ライフサイエンスコーパス: uremic

1 Parathyroids from uremic and normal rats segregated on the basis of their

2 ney disease (ESKD) are considered at risk of uremic anorexia and underweight they are also exposed to

3 identification of risk factors for calcific uremic arteriolopathy (CUA) is necessary to develop prev

4 the terms "calciphylaxis and warfarin," "non-uremic calciphylaxis," and "nonuremic calciphylaxis." We

5 gans have a survival advantage compared with uremic candidates who receive neither (SPK waitlist).

6 essing echocardiographic technique to detect uremic cardiomyopathy and predict cardiovascular mortali

7 cretion of water and urea, but the effect on uremic cardiomyopathy has not been studied.

8 utine echocardiography in early detection of uremic cardiomyopathy in animal models and whether it pr

9 te of adipocytes controls the development of uremic cardiomyopathy in mice subjected to partial nephr

10 cantly ameliorated adipocyte dysfunction and uremic cardiomyopathy in partially nephrectomized mice.

11 amplification might ameliorate experimental uremic cardiomyopathy induced by partial nephrectomy (PN

12 To determine whether T cells contribute to uremic cardiomyopathy pathogenesis, we modeled this cond

13 istration of pNaKtide after the induction of uremic cardiomyopathy reversed many of the phenotypical

14 acking echocardiography in two rat models of uremic cardiomyopathy soon (4-6 weeks) after induction o

15 Uremic cardiomyopathy, characterized by hypertension, ca

16 Uremic cardiomyopathy, characterized by left ventricular

17 romoter into the mouse model of experimental uremic cardiomyopathy, intraperitoneally.

18 the development of phenotypical features of uremic cardiomyopathy.

19 nd biochemical changes consistent with human uremic cardiomyopathy.

20 iac death and recurrent heart failure due to uremic cardiomyopathy.

21 ephrectomy serve as an experimental model of uremic cardiomyopathy.

22 er correlations with histologic hallmarks of uremic cardiomyopathy.

23 st functional deteriorations were related to uremic cardiovascular disease and kidney damage.

24 ding volume overload, electrolyte disorders, uremic complications, and drug toxicity.

25 serum PTH and FGF23 significantly less than uremic controls.

26 ssive daily dialysis can reverse many of the uremic derangements.

27 Compared with uremic diabetic waitlist patients, SPK and PAK recipient

28 Uremic dysbiosis and intestinal barrier dysfunction may

29 s indicate that IS can be one of the crucial uremic factors responsible for altered mental status in

30 at can mimic mental health problems, such as uremic, hepatic, or hypoxic encephalopathy, should be id

31 to increase FGF23 expression as observed in uremic KL(fl/fl) mice.

32 or CD14 reduced the profibrotic responses of uremic leukocytes to endogenous components present in th

33 effects of acute and continuous exposure to uremic levels of indoxylsulfate (IS), p-cresylsulfate (p

34 independently and synergistically regulating uremic metabolism.

35 metabolic profiling to identify and validate uremic metabolites associated with impairment in executi

36 Retention of uremic metabolites is a proposed cause of cognitive impa

37 Uremic metabolites, some of which are anorexigenic and m

38 y to the internal jugular vein in normal and uremic mice and compared these findings with those in fa

39 with wild-type uremic mice, Npt2b-deficient uremic mice had significantly lower levels of serum phos

40 Compared with wild-type mice, normal, or uremic mice lacking Cyp27b1 had lower levels of serum FG

41 Endothelial cells (ECs) of AVFs in uremic mice or patients expressed mesenchymal markers (F

42 To address this, calcified aortas from uremic mice were transplanted orthotopically into normal

43 Compared with wild-type uremic mice, Npt2b-deficient uremic mice had significant

44 tch target genes increased in ECs of AVFs in uremic mice.

45 The uremic milieu is profoundly thrombogenic and upregulates

46 The uremic milieu provides a perfect storm of risk factors f

47 The plasmas of diabetic or uremic patients and of those receiving peritoneal dialys

48 o the analyses of 15 healthy subjects and 24 uremic patients undergoing hemodialysis.

49 ve role in the increased ST risk observed in uremic patients.

50 oneal dialysis effluent (PDE) of noninfected uremic patients.

51 Compared with long-term PD control and uremic peritoneum, EPS peritoneum showed thicker submeso

52 sociated with morbidity and mortality in non-uremic populations, ScvO2 has received little attention

53 Uremic pruritus with elevated levels of calcium phosphat

54 Moreover, uremic PT-Dicer(-/-) mice increased serum PTH and FGF23

55 sulfate and p-cresyl sulfate remained in the uremic range.

56 ary hyperparathyroidism rats and in vitro in uremic rat parathyroid glands in organ culture.

57 prevented the increase in serum PTH level in uremic rats and decreased levels of secreted PTH in para

58 controls and uremic rats fed a normal diet, uremic rats fed a high-phosphorous diet had lower levels

59 Compared with controls and uremic rats fed a normal diet, uremic rats fed a high-ph

60 of the 11betaHSD inhibitor carbenoxolone to uremic rats for 2 wk improved glucose tolerance and insu

61 tho and FGF receptor (FEFR)-1 in healthy and uremic rats induced by 5/6 nephrectomy.

62 Uremic rats on a high-phosphate (HP) diet presented hype

63 hyroid hormone (PTH) secretion in normal and uremic rats, as well as in mouse parathyroid organ cultu

64 tion of renal Klotho and FGFR1 in normal and uremic rats.

65 e colonic microbiota as a relevant source of uremic retention solutes accumulating in CKD.

66 ports a biologic effect of the protein-bound uremic retention solutes indoxyl sulfate and p-cresyl su

67 tal in vitro data link several protein-bound uremic retention solutes to the modulation of inflammato

68 Uremic rpS6(p-/-) mice had no increase in parathyroid ce

69 Uremic sera induced 2- to 3-fold higher TF expression an

70 smooth muscle cells (vSMCs) pretreated with uremic serum (obtained from ESRD patients on hemodialysi

71 o in vitro models of vascular calcification (uremic serum and high-calcium and -phosphorus medium), a

72 d significantly greater clot formation after uremic serum exposure, which was substantially reduced w

73 activation elicited by octylamine and human uremic serum increased FMO-mediated TMAO formation.

74 were examined after vSMCs were treated with uremic serum or solutes.

75 The FMO activator octylamine and human uremic serum were evaluated.

76 ndergoes ubiquitination at baseline and that uremic serum, indole-3-acetic acid, and indoxyl sulfate

77 In VSMC, Bbetaglucans prevented LPS- or uremic serum-induced rapid increases in ADAM17, TNFalpha

78 We investigated whether the uremic solute indole-3 acetic acid (IAA) predicts clinic

79 bial metabolism substantially contributes to uremic solute production.

80 es of OAT1 and OAT3 in the regulation of the uremic solutes and supports the centrality of these "dru

81 In CKD, uremic solutes may induce endothelial dysfunction, infla

82 reatment used lowered plasma levels of small uremic solutes other than urea.

83 duce vSMC TF may help to prevent ST and that uremic solutes should be considered as novel risk factor

84 Relevant concentrations of isolated uremic solutes such as indole-3-acetic acid (3.5 mug/mL)

85 ules, antioxidants, gut microbiome products, uremic solutes, and uremic toxins.

86 Despite their uremic state, the D25V-carriers exhibit low triglyceride

87 alysis fluid exposure under either normal or uremic status.

88 y UF attenuates sleep apnea without altering uremic status.

89 y efficient metabolic machinery to alleviate uremic symptoms.

90 to that of patients with atypical hemolytic uremic syndrome (51.5%).

91 Complement mediated hemolytic uremic syndrome (aHUS) accounts for a significant propor

92 -related diseases such as atypical hemolytic uremic syndrome (aHUS) and age-related macular degenerat

93 the human kidney diseases atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy.

94 therapy in patients with atypical hemolytic uremic syndrome (aHUS) are remarkable in contrast to the

95 een well characterized in atypical hemolytic uremic syndrome (aHUS) but have been less well described

96 Patients with atypical hemolytic uremic syndrome (aHUS) develop a thrombotic microangiopa

97 assay that could convert atypical hemolytic uremic syndrome (aHUS) from a diagnosis of exclusion int

98 shares similarities with atypical hemolytic uremic syndrome (aHUS) in the underlying pathomechanisms

99 Atypical hemolytic uremic syndrome (aHUS) is a genetic ultrarare renal dise

100 Atypical hemolytic uremic syndrome (aHUS) is a genetic, life-threatening di

101 Atypical hemolytic uremic syndrome (aHUS) is a rare disease with a high rec

102 Atypical hemolytic uremic syndrome (aHUS) is a severe thrombotic microangio

103 Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy (

104 Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy c

105 Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy w

106 Atypical hemolytic uremic syndrome (aHUS) is an orphan disease with a high

107 Atypical hemolytic-uremic syndrome (aHUS) is associated with genetic comple

108 Atypical hemolytic uremic syndrome (aHUS) is characterized by complement at

109 Atypical hemolytic uremic syndrome (aHUS) is characterized by dysregulated

110 Atypical hemolytic uremic syndrome (aHUS) is characterized by genetic and a

111 Atypical hemolytic uremic syndrome (aHUS) is classically described to resul

112 Atypical hemolytic uremic syndrome (aHUS) is frequently associated in human

113 Atypical hemolytic uremic syndrome (aHUS) is life-threatening condition par

114 The pathogenesis of atypical hemolytic uremic syndrome (aHUS) is strongly linked to dysregulati

115 Atypical hemolytic uremic syndrome (aHUS) is usually characterized by uncon

116 mplement C3 identified in atypical hemolytic uremic syndrome (aHUS) patients cause dysregulation in t

117 tic microangiopathy (TMA) atypical hemolytic uremic syndrome (aHUS) resulted in the successful introd

118 glomerulopathy (C3G) and atypical hemolytic uremic syndrome (aHUS) strongly associate with inherited

119 escribed in patients with atypical hemolytic uremic syndrome (aHUS), a rare condition characterized b

120 Atypical hemolytic uremic syndrome (aHUS), a rare form of thrombotic microa

121 ribed in association with atypical hemolytic uremic syndrome (aHUS), also confers high risk of age-re

122 nal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), and various glomerular diseases.

123 reportedly contribute to atypical hemolytic uremic syndrome (aHUS), but incomplete penetrance sugges

124 native pathway results in atypical hemolytic uremic syndrome (aHUS), the prototypes of thrombotic mic

125 ereas R53H-CFH, linked to atypical hemolytic uremic syndrome (aHUS), was defective in C3bBb decay-acc

126 nt dysregulation leads to atypical hemolytic uremic syndrome (aHUS), while ADAMTS13 deficiency causes

127 hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS).

128 al to the pathogenesis of atypical hemolytic uremic syndrome (aHUS).

129 ngiopathy (TMA), known as atypical hemolytic uremic syndrome (aHUS).

130 gnose complement-mediated atypical hemolytic uremic syndrome (aHUS; a diagnosis of exclusion).

131 ia coli causes diarrhea-associated hemolytic-uremic syndrome (DHUS), a severe renal thrombotic microa

132 42 cases, including 855 cases with hemolytic uremic syndrome (HUS) and 53 deaths.

133 x2) responsible for development of hemolytic uremic syndrome (HUS) and acute kidney injury (AKI).

134 e symptoms of the life-threatening hemolytic uremic syndrome (HUS) and are the main virulence factors

135 histomorphologic similarities with hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic pu

136 thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are appropriately at the top of a

137 Hemolytic uremic syndrome (HUS) caused by intestinal Shiga toxin-p

138 Hemolytic-uremic syndrome (HUS) features episodes of small-vessel

139 rhea or developed life-threatening hemolytic uremic syndrome (HUS) in any of 6 closed cohorts from 4

140 sed an outbreak with >800 cases of hemolytic uremic syndrome (HUS) in Germany, including 90 children.

141 Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy ch

142 Hemolytic-uremic syndrome (HUS) is a thrombotic microangiopathy th

143 Atypical hemolytic uremic syndrome (HUS) is associated with high recurrence

144 scherichia coli O157:H7-associated hemolytic-uremic syndrome (HUS) is characterized by profound proth

145 Hemolytic uremic syndrome (HUS) is the life-threatenig sequela of

146 Hemolytic uremic syndrome (HUS) occurred in 12 patients (10 infect

147 2011 the largest known outbreak of hemolytic uremic syndrome (HUS) occurred in northern Germany.

148 Identifying hemolytic uremic syndrome (HUS) risk factors is needed to guide ca

149 the 62 individuals with diarrheal hemolytic uremic syndrome (HUS) seen at our institution during the

150 tening sequela of infection called hemolytic-uremic syndrome (HUS) than isolates that make Stx1a only

151 g agent of postdiarrhea-associated hemolytic uremic syndrome (HUS), a disorder of glomerular ischemic

152 cytotoxic proteins that can cause hemolytic-uremic syndrome (HUS), a thrombotic microangiopathy, fol

153 s, the development and severity of hemolytic uremic syndrome (HUS), and adverse outcomes in STEC-infe

154 Hemolytic-uremic syndrome (HUS), caused by Shiga toxin (Stx)-produ

155 es to hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS), due to the expression of one or m

156 e pathogenesis of postenteropathic hemolytic uremic syndrome (HUS), most commonly caused by Shiga tox

157 complicated by potentially lethal hemolytic uremic syndrome (HUS), particularly in children.

158 b pasudotox for 10 doses developed hemolytic uremic syndrome (HUS), thrombotic microangiopathy (TMA),

159 uding hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS), which is the most common cause of

160 is associated with development of hemolytic uremic syndrome (HUS).

161 outcomes of waitlisted adults with hemolytic uremic syndrome (HUS).

162 cing Escherichia coli (STEC) cause hemolytic uremic syndrome (HUS).

163 kidney-damaging sequela called the hemolytic uremic syndrome (HUS).

164 causes hemorrhagic colitis and the hemolytic-uremic syndrome (HUS).

165 ere hospitalized, including 4 with hemolytic uremic syndrome (HUS).

166 22% of these individuals developed hemolytic-uremic syndrome (HUS).

167 r the serious disease consequence, hemolytic-uremic syndrome (HUS).

168 oli (EHEC) O26 causes diarrhea and hemolytic uremic syndrome (HUS).

169 tery, hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS).

170 y congenital; n = 650), glomerular-hemolytic uremic syndrome (HUS; n = 49), or glomerular-non-HUS (he

171 treptococcus pneumoniae associated hemolytic uremic syndrome (SpHUS) is defined by the occurrence of

172 renal diseases, including atypical hemolytic uremic syndrome and C3 glomerulopathies, and age-related

173 t-driven diseases such as atypical hemolytic uremic syndrome and catastrophic antiphospholipid antibo

174 d with the renal diseases atypical hemolytic uremic syndrome and dense deposit disease and the ocular

175 The outbreak of hemolytic-uremic syndrome and diarrhea caused by Shiga toxin-produ

176 foodborne pathogens that can cause hemolytic uremic syndrome and infantile diarrhea, respectively.

177 iated endothelial damage: atypical hemolytic uremic syndrome and thrombotic thrombocytopenic purpura.

178 of clinical presentation (atypical hemolytic uremic syndrome as thrombotic microangiopathy), biopsy a

179 n (Stx) causes diarrhea-associated hemolytic uremic syndrome by damaging renal microvascular endothel

180 nticomplement therapy for atypical hemolytic uremic syndrome during pregnancy, and implications of th

181 toxin-producing E. coli-associated hemolytic uremic syndrome during this outbreak.

182 We report a case of hemolytic uremic syndrome in a 69-year-old woman due to Shiga toxi

183 TEC) O146:H28 infection leading to hemolytic uremic syndrome in a neonate.

184 toxin-producing E. coli-associated hemolytic uremic syndrome in six hospitals in Hamburg, Germany, be

185 s can trigger episodes of atypical hemolytic uremic syndrome in susceptible patients.

186 Hemolytic uremic syndrome is a disease characterized by hemolytic

187 Atypical hemolytic-uremic syndrome is a genetic, life-threatening, chronic

188 and autoantibody-positive form of hemolytic uremic syndrome is characterized by the presence of auto

189 ife-threatening sequela called the hemolytic uremic syndrome is unpredictable.

190 a coli serotype O104:H4-associated hemolytic uremic syndrome occurred in Northern Germany.

191 toxin-producing E. coli-associated hemolytic uremic syndrome outbreak in Germany, critical illness de

192 en that causes bloody diarrhea and hemolytic uremic syndrome throughout the world.

193 toxin-producing E. coli-associated hemolytic uremic syndrome were admitted to eight ICUs.

194 ls in which patients with atypical hemolytic-uremic syndrome who were 12 years of age or older receiv

195 In hemolytic uremic syndrome with brain involvement symptoms develop

196 ks of gastrointestinal illness and hemolytic uremic syndrome worldwide.

197 esponsible for bloody diarrhea and hemolytic-uremic syndrome worldwide.

198 Uraemic syndrome (also known as uremic syndrome) in patients with advanced chronic kidne

199 ive regulation of the AP (atypical hemolytic-uremic syndrome) or with inadequate cleavage by ADAMTS-1

200 The Oklahoma TTP-HUS (hemolytic uremic syndrome) Registry enrolled 70 consecutive patien

201 macular degeneration and atypical hemolytic uremic syndrome, a form of thrombotic microangiopathy.

202 Hemolytic uremic syndrome, a life-threatening disease often accomp

203 FH and MCP are linked to atypical hemolytic uremic syndrome, a type of thrombotic microangiopathy (T

204 04 were hospitalized, 28 developed hemolytic uremic syndrome, and 5 died.

205 ted macular degeneration, atypical hemolytic uremic syndrome, and C3 glomerulopathies.

206 04 were hospitalized, 28 developed hemolytic uremic syndrome, and five died.

207 diseases such as AMD and atypical hemolytic uremic syndrome, and leads to a better understanding of

208 es have been described in atypical hemolytic uremic syndrome, arising commonly through nonallelic hom

209 hemoglobinuria (PNH) and atypical hemolytic uremic syndrome, blocks the terminal complement pathway

210 croangiopathies including atypical hemolytic uremic syndrome, C3 and C1q glomerulopathies, and preecl

211 botic thrombocytopenic purpura and hemolytic-uremic syndrome, have been reported to have a drug-induc

212 tients with the autoimmune form of hemolytic uremic syndrome, is involved in B cell regulation.

213 ted macular degeneration, atypical hemolytic uremic syndrome, membranoproliferative glomerulonephriti

214 obinuria, cold agglutinin disease, hemolytic uremic syndrome, nephropathies, HELLP syndrome, transpla

215 O157:H7 can cause bloody diarrhea, hemolytic uremic syndrome, or even death.

216 of rare diseases such as atypical hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, C3

217 binding sites and causing atypical hemolytic uremic syndrome, we found that it detached more uniforml

218 d with wild type FH19-20, atypical hemolytic uremic syndrome-associated mutants were less able to com

219 ve or therapeutic ends, for use in hemolytic uremic syndrome-endemic areas or during future outbreaks

220 mbomicroangiopathy called atypical hemolytic uremic syndrome.

221 turnal hemoglobinuria and atypical hemolytic uremic syndrome.

222 HR5 genes are reported in atypical hemolytic uremic syndrome.

223 ings in a four-month-old male with hemolytic uremic syndrome.

224 sy of a child with EHEC-associated hemolytic uremic syndrome.

225 luding hemorrhagic colitis and the hemolytic uremic syndrome.

226 es such as hemorrhagic colitis and hemolytic uremic syndrome.

227 s the cause of bloody diarrhea and hemolytic-uremic syndrome.

228 infections, as well as sepsis and hemolytic uremic syndrome.

229 s, such as hemorrhagic colitis and hemolytic uremic syndrome.

230 en causing hemorrhagic colitis and hemolytic uremic syndrome.

231 and disseminated malignancy or in hemolytic uremic syndrome.

232 litis that sometimes progresses to hemolytic-uremic syndrome.

233 izumab after a relapse of atypical hemolytic uremic syndrome.

234 erleukin-1beta, has been linked to hemolytic uremic syndrome.

235 hat causes hemorrhagic colitis and hemolytic uremic syndrome.

236 an experimental model for atypical hemolytic uremic syndrome.

237 O157 strains (P = 0.03) developing hemolytic-uremic syndrome.

238 ology of neuronal complications in hemolytic-uremic syndrome.

239 function in patients with atypical hemolytic-uremic syndrome.

240 evelopment of the life-threatening hemolytic uremic syndrome.

241 nsidered in the workup of neonatal hemolytic uremic syndrome.

242 ienced fatal chronic rejection and hemolytic uremic syndrome.

243 kinase epsilon result in atypical hemolytic-uremic syndrome.

244 c thrombocytopenic purpura and the hemolytic uremic syndrome.

245 causes severe bloody diarrhea and hemolytic uremic syndrome.

246 ar degeneration (AMD) and atypical hemolytic uremic syndrome.

247 r and renal injury and can trigger hemolytic uremic syndrome.

248 re hospitalized and 6.4% developed hemolytic uremic syndrome.

249 renal diseases, including atypical hemolytic uremic syndrome.

250 ribed in association with atypical hemolytic uremic syndrome.

251 anging from hemorrhagic colitis to hemolytic uremic syndrome.

252 iated with hemorrhagic colitis and hemolytic uremic syndrome.

253 loody diarrhea, renal failure, and hemolytic uremic syndrome.

254 share features with human atypical hemolytic uremic syndrome.

255 y sera from patients with atypical hemolytic uremic syndrome.

256 with the related disease atypical hemolytic uremic syndrome; 6.8% in cases versus 5.9% in controls)

257 Uremic toxicity may play a role in the elevated risk of

258 e systemic circulation, which contributes to uremic toxicity, inflammation, progression of CKD, and a

259 emodialysis, although beneficial in terms of uremic toxin clearance, also contributes to cognitive de

260 We tested whether the uremic toxin indoxyl sulfate (IS), an endogenous ligand

261 icrobiome and demonstrate that levels of the uremic toxin indoxyl sulfate can be modulated in vivo by

262 The putative uremic toxin indoxyl sulfate induces oxidative stress an

263 principles for potential MOFs candidates for uremic toxin removal.

264 d is p-cresyl sulfate (PCS), a protein-bound uremic toxin that originates from tyrosine metabolism by

265 ion of diabetes in rats overexpressing human uremic toxin transporter SLCO4C1 in the kidney, and are

266 AhR activation by indoxyl sulfate, a uremic toxin, leads to blood-brain barrier disruption as

267 uggest that indoxyl sulfate, a protein-bound uremic toxin, may induce vascular dysfunction and thromb

268 of resistin, a proinflammatory cytokine and uremic toxin, were significantly elevated during both fo

269 This reduced uremic toxin-producing activity and ameliorated progress

270 ototypical microbiome-derived metabolite and uremic toxin.

271 egard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1

272 Protein-bound uremic toxins (PBUTs) are difficult to remove by convent

273 Protein-bound uremic toxins (PBUTs) are poorly removed during hemodial

274 acid, gut microbiome products, and so-called uremic toxins accumulating in chronic kidney disease.

275 kidney proximal tubule (PT) transporters of uremic toxins and solutes (e.g., indoxyl sulfate, p-cres

276 OAT1 and/or OAT3 in the handling of over 35 uremic toxins and solutes, including those derived from

277 om human serum albumin, a protein that these uremic toxins bind to in the body.

278 rogram suggested that increased clearance of uremic toxins by intensified hemodialysis improves pregn

279 Uremic toxins could modify the expression and/or activit

280 bacterial endotoxins, or adsorb gut-derived uremic toxins have been developed.

281 To characterize involvement of uremic toxins in cerebral and neurobehavioral abnormalit

282 Protein-bound uremic toxins indoxyl sulfate (IS) and p-cresyl sulfate

283 he interactions between an adsorbent and the uremic toxins is critical for designing effective materi

284 Uremic toxins often accumulate in patients with compromi

285 However, the impact of these uremic toxins on the crosstalk between endothelium and l

286 P and history of cardiovascular disease; and uremic toxins p-cresyl sulfate and indoxyl sulfate.

287 s (including tryptophan-derivatives that are uremic toxins), and lipids.

288 ic solutes and uraemic toxins (also known as uremic toxins), dysfunction of multiple organs and dysbi

289 The latter are uremic toxins, and H(2)S has diverse physiological funct

290 t understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac

291 hanisms, including direct neuronal injury by uremic toxins, could also be involved, especially in the

292 In CKD, uremic toxins, hyperparathyroidism and Klotho deficiency

293 Emerging evidence suggests that uremic toxins, in particular indoxyl sulfate (IS) and p-

294 Some uremic toxins, like indoxyl sulfate, are agonists of the

295 ein, we study the adsorption behavior of the uremic toxins, p-cresyl sulfate, indoxyl sulfate, and hi

296 Altogether, these results suggest that uremic toxins, such as IS, through effects on drug trans

297 doxyl sulfate (IS) is one of the most potent uremic toxins.

298 gut microbiome products, uremic solutes, and uremic toxins.

299 volving amino acids, lipids, bile acids, and uremic toxins.

300 Uremic wild-type (KL(fl/fl) ) and knockout (Prx1-Cre;KL(

301 iferation compared with a marked increase in uremic wild-type mice.