease progression that will be useful for identifi
101 venous fluid administration up to the day
of HUS diagnosis was associated with a decreased risk of re
102 those employing an appropriate definition
of HUS yielded an OR of 2.24 (95% CI, 1.45-3.46; I(2) = 0%)
103 t did not employ an acceptable definition
of HUS, there was a significant association.
104 tify features associated with development
of HUS (primary outcome) and need for renal replacement the
105 antibiotic administration and development
of HUS was 1.33 (95% confidence interval [CI], .89-1.99; I(
106 Development
of HUS, complications (ie, oligoanuric renal failure, invol
107 independently associated with development
of HUS.
108 tory response involved in the development
of HUS.
109 tric patients with the clinical diagnosis
of HUS were registered in Austria and Germany, and a subset
110 uid administration prior to establishment
of HUS and (2) a higher hematocrit value at presentation.
111 Renal failure is a key feature
of HUS and a major cause of childhood renal failure worldwi
112 or presumed STEC infection, and some form
of HUS that developed.
113 g the pathogenesis of the different forms
of HUS may prove helpful in clinical practice.
114 iga toxin mediated and the atypical forms
of HUS, with a focus on genetic variations in the complemen
115 inach, there was a notably high frequency
of HUS.
116 Management
of HUS remains supportive; there are no specific therapies
117 nfected outpatients without manifestation
of HUS, were investigated between May 15 and July 26, 2011,
118 osystem can function as an in vitro model
of HUS and showed that shear stress influences microvascula
119 We have developed a mouse model
of HUS by administering endotoxin-free Stx2 in multiple dos
120 A mouse model
of HUS designed to mirror human mutations in FH has now bee
121 at this C57BL/6 mouse is a complete model
of HUS that includes the thrombocytopenia, hemolytic anemia
122 he contribution of CCR1 in a murine model
of HUS.
123 the frequency of bloody diarrhea but not
of HUS and the length of the incubation period depended on
124 dy their efficacy in preventing the onset
of HUS during the systemic blood phase of Stx.
125 type have been linked to the pathogenesis
of HUS.
126 nd their contribution to the pathogenesis
of HUS.
127 the understanding of the pathophysiology
of HUS and could have an important effect on the developmen
128 apheresis (n = 13) during the acute phase
of HUS had comparable outcomes.
129 e that, when performed during progression
of HUS, passive immunization of mice with anti-Stx2 antibod
130 The higher rate
of HUS was observed across all antibiotic classes used.
131 e farm prior to the first clinical report
of HUS.
132 uraged because it might increase the risk
of HUS development.
133 trongly associated with an increased risk
of HUS, and eae was strongly associated with an increased r
134 Sera
of HUS patients, but not healthy individuals, recognized Hc
135 fice, moribund animals demonstrated signs
of HUS: increased blood urea nitrogen and serum creatinine
136 accharide (LPS) caused signs and symptoms
of HUS in mice, but the mechanism leading to renal failure
137 This type
of HUS is characterized by obstruction of the glomeruli and
138 per limit of normal for age) and
oligoanuric HUS.
139 sociated with the development of
oligoanuric HUS (OR, 2.38 [95% CI, 1.30-4.35]; I2 = 2%), renal repla
140 sociated with the development of
oligoanuric HUS.
141 104:H4 was equivalent to previous reports
on HUS due to other types of Shiga toxin-producing E. coli
142 (HUS), thrombotic microangiopathy (TMA),
or HUS-like events, exceeding the MTCD.
143 During 2000-2007, 627
pediatric HUS cases were reported.
144 ho had been included in the German
Pediatric HUS Registry during the 2011 outbreak.
145 s population-based surveillance of
pediatric HUS to measure the incidence of disease and to validate
146 nce rate for all reported cases of
pediatric HUS was 0.78 per 100,000 children <18 years.
147 The overall incidence of
pediatric HUS was affected by key characteristics of the surveilla
148 We report the incidence of
pediatric HUS, which is defined as HUS in children <18 years.
149 re significantly different in HUS vs the
pre-
HUS phase of illness or uncomplicated infection.
150 Angiopoietin dysregulation
preceded HUS and worsened as HUS developed.
151 The best way to
prevent HUS is to prevent primary infection with Shiga-toxin-pro
152 erstanding of bacterial factors that
promote HUS is incomplete.
153 Both patients had a history of
recurrent HUS after transplantation.
154 t to index visit was associated with
reduced HUS risk (OR, 0.70 [95% CI, .54-.90]).
155 s are hampered by the inability to
reproduce HUS with thrombotic microangiopathy, hemolytic anemia, a
156 Herein are
reviewed HUS and TTP along with recent progress shedding new ligh
157 athogenesis of STEC-HUS, aHUS, and
secondary HUS are discussed.
158 ic features in STEC-HUS, aHUS, and
secondary HUS are simultaneous damage to endothelial cells, intrav
159 olled complement activation, or as
secondary HUS with a coexisting disease.
160 Some have
secondary HUS with a coexisting disease or trigger such as autoimm
161 and some patients with STEC-HUS or
secondary HUS.
162 xin-free Stx challenge exhibit full
spectrum HUS, including thrombocytopenia, hemolytic anemia, and A
163 cting data for the use of eculizumab in
STEC HUS.
164 associated haemolytic uraemic syndrome (
STEC HUS) is also provided.
165 isits in patients are recommended after
STEC-
HUS.
166 the hemolytic process occurring during
STEC-
HUS.
167 ent and future choices of therapies for
STEC-
HUS.
168 is evident in Shiga toxin-induced HUS (
STEC-
HUS).
169 Typical HUS (ie,
STEC-
HUS) follows a gastrointestinal infection with STEC, whe
170 The common pathogenetic features in
STEC-
HUS, aHUS, and secondary HUS are simultaneous damage to
171 and similarities in the pathogenesis of
STEC-
HUS, aHUS, and secondary HUS are discussed.
172 erived microvesicles from patients with
STEC-
HUS (n = 25) were investigated for the presence of C3 an
173 psilon mutation, and some patients with
STEC-
HUS or secondary HUS.
174 identified in 1 patient each with fatal
Stx-
HUS, the HELLP (hemolysis, elevated liver enzymes, and l
175 ogy of renal microvascular thrombosis in
Stx-
HUS is still ill-defined.
176 ding to podocyte dysfunction and loss in
Stx-
HUS.
177 nction may adversely affect evolution of
Stx-
HUS.
178 for using soluble TM in the treatment of
Stx-
HUS.
179 associated with a higher rate of
subsequent HUS and should be avoided.
180 hoea-associated haemolytic uraemic
syndrome (
HUS) are caused by Shiga-toxin-producing bacteria; the p
181 ng 855 cases with hemolytic uremic
syndrome (
HUS) and 53 deaths.
182 or development of hemolytic uremic
syndrome (
HUS) and acute kidney injury (AKI).
183 e major causes of hemolytic uremic
syndrome (
HUS) and acute renal failure in children.
184 life-threatening hemolytic uremic
syndrome (
HUS) and are the main virulence factors of enterohemorrh
185 ngiopathy are the hemolytic-uremic
syndrome (
HUS) and thrombotic thrombocytopenic purpura (TTP), the
186 similarities with hemolytic uremic
syndrome (
HUS) and thrombotic thrombocytopenic purpura (TTP).
187 purpura (TTP) and hemolytic uremic
syndrome (
HUS) are appropriately at the top of a clinician's diffe
188 hagic colitis and hemolytic uremic
syndrome (
HUS) by colonizing the gut mucosa and producing Shiga to
189 are isolated from hemolytic-uremic
syndrome (
HUS) cases more frequently than are strains that produce
190 Hemolytic uremic
syndrome (
HUS) caused by intestinal Shiga toxin-producing Escheric
191 Hemolytic-uremic
syndrome (
HUS) caused by Shiga toxin-producing Escherichia coli in
192 Hemolytic-uremic
syndrome (
HUS) features episodes of small-vessel thrombosis result
193 STEC) can lead to hemolytic-uremic
syndrome (
HUS) in 5 to 10% of patients.
194 he development of hemolytic-uremic
syndrome (
HUS) in a small percentage of infected humans.
195 life-threatening hemolytic uremic
syndrome (
HUS) in any of 6 closed cohorts from 4 countries (1 coho
196 ith >800 cases of hemolytic uremic
syndrome (
HUS) in Germany, including 90 children.
197 Hemolytic uremic
syndrome (
HUS) is a potentially life-threatening condition.
198 Hemolytic uremic
syndrome (
HUS) is a thrombotic microangiopathy characterized by in
199 Hemolytic-uremic
syndrome (
HUS) is a thrombotic microangiopathy that is characteriz
200 The hemolytic uremic
syndrome (
HUS) is a triad of microangiopathic hemolytic anemia, th
201 Atypical hemolytic uremic
syndrome (
HUS) is associated with high recurrence rates after kidn
202 157:H7-associated hemolytic-uremic
syndrome (
HUS) is characterized by profound prothrombotic abnormal
203 Hemolytic uremic
syndrome (
HUS) is the life-threatenig sequela of intestinal infect
204 Postdiarrheal hemolytic uremic
syndrome (
HUS) is the most common cause of acute kidney failure am
205 The hemolytic uremic
syndrome (
HUS) is the most common cause of acute renal failure in
206 Brain injury in hemolytic-uremic
syndrome (
HUS) may be enhanced by inflammatory cytokine up-regulat
207 Hemolytic uremic
syndrome (
HUS) occurred in 12 patients (10 infected with STEC O157
208 high incidence of hemolytic uremic
syndrome (
HUS) occurred in Germany in May 2011.
209 known outbreak of hemolytic uremic
syndrome (
HUS) occurred in northern Germany.
210 , 8 patients with hemolytic uremic
syndrome (
HUS) or bloody diarrhea were reported in France.
211 nfection leads to hemolytic uremic
syndrome (
HUS) or other complications.
212 Hemolytic-uremic
syndrome (
HUS) results from infection by Shiga toxin (Stx)-produci
213 Identifying hemolytic uremic
syndrome (
HUS) risk factors is needed to guide care.
214 ls with diarrheal hemolytic uremic
syndrome (
HUS) seen at our institution during the study period, 16
215 infection called hemolytic-uremic
syndrome (
HUS) than isolates that make Stx1a only or produce both
216 arrhea-associated hemolytic uremic
syndrome (
HUS), a disorder of glomerular ischemic damage and wides
217 arrhea-associated hemolytic uremic
syndrome (
HUS), a disorder of thrombocytopenia, microangiopathic h
218 s and can lead to hemolytic-uremic
syndrome (
HUS), a life-threatening condition that principally affe
219 agent that causes hemolytic uremic
syndrome (
HUS), a microangiopathic disease characterized by hemoly
220 ction can lead to hemolytic-uremic
syndrome (
HUS), a severe disease characterized by hemolysis and re
221 t can progress to hemolytic uremic
syndrome (
HUS), a systematic microvascular syndrome with predomina
222 ns that can cause hemolytic-uremic
syndrome (
HUS), a thrombotic microangiopathy, following infections
223 t and severity of hemolytic uremic
syndrome (
HUS), and adverse outcomes in STEC-infected individuals.
224 Hemolytic-uremic
syndrome (
HUS), caused by Shiga toxin (Stx)-producing Escherichia
225 colitis (HC) and hemolytic uremic
syndrome (
HUS), due to the expression of one or more Shiga toxins
226 ations, including hemolytic-uremic
syndrome (
HUS), in animal models of disease.
227 e associated with hemolytic uremic
syndrome (
HUS), membranoproliferative glomerulonephritis (dense de
228 postenteropathic hemolytic uremic
syndrome (
HUS), most commonly caused by Shiga toxin (Stx)-producin
229 otentially lethal hemolytic uremic
syndrome (
HUS), particularly in children.
230 disease (SCD) and hemolytic uremic
syndrome (
HUS), pathological biophysical interactions among blood
231 Hemolytic-uremic
syndrome (
HUS), the life-threatening complication following infect
232 0 doses developed hemolytic uremic
syndrome (
HUS), thrombotic microangiopathy (TMA), or HUS-like even
233 Hemolytic uremic
syndrome (
HUS), which is caused by Shiga toxin-producing Escherich
234 colitis (HC) and hemolytic-uremic
syndrome (
HUS), which is the most common cause of acute renal fail
235 nfection, such as hemolytic-uremic
syndrome (
HUS), zinc might be capable of preventing severe sequela
236 isted adults with hemolytic uremic
syndrome (
HUS).
237 coli (STEC) cause hemolytic uremic
syndrome (
HUS).
238 equela called the hemolytic uremic
syndrome (
HUS).
239 c colitis and the hemolytic-uremic
syndrome (
HUS).
240 including 4 with hemolytic uremic
syndrome (
HUS).
241 viduals developed hemolytic-uremic
syndrome (
HUS).
242 ease consequence, hemolytic-uremic
syndrome (
HUS).
243 uses diarrhea and hemolytic uremic
syndrome (
HUS).
244 life-threatening hemolytic uremic
syndrome (
HUS).
245 leading cause of hemolytic uremic
syndrome (
HUS).
246 of children with hemolytic uremic
syndrome (
HUS).
247 purpura (TTP) and hemolytic uremic
syndrome (
HUS).
248 leading cause of hemolytic-uremic
syndrome (
HUS).
249 n associated with hemolytic-uremic
syndrome (
HUS).
250 t common cause of hemolytic-uremic
syndrome (
HUS).
251 spose to atypical hemolytic uremic
syndrome (
HUS).
252 oody diarrhea and hemolytic-uremic
syndrome (
HUS).
253 arrhea-associated hemolytic uremic
syndrome (
HUS).
254 colitis (HC) and hemolytic uremic
syndrome (
HUS).
255 th development of hemolytic uremic
syndrome (
HUS).
256 650), glomerular-hemolytic uremic
syndrome (
HUS; n = 49), or glomerular-non-HUS (heterogeneous child
257 Of
the HUS cases in which STEC was isolated, 28 (90%) were attr
258 n the dialysis-maintained cohorts within
the HUS (HR, 0.56; 95% CI, 0.35-0.91), HTN (HR, 0.50; 95% CI
259 = 11) exceeded the MTCD because of 2 HUS/
TMA/
HUS-like events.
260 mined, suggesting that several approaches
to HUS surveillance can be used to track trends.
261 he inflammatory response that contributes
to HUS development.
262 The vascular injury leading
to HUS is likely to be well under way by the time infected
263 sis and direct endothelial injury leading
to HUS phenotype.
264 toxin-producing Escherichia coli leading
to HUS was suspected following histology obtained at colono
265 re elevated in individuals who progressed
to HUS.
266 of antibiotic administration in relation
to HUS.
267 a significant proportion of non-shiga
toxin HUS.
268 The Oklahoma
TTP-
HUS (hemolytic uremic syndrome) Registry enrolled 70 con
269 <10%) in women enrolled in the Oklahoma
TTP-
HUS Registry from 1995 to 2012.
270 Typical HUS (ie, STEC-HUS) follows a gastrointestinal infection
271 iopoietins 1 and 2 (Ang-1/2), could
underlie HUS pathophysiology.
272 risk-of-bias studies employing commonly
used HUS criteria.
273 ransplantation probability in the
waitlisted HUS cohort was 60% versus 42% to 49% (P < 0.001) in the
274 The primary and secondary outcomes
were HUS (hematocrit <30% with smear evidence of hemolysis, p
275 efit over dialysis in waitlisted adults
with HUS.
276 tx2a only were significantly associated
with HUS (odds ratio, 14.2; 95% confidence interval, 7.9-25.6
277 iotic use were independently associated
with HUS and, additionally, these variables were each associa
278 strains are more frequently associated
with HUS than Stx1-producing strains.
279 of Stx2a, the major Stx type associated
with HUS, on human renal glomerular endothelial cells (HRGEC)
280 ophage to the kidney disease associated
with HUS.
281 ntribute to the renal damage associated
with HUS.
282 promote the renal thrombosis associated
with HUS.
283 Two cases
with HUS died.
284 ation and adverse outcomes for children
with HUS.
285 s (GN) were analyzed, and then compared
with HUS patients.
286 ted by the bacteria, is directly linked
with HUS.
287 ed by the bacterium, is directly linked
with HUS.
288 TM(LeD/LeD) mice
with HUS had a higher mortality rate than TM(wt/wt) mice.
289 associated with bloody diarrhea but not
with HUS.
290 be an effective treatment for patients
with HUS and/or individuals at high risk of developing HUS du
291 with STEC infection, including patients
with HUS as well as STEC-infected outpatients without manifes
292 Patients
with HUS receive only supportive treatment as the benefit of
293 Among the 30% to 50% of patients
with HUS who have no detectable complement defect, some have
294 ed in vitro and as observed in patients
with HUS.
295 IF mutations in a panel of 76 patients
with HUS.
296 ure of hydration status at presentation
with HUS was associated with the development of oligoanuric H
297 Two hundred nine patients presented
with HUS.
298 Patients presenting
with HUS had a significantly shortened shedding duration (med
299 has the strongest association worldwide
with HUS.
300 y outcome) in STEC-infected children
without HUS at initial presentation.