ライフサイエンスコーパス: suPAR

1 suPAR also was increased in plasma from patients with EG

2 suPAR by itself is not the cause for direct podocyte inj

3 suPAR correlated significantly with urinary nephrin, IgG

4 suPAR did not significantly stimulate cell signaling or

5 suPAR levels >2.82 ng/ml had a 3.38-fold increase in the

6 suPAR levels were associated with height-adjusted total

7 suPAR levels were associated with progressive decline in

8 suPAR predicts all-cause and cardiovascular death over a

9 suPAR was measured by enzyme-linked immunosorbent assay,

10 suPAR was measured using a commercially available enzyme

11 suPAR was superior to the combination of conventional pl

12 suPAR-K139A/H143A displayed a 50% reduction in scuPA-med

13 asma biomarkers (TNFR1, FGF23, TNFR2, KIM-1, suPAR, and others) and urine biomarkers (KIM-1, NGAL, an

14 asma levels of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were associated with increased risk of

15 centrations of KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40 were each associated with a greater ri

16 Plasma MCP-1, suPAR, and YKL-40 were not independently associated with

17 and fibrosis (KIM-1, TNFR-1, TNFR-2, MCP-1, suPAR, and YKL-40).

18 as YKL-40), or inflammation (such as MCP-1, suPAR, TNF receptor-1 [TNFR-1], and TNFR-2) may identify

19 tigated whether plasma KIM-1, YKL-40, MCP-1, suPAR, TNFR-1, and TNFR-2 are associated with GFR declin

20 uma was significantly associated with age 24 suPAR (beta = 0.06, 95 % CI [.03, 0.1], p = 0.001), CRP

21 tivation and causes proteinuria in mice in a suPAR-dependent manner.

22 Adding suPAR to clinical scores could improve the recognition a

23 Admission suPAR levels in patients hospitalized for COVID-19 are p

24 0.6-44.2) to 39.3 (28.8-63.4; P<0.0001), and suPAR levels decreased from a median of 6.781 to 4.129 p

25 (odds ratio[OR] 1.68, 95 %CI 1.20-2.34) and suPAR (OR 1.74, 95 %CI 1.17-2.58).

26 radation product, heat shock protein-70, and suPAR were measured in 3278 patients undergoing coronary

27 sociation of adult stressful life events and suPAR at age 45-children with more ACEs showed higher su

28 treatment of piglets with RAP, anti-LRP, and suPAR completely prevented, and the ERK MAPK antagonist

29 ta-2 microglobulin (beta-2 m), neopterin and suPAR soluble urokinase-type plasminogen activator recep

30 study, we examined associations of PTSD and suPAR in two research cohorts-the E-Risk Study (United K

31 r, the possible relationship between SRH and suPAR in the assessment of hospitalization and mortality

32 Both SRH and suPAR were independently associated with risk of acute h

33 In unadjusted analyses, SRH and suPAR were individually associated with higher risks of

34 We assessed suPAR levels in 649 patients with ADPKD who underwent sc

35 only significant predictors of the augmented suPAR levels in plasma and saliva, respectively.

36 o characterize associations between baseline suPAR levels and follow-up eGFR or incident ESRD.

37 We examined the association between suPAR levels and incident in-hospital AKI.

38 ormation of a zinc-dependent complex between suPAR and HKa.

39 dentified high-affinity interactions between suPAR, APOL1 and alphavbeta3 integrin, whereby APOL1 pro

40 We investigated the relationship between suPAR levels and podocyte changes and the impact of ther

41 The relationship between suPAR levels and the eGFR at baseline, the change in the

42 gonist of alphavbeta3 integrin RGDfv blocked suPAR-induced suppression of nephrin.

43 Both suPAR (b = 0.015; 95% CI, 0.002-0.037) and sleep problem

44 tions to reduce inflammation, as measured by suPAR, for adolescents at high risk of MDD to potentiall

45 Circulating suPAR levels were elevated in 84.3% and 55.3% of patient

46 Here, we analyzed circulating suPAR levels in two cohorts of children and adults with

47 associations between a change in circulating suPAR with different therapeutic regimens and with remis

48 We show that circulating suPAR activates podocyte beta(3) integrin in both native

49 In conclusion, suPAR levels are elevated in geographically and ethnical

50 Among PWH, higher CSF suPAR levels correlated with higher CSAR values (r = 0.4

51 dance with the previous study, the delivered suPARs are deposited in the glomeruli.

52 In adult dengue, suPAR may be a reliable prognostic biomarker for severe

53 EGFRvIII-expressing GBM cells, tumor-derived suPAR was detected in the plasma, and the level was sign

54 Early suPAR-guided anakinra decreased SRF and restored the pro

55 It was studied if early suPAR-guided anakinra treatment can prevent severe respi

56 l life events from age 38 to 44 had elevated suPAR at age 45, and had significantly greater increases

57 loneliness at age 38 or age 45 had elevated suPAR at age 45.

58 those with depressive disorder had elevated suPAR levels relative to controls (k = 3, SMD = 0.61, 95

59 The cellular source(s) of elevated suPAR associated with future and progressing kidney dise

60 For plasma, elevated suPAR concentrations were also identified for those with

61 To determine whether elevated suPAR levels are associated with renal disease progressi

62 It is unknown whether elevated suPAR levels in patients with normal kidney function are

63 from 0-17 years was associated with elevated suPAR (beta = 0.04, 95 % CI [.005, 0.07], p = 0.025) and

64 f 70 sessions of PE, which partly eliminated suPAR, with a mean reduction of 37 +/- 12% of serum conc

65 levels in plasma and saliva and to evaluate suPAR as a biomarker of periodontitis and CHD.

66 Further research should examine suPAR as potential marker of chronic systemic inflammati

67 The synergy of circulating factor suPAR and APOL1 G1 or G2 on alphavbeta3 integrin activat

68 tudies); and 1.42 (95% CI, 1.30 to 1.55) for suPAR (12 studies).

69 ants G1 and G2 exhibited higher affinity for suPAR-activated avb3 integrin than APOL1 G0.

70 lapping 20-amino acid peptides prepared from suPAR, two regions for HK binding were identified.

71 High suPAR levels correlated with incident CVD and atheroscle

72 High suPAR levels were associated with acute kidney injury in

73 A high suPAR level >/=3.5 ng/mL was associated with all-cause d

74 ed an independent association between a high suPAR level at baseline and increased hazard rates for b

75 in the BM of proteinuric animals having high suPAR, and these cells efficiently transmit proteinuria

76 Patients with high suPAR levels were more likely to have progression of the

77 A higher suPAR level at baseline was associated with a greater de

78 , patients with an NPHS2 mutation had higher suPAR levels than those without a mutation.

79 tis and periodontitis + CHD presented higher suPAR levels in both plasma and saliva in comparison wit

80 d CRP (C-reactive protein), each 1-SD higher suPAR was associated with a 21% to 31% increased risk of

81 age 45-children with more ACEs showed higher suPAR levels after experiencing stressful life events as

82 , confirmed experimentally to lead to higher suPAR levels.

83 al discrimination was associated with higher suPAR levels (b = 0.006; 95% CI, 0.001-0.011; P = .01) a

84 suPAR, and strengthened in those with higher suPAR levels.

85 The highest suPAR quartile (vs.

86 In multivariable analysis, the highest suPAR tertile was associated with a 9.15-fold increase i

87 Together, these results identify suPAR as a functional connection between the BM and the

88 there was no sustained significant change in suPAR levels before and after the course of intensified

89 binding of scuPA to more than one epitope in suPAR is required for its optimal activation and associa

90 the gene encoding uPAR, forced increases in suPAR concentration result in FSGS-like glomerular lesio

91 e 45 in Dunedin had significant increases in suPAR from age 38 to 45 (beta = 0.45, p = 0.034).

92 , and had significantly greater increases in suPAR from baseline to follow-up across the same period.

93 Increases in suPAR were significantly related to concomitant declines

94 oclonal antibody attenuated kidney injury in suPAR-overexpressing mice and normalized bioenergetic ch

95 In accordance with the results seen in suPAR-associated proteinuric animal models, in which kid

96 rrelates with inflammatory markers including suPAR, nadir CD4 count, and prevalence of age-associated

97 coronavirus 2 (SARS-CoV-2) causes increased suPAR levels and glomerulopathy in African green monkeys

98 AKI incidence rose with increasing suPAR tertiles, from a 6.0% incidence in patients with s

99 Binding of labeled suPAR/scuPA was inhibited by unlabeled complex, but not

100 e per 1.73 m(2)) at baseline had the largest suPAR-related decline in the eGFR.

101 the maximum activity induced by full-length suPAR (5 nM), respectively.

102 udy unveiled that interaction of full-length suPAR with alphavbeta3 integrin expressed on podocytes r

103 s phenomenon is mediated only by full-length suPAR, is time-and dose-dependent and is associated with

104 ple regression analysis suggested that lower suPAR levels associated with higher estimated GFR, male

105 d risk was attenuated in patients with lower suPAR, and strengthened in those with higher suPAR level

106 Patients in the lowest suPAR tertile (<2.18 ng/ml) had a 6.8% decline in eGFR a

107 ients hospitalized for COVID-19, we measured suPAR levels in plasma samples from 352 adult patients t

108 Biobank (mean age, 63 years; 65% men; median suPAR level, 3040 pg per milliliter) and determined rena

109 The median suPAR concentration was 3010 pg/mL (interquartile range,

110 The median suPAR level was 2.47 ng/ml and median height-adjusted to

111 The median suPAR level was 5.61 ng/ml.

112 ted with suPAR and together explained 14% of suPAR phenotypic variation.

113 surgery.Objectives: To study the ability of suPAR (soluble urokinase plasminogen activator receptor)

114 The activities of suPAR were replicated by conditioned medium (CM) from EG

115 Addition of suPAR to the 3-BRS significantly improved the C statisti

116 Cross-sectional associations of suPAR with lifestyle and CVD risk factors were assessed,

117 ere used to evaluate genetic associations of suPAR, and relationships of suPAR with incident CVD outc

118 ct synergistically to inhibit the binding of suPAR and to stimulate plasminogen activator activity.

119 Binding of suPAR to alpha4beta1 and alphavbeta3 is blocked by known

120 scuPA induced the binding of suPAR to LM-TK- cells.

121 uPAR antibodies effectively block binding of suPAR to these integrins.

122 further find that a higher concentration of suPAR before transplantation underlies an increased risk

123 studies observed increased concentration of suPAR in various glomerular diseases and in other human

124 characterized by increased concentration of suPAR.

125 Further, little degradation of suPAR was detected, suggesting that cell-bound complex d

126 findings suggest that glomerular deposits of suPAR caused by elevated plasma levels are not sufficien

127 d-childhood trauma) for the dysregulation of suPAR in early adulthood and support the measurement of

128 roduced conflicting results on the effect of suPAR on podocyte injury, effacement of foot processes,

129 hree mouse models, we explore the effects of suPAR on kidney function and morphology.

130 However, such deposition of either form of suPAR in the kidney did not result in increased glomerul

131 d provide new insights into the influence of suPAR and YKL-40 as plasma biomarkers that require valid

132 model by demonstrating that the infusion of suPAR inhibits expression of nephrin and WT-1 in podocyt

133 Injection of suPAR resulted in its deposition exclusively in the glom

134 We investigated whether a high level of suPAR predisposed patients to acute kidney injury in mul

135 An elevated level of suPAR was independently associated with incident chronic

136 e) had significantly higher median levels of suPAR (but not CRP or IL-6) compared with patients not l

137 ed psychiatric disorder had higher levels of suPAR compared to propensity score-matched patients with

138 We measured plasma levels of suPAR preprocedurally in patients who underwent coronary

139 ile) had significantly higher mean levels of suPAR six years later than adolescents who had been iden

140 At all time points, higher levels of suPAR were associated with increased risk of non-AIDS ev

141 Elevated levels of suPAR were strongly, consistently, and independently pre

142 ble for the elevated, pathological levels of suPAR, as evidenced by BM chimera and BM ablation and ce

143 rly adulthood and support the measurement of suPAR in combination with other markers to better charac

144 However, whether overexpression of suPAR, per se, contributes to the pathogenesis of FSGS i

145 roceeded less efficiently in the presence of suPAR.

146 Using the lowest quartile of suPAR as the reference, crude hazard ratio for cardiovas

147 secondary outcome, according to quartile of suPAR level.

148 among participants in the lowest quartile of suPAR levels as compared with -4.2 ml per minute per 1.7

149 ic kidney disease in the highest quartile of suPAR levels was 3.13 times as high (95% confidence inte

150 hazards regression according to quartiles of suPAR, including age, sex, use of lipid-lowering drugs,

151 ssociation between the relative reduction of suPAR after 26 weeks of treatment and reduction of prote

152 therapy results in significant reduction of suPAR levels and complete or significant improvement of

153 associations of suPAR, and relationships of suPAR with incident CVD outcomes and overall mortality w

154 nvestigation into a potential causal role of suPAR in cardiovascular disease is warranted.

155 complex and still poorly understood role of suPAR in FSGS.

156 imens and with remission support the role of suPAR in the pathogenesis of FSGS.

157 f gingival health, periodontitis, and CHD on suPAR levels in plasma and saliva and to evaluate suPAR

158 ed by unlabeled complex, but not by scuPA or suPAR added separately, indicating cellular binding site

159 of plasma exchange (PE) on clinical outcome, suPAR levels, and in vitro podocyte beta3-integrin activ

160 (Pcsk9) transfection in mice overexpressing suPAR (suPARTg) led to substantially increased atheroscl

161 In a cohort of 1991 COVID-19 patients, suPAR levels exhibit a stepwise association with protein

162 In the febrile phase, suPAR was a prognostic biomarker of severe dengue, with

163 Furthermore, studies that analysed plasma suPAR concentrations found elevated plasma suPAR levels

164 a suPAR concentrations found elevated plasma suPAR levels in individuals with any psychiatric disorde

165 (lo) cells in the BM, leading to high plasma suPAR and proteinuric kidney disease.

166 PAR-encoding gene (PLAUR) with higher plasma suPAR levels.

167 However, plasma suPAR levels were significantly elevated in those with a

168 We measured plasma suPAR levels in 3683 persons enrolled in the Emory Cardi

169 was the only significant predictor of plasma suPAR (P = .035) while hs-CRP was the only significant p

170 rent FSGS and a temporary lowering of plasma suPAR as well as podocyte beta3-integrin activation.

171 APOL1 risk variants was dependent on plasma suPAR levels: APOL1-related risk was attenuated in patie

172 Pleural suPAR could more accurately predict the subsequent inser

173 C 0.92 vs. 0.76).Conclusions: Raised pleural suPAR was predictive of patients receiving more invasive

174 ions).Measurements and Main Results: Pleural suPAR levels were significantly higher in effusions that

175 Median pretreatment suPAR levels were higher among those with severe (>/=75%

176 Purified suPAR was biologically active when added to cultures of

177 e urokinase plasminogen activation receptor (suPAR) is risk factor for kidney disease and biomarker f

178 le urokinase plasminogen activator receptor (suPAR) and incident non-AIDS comorbidity and all-cause m

179 le urokinase plasminogen activator receptor (suPAR) and olfactomedin 4, and mast cell mediators, chym

180 okinase-type plasminogen activator receptor (suPAR) are generally elevated in sera from children and

181 okinase-type plasminogen activator receptor (suPAR) as a circulating factor implicated in FSGS.

182 le urokinase plasminogen activator receptor (suPAR) has been identified as an immunologic risk factor

183 okinase-type plasminogen activator receptor (suPAR) have been associated with focal segmental glomeru

184 le urokinase plasminogen activator receptor (suPAR) in focal segmental glomerulosclerosis (FSGS) as t

185 le urokinase plasminogen activator receptor (suPAR) independently predicts chronic kidney disease (CK

186 le urokinase plasminogen activator receptor (suPAR) is a circulating factor implicated in the onset a

187 le urokinase plasminogen activator receptor (suPAR) is a signaling glycoprotein thought to be involve

188 le urokinase plasminogen activator receptor (suPAR) is an immune-derived circulating signaling molecu

189 okinase-type plasminogen activator receptor (suPAR) is implicated in the pathogenesis of native and r

190 asma soluble plasminogen activator receptor (suPAR) levels, which in turn induces chemotaxis of CD34

191 okinase-type plasminogen activator receptor (suPAR) plays an essential function in leukocytes and end

192 le urokinase plasminogen activator receptor (suPAR) prevents impairment of cerebrovasodilation induce

193 okinase-type plasminogen activator receptor (suPAR) was associated recently with focal segmental glom

194 okinase-type plasminogen activator receptor (suPAR) was performed with archived plasma samples to pre

195 le urokinase plasminogen activator receptor (suPAR), a marker of immune activation, is predictive of

196 le urokinase plasminogen activator receptor (suPAR), a proposed pathomechanically involved molecule i

197 le urokinase plasminogen activator receptor (suPAR), an inflammation marker, are strongly predictive

198 le urokinase plasminogen activator receptor (suPAR), lipopolysaccharide binding protein (LBP), beta-D

199 le urokinase plasminogen activator receptor (suPAR), which contains the three domains of the wild-typ

200 le urokinase plasminogen activator receptor (suPAR).

201 and His(143) to alanine in soluble receptor (suPAR) reduced the affinity for scuPA approximately 5-fo

202 mposed of recombinant, soluble uPA receptor (suPAR) and single chain uPA (scuPA) to a cell line (LM-T

203 Elevation in soluble urokinase receptor (suPAR) and proteinuria are common signs in patients with

204 verexpression of soluble urokinase receptor (suPAR) causes pathology in animal models similar to prim

205 Recently, serum soluble urokinase receptor (suPAR) has been proposed as a cause of two thirds of cas

206 Soluble urokinase receptor (suPAR) is a circulatory molecule that activates alphavbe

207 eport that serum soluble urokinase receptor (suPAR) is elevated in two-thirds of subjects with primar

208 Serum soluble urokinase receptor (suPAR) levels strongly predict incident CKD stage 3 in a

209 le urokinase plasminogen activator receptor [suPAR]) and sleep problems were collected to consider as

210 okinase-type plasminogen activator receptor, suPAR and neutrophil gelatinase-associated lipocalin, NG

211 and well characterized forms of recombinant suPAR produced by eukaryotic cells were administered ove

212 HK-2) cells that were exposed to recombinant suPAR.

213 nded within 4 days concomitant with a rising suPAR level.

214 mage markers, VEGF, syndecan-1, TM, S100A10, suPAR and HcDNA were associated with blunt mechanism of

215 presented higher median plasma and salivary suPAR levels compared with CHD and healthy controls.

216 rotein (hs-CRP), and for plasma and salivary suPAR levels.

217 ve direct effect on both plasma and salivary suPAR levels.

218 s the only significant predictor of salivary suPAR (P <.001).

219 inhibited the enzymatic activity of WT-scuPA-suPAR unlike comparable concentrations of GFD.

220 Inhibition of scuPA/suPAR activity was evident at a Glu-plasminogen concentr

221 Inhibition of scuPA/suPAR by plasminogen was completely abolished in the pre

222 creased the Michaelis constant (Km) of scuPA/suPAR from 18 nM to 49 nM, and decreased the catalytic c

223 -3 inhibited the enzymatic activity of scuPA/suPAR with an inhibition constant (Ki) equal to 1.9 micr

224 plasminogen activator activity of the scuPA/suPAR complex is inhibited by Glu- and Lys-plasminogen,

225 by which the enzymatic activity of the scuPA/suPAR complex is regulated is only partially understood.

226 Serum suPAR level was measured at enrollment, and eGFR was mea

227 Serum suPAR was found to be elevated in all transplant candida

228 tly increased urinary nephrin, IgG and serum suPAR concentrations compared to healthy controls.

229 Pleural fluid and serum suPAR levels were measured using the suPARnostic double-

230 In advanced renal disease, elevated serum suPAR is not unique to FSGS cases.

231 Our study identifies serum suPAR as a circulating factor that may cause FSGS.

232 e disease can be abrogated by lowering serum suPAR concentrations through plasmapheresis, or by inter

233 [0.38, 1.29]), while studies measuring serum suPAR levels in any psychiatric disorder did not find a

234 study demonstrated elevated levels of serum suPAR in patients with the disease.

235 07) and the 4C Study (2010-2016), with serum suPAR level measured at enrollment and longitudinal eGFR

236 To hus, we studied suPAR in participants of the Ludwigshafen Risk and Cardi

237 nephrin, IgG and albumin levels, suggesting suPAR as a pathophysiological mediator in podocyte dysfu

238 age 3, whereas those in the highest tertile (suPAR>2.83 ng/ml) had a 19.4% decline in eGFR at 3 years

239 R is a low percentage binding event and that suPAR and full-length uPAR bind the Man-6-P/IGF2R by dif

240 Here, we show that suPAR induces nephrin down-modulation in human podocytes

241 These results suggest that suPAR may function as an important paracrine signaling f

242 The suPAR level was assessed in 3827 patients who were under

243 The suPAR-overexpressing mice that were given contrast mater

244 The suPAR-treated HK-2 cells showed heightened energetic dem

245 Indeed, the suPAR-Man-6-P/IGF2R interaction was inhibited by Man-6-P

246 epresented a minor percentage (8-30%) of the suPAR present.

247 signature that includes upregulation of the suPAR receptor Itgb3, encoding beta3 integrin.

248 Interventions that target the suPAR pathway should be investigated to explore its role

249 h plasmapheresis, or by interfering with the suPAR-beta(3) integrin interaction through antibodies an

250 is revealed two variants associated with the suPAR-encoding gene (PLAUR) with higher plasma suPAR lev

251 Binding of PaI-1 to suPAR/scuPA complexes is totally reversible and can be o

252 In addition to suPAR, proteolysis of membrane-bound uPAR results in cir

253 utrophils demonstrated increased adhesion to suPAR, which was abrogated by blocking of low-density li

254 of D2 (Leu166-Thr195) blocked HK binding to suPAR and to human umbilical vein endothelial cells (HUV

255 ely inhibited biotin-HK or -46HKa binding to suPAR.

256 HK predominantly bound to suPAR fragments containing domains 2 and 3 (S-D2D3).

257 When scuPA bound to suPAR, a binding site for alpha 2-macroglobulin receptor

258 Binding of biotin-HK to suPAR was inhibited by HK, 56HKa, and 46HKa with an IC50

259 and urokinase inhibited the binding of HK to suPAR.

260 Binding of scuPA to suPAR also retards its cleavage by plasmin.

261 nding of Delta K-scuPA, but not WT-scuPA, to suPAR was comparably inhibited by its growth factor doma

262 of a lasting reduction in the level of total suPAR because there was no sustained significant change

263 Whether a sustained lowering of total suPAR results in further improved outcomes requires addi

264 an 40 mL/min/1.73 m2, higher log-transformed suPAR levels were associated with a higher risk of CKD p

265 We identified two suPAR-binding sites, a higher affinity site in the light

266 says revealed that soluble recombinant uPAR (suPAR) bound the Man-6-P/IGF2R at two distinct sites, on

267 3 antibodies and soluble, recombinant uPAR (suPAR), but not by antibody 7E3, which recognizes the be

268 the interaction sites between soluble uPAR (suPAR) and high molecular mass kininogen (HK).

269 of scuPA bound to recombinant, soluble uPAR (suPAR) is also fivefold less sensitive to inhibition by

270 We provide evidence that soluble uPAR (suPAR) specifically binds to integrins alpha4beta1, alph

271 ing of recombinant full-length soluble uPAR (suPAR) to scuPA with an IC50 = 253 nM and an IC50 = 1569

272 ingle (Delta K-scuPA) bound to soluble uPAR (suPAR) with the similar "on-rate" but with a faster "off

273 s abrogated by incubation with soluble uPAR (suPAR), arginine-glycine-aspartic acid (RGD)-containing

274 d release increased amounts of soluble uPAR (suPAR).

275 Urinary suPAR appears to be higher in cases of FSGS destined for

276 Urinary suPAR was indexed to creatinine.

277 However, elevated urinary suPAR showed a trend in providing additional prognostic

278 Urine suPAR was elevated in cases of recurrent FSGS compared w

279 Both serum and urine suPAR correlated with proteinuria and albuminuria.

280 We studied serum and urine suPAR from pretransplantation banked samples from 86 wel

281 Future studies should use suPAR in combination with CRP and IL-6 to further explor

282 st that the renal disease only develops when suPAR sufficiently activates podocyte beta(3) integrin.

283 Whether suPAR is associated with COVID-19-related AKI is unknown

284 Whether suPAR levels are predictive of declining kidney function

285 Further studies should determine whether suPAR levels can identify children at risk for future CK

286 ental models to identify mechanisms by which suPAR acts and to assess it as a therapeutic target.

287 e 19 were each independently associated with suPAR and together explained 14% of suPAR phenotypic var

288 the consistently stronger associations with suPAR than other inflammation biomarkers.

289 or uPAR(-/-) macrophages, but not both, with suPAR enhanced the uptake of viable uPAR(-/-) neutrophil

290 s 64.5% (95% CI, 57.4-71.7) in children with suPAR levels in the lowest quartile compared with 35.9%

291 egree of podocyte effacement correlates with suPAR levels at time of diagnosis.

292 Therefore, HK interacts with suPAR at several sites.

293 Incubation of uPAR(-/-) neutrophils with suPAR or anti-integrin antibodies diminished uptake by W

294 iles, from a 6.0% incidence in patients with suPAR <4.60 ng/ml (first tertile) to a 45.8% incidence o

295 None of the patients with suPAR <4.60 ng/ml required dialysis during their hospita

296 A total of 130 patients with suPAR 6 ng/ml were assigned to subcutaneous anakinra 100

297 to a 45.8% incidence of AKI in patients with suPAR levels >6.86 ng/ml (third tertile).

298 tencies of the previous studies results with suPAR by using uniform methods and studies in different

299 rebound was observed between sessions, with suPAR levels reaching 99 +/- 22% of the pretreatment lev

300 cell binding epitopes were generated within suPAR itself by the aminoterminal fragment of scuPA, whi