ライフサイエンスコーパス: CKD

1 restore fertility in chronic kidney disease (CKD).

2 ascular morbidity in chronic kidney disease (CKD).

3 at increased risk of chronic kidney disease (CKD).

4 ted with the risk of chronic kidney disease (CKD).

5 of organs, including chronic kidney disease (CKD).

6 sease requiring long-term dialysis (stage 5D CKD).

7 ss in progression of chronic kidney disease (CKD).

8 ity in patients with chronic kidney disease (CKD).

9 -naive patients with chronic kidney disease (CKD).

10 or with hypertensive chronic kidney disease (CKD).

11 induced in mice with chronic kidney disease (CKD).

12 e quantity and quality of clinical trials in CKD.

13 e been evaluated in animal models of AKI and CKD.

14 16.6 years, 31.7% of participants developed CKD.

15 ompanied by improved cardiorenal outcomes in CKD.

16 increased risk of mortality in patients with CKD.

17 a metric of beta-oxidation, across stages of CKD.

18 KD, 61 with stage 4 CKD, and 18 with stage 5 CKD.

19 pid metabolism changes that typify advancing CKD.

20 lso correlated statistically with stage 3b-5 CKD.

21 we identified new potential target genes for CKD.

22 resent a therapeutic target in late stage of CKD.

23 ha has been implicated in the progression of CKD.

24 % of children and 8% of adults had stage 4-5 CKD.

25 sposes to the development and progression of CKD.

26 tension, polycystic kidney disease, AKI, and CKD.

27 9-year follow-up, 404 participants developed CKD.

28 farction, and heart failure in patients with CKD.

29 may contribute to endothelial dysfunction in CKD.

30 y for myocardial infarction in patients with CKD.

31 fibrotic macrophage phenotype in UUO-induced CKD.

32 ight mitigate cardiovascular disease risk in CKD.

33 d rapid renal deterioration in patients with CKD.

34 ation of HCV infection with the incidence of CKD.

35 ng that MANBA is a potential target gene for CKD.

36 hyperoxaluric mice from nephrocalcinosis and CKD.

37 nephropathy frequently leads to progressive CKD.

38 varies significantly among individuals with CKD.

39 jected to renal mass reduction as a model of CKD.

40 e system has been implicated in both AKI and CKD.

41 LDL may underlie downregulation of KChIP2 in CKD.

42 shed LVH in the 5/6 nephrectomy rat model of CKD.

43 onset dialysis in HCV-infected patients with CKD.

44 ity and mortality through the development of CKD.

45 progression in individuals with nondiabetic CKD.

46 D4(+)CD25(+)CD127(lo) T cells in humans with CKD.

47 o the high rates of LVH and cardiac death in CKD.

48 h renal disease progression in children with CKD.

49 d to an eGFR category indicating more severe CKD.

50 athway as a promising therapeutic target for CKD.

51 mortality among dialysis-naive patients with CKD.

52 sing therapeutic target for the treatment of CKD.

53 a key process in the development of AKI and CKD.

54 h changes in renal function in patients with CKD.

55 , and stroke in participants with vs without CKD.

56 n variants have in complex diseases, such as CKD.

57 acidosis is associated with poor outcomes in CKD.

58 odium restriction on residual albuminuria in CKD.

59 minimal data on serial FGF23 measurements in CKD.

60 hort (n=161) comprising 36 participants with CKD, 100 participants with ESRD, and 25 controls.

61 points from 3 males with rapidly-progressing CKD, 3 males with slowly-progressing CKD, and 2 age-matc

62 sis (3 trials), or postmenopausal women with CKD (4 trials).

63 he calf in 99 patients with mild to moderate CKD (42 women; median [range] age, 65 [23-78] years).

64 erall, 31% of children and 42% of adults had CKD; 6% of children and 8% of adults had stage 4-5 CKD.

65 14 36 with stage 1 or 2 CKD, 99 with stage 3 CKD, 61 with stage 4 CKD, and 18 with stage 5 CKD.

66 ey injury (8 countries [7%]) and nondialysis CKD (9 countries [8%]).

67 selected a panel of 214 36 with stage 1 or 2 CKD, 99 with stage 3 CKD, 61 with stage 4 CKD, and 18 wi

68 clinically significant (stage 4 and higher) CKD after radical or partial nephrectomy among veterans

69 cted patients and the incidence reduction of CKD after receipt of HCV treatment.

70 The median time to stage 4 or higher CKD after surgery was 5 months, after which few patients

71 ly to have stage 3-5 chronic kidney disease (CKD), alcohol or drug abuse or dependence diagnosis, and

72 HCV infection can prevent the development of CKD, although the association was not significant for al

73 African ancestry alleles may contribute to CKD among Hispanics/Latinos, but whether associations di

74 endothelin-1 levels associated with incident CKD and all-cause mortality during follow-up in this gen

75 ary hyperparathyroidism commonly complicates CKD and associates with morbidity and mortality.

76 participants >/=18 years of age with stage 3 CKD and asymptomatic hyperuricemia (>/=7 mg/dl in men an

77 erum uric acid levels in adults with stage 3 CKD and asymptomatic hyperuricemia but did not improve e

78 an interaction (p = 0.329 and p = 0.291 for CKD and CVD, respectively).

79 persisted despite the presence of underlying CKD and decreasing ejection fraction.

80 nd death, but their association with risk of CKD and ESRD is unknown.

81 Diabetes is the main cause of CKD and ESRD worldwide.

82 e appropriate target for BP in patients with CKD and hypertension remains uncertain.

83 Thus, among patients with CKD and hypertension without diabetes, targeting an SBP<

84 uble-blind clinical trial in adults with NDD-CKD and iron deficiency anemia to compare the safety and

85 Metabolic acidosis is not uncommon in CKD and is linked with bone demineralization, muscle cat

86 Among patients with non-dialysis-dependent CKD and MDD, treatment with sertraline compared with pla

87 mproves depressive symptoms in patients with CKD and MDD.

88 onium excretion could identify patients with CKD and normal bicarbonate levels who might benefit from

89 gnificantly associated (P < 1e-07) with eGFR/CKD and replicated, five also associate with renal fibro

90 Thus, in nondiabetic patients with stage 3-4 CKD and vitamin D deficiency, vitamin D supplementation

91 ted in patients with chronic kidney disease (CKD), and it is likely that FGF23 directly contributes t

92 betes mellitus (DM), chronic kidney disease (CKD), and treated hypertension (HTN) by age, sex, and ra

93 rage about 75%), 610 live-born singletons in CKD, and 1418 low-risk controls recruited in 2 large Ita

94 2 CKD, 99 with stage 3 CKD, 61 with stage 4 CKD, and 18 with stage 5 CKD.

95 ressing CKD, 3 males with slowly-progressing CKD, and 2 age-matched controls.

96 Racial disparities in the occurrence of DM, CKD, and HTN emphasize the need for prevention and treat

97 y associates with mortality in patients with CKD, and vitamin D supplementation might mitigate cardio

98 osteoporosis medications among patients with CKD; and reported on BMD, fractures, or safety (mortalit

99 CKD appears to be a condition of soluble klotho deficien

100 Children with CKD are at increased risk for neurocognitive impairment,

101 People with CKD are five to ten times more likely to die prematurely

102 n lipid-lowering therapy in individuals with CKD are needed.

103 racture risk, and safety among patients with CKD are not clearly established.

104 nephritis or systemic diseases ("progressive CKD") are compared with KT.

105 We defined incident CKD as eGFR<60 ml/min per 1.73 m(2) and >/=30% eGFR decl

106 prove understanding of the natural course of CKD; assess and implement established treatment options

107 e intensive BP lowering arm of two trials in CKD associated with higher risk of ESRD, we performed a

108 ing this inflammation and thereby preventing CKD-associated cardiovascular disease.

109 Variants in linkage with the CKD-associated single-nucleotide polymorphism rs11959928

110 otated multiple genes to previously reported CKD-associated single-nucleotide polymorphisms and provi

111 Our 4C analyses revealed interactions of CKD-associated susceptibility regions with the transcrip

112 at genes regulated by DREs colocalizing with CKD-associated variation can be dysregulated and therefo

113 w the progression of chronic kidney disease (CKD), but their use is limited by hyperkalemia, especial

114 e over time in the majority of patients with CKD, but serial measurements identify subpopulations wit

115 increase the cost of testing and monitoring CKD by approximately pound31 million per year.

116 many elderly individuals considered to have CKD by current criteria.

117 trasound alone can attenuate AKI and prevent CKD by stimulating the splenic cholinergic anti-inflamma

118 the progression of chronic kidney diseases (CKD) by producing renal tubulointerstitial fibrosis.

119 But CKD can also be viewed conceptually as an accelerator of

120 be dysregulated and therefore, considered as CKD candidate genes.

121 h into mineral bone disorder associated with CKD (CKD-MBD) could help the medical community to better

122 tion in an all-cause chronic kidney disease (CKD) cohort.

123 sis of 2 prospectively followed up pediatric CKD cohorts, ie, the ESCAPE Trial (1999-2007) and the 4C

124 nfected patients had a 27% increased risk of CKD compared with non-HCV patients (hazard ratio [HR], 1

125 rventions to slow CKD progression and reduce CKD complications; and increase the quantity and quality

126 d moderate to severe chronic kidney disease (CKD), congestive heart failure (CHF), or chronic liver d

127 iabetes nephropathy vs. other etiologies) of CKD could be associated with mortality.

128 management of symptoms and complications of CKD; develop novel therapeutic interventions to slow CKD

129 ffect of renal GPCR-Gbetagamma inhibition in CKD developed in a clinically relevant murine model of n

130 can highlight potential new target genes for CKD development.

131 mL/min/1.73 m(2)), and those with stage 4-5 CKD (eGFR < 30 mL/min/1.73 m(2)) and separately underwen

132 >/= 60 mL/min/1.73 m(2)), those with stage 3 CKD (eGFR, 30-59 mL/min/1.73 m(2)), and those with stage

133 tween exposure to PM2.5 and risk of incident CKD, eGFR decline, and ESRD.

134 increased inflammation, and in patients with CKD, elevated C-reactive protein level predicts cardiova

135 cute kidney injury-a special risk factor for CKD; enhance understanding of the genetic causes of CKD;

136 set from patients with cancer, BSA-adjusted CKD-EPI is the most accurate published model to predict

137 c Kidney Disease Epidemiology Collaboration (CKD-EPI) equations, we compared GFR estimated from creat

138 djusted chronic kidney disease epidemiology (CKD-EPI) was the most accurate published model for eGFR

139 s, monitoring, and treatment of both AKI and CKD, especially considering recent advances in this tech

140 Prevalence and outcomes of patients with CKD, especially those with end-stage renal disease (ESRD

141 with CKD or ESRD with those patients with no CKD/ESRD.

142 hance understanding of the genetic causes of CKD; establish better diagnostic methods in CKD; improve

143 those with stage 1-2 chronic kidney disease (CKD) (estimated glomerular filtration rate [eGFR], >/= 6

144 In population studies, CKD etiology is often uncertain.

145 common variants to genes that are causal for CKD etiology remains challenging.

146 We calculated CVD and CKD event rates by predicted 5-year CVD and CKD risk gro

147 CVD and CKD event rates by predicted risk group were multiplicat

148 substantially greater risks for both CVD and CKD events compared with those at low predicted risk for

149 ive SBP lowering increased risk for incident CKD events, but this was outweighed by cardiovascular an

150 those at high predicted risk for only CVD or CKD events.

151 KD would be at even greater risk for CVD and CKD events.

152 ences comparing participants with vs without CKD for HF were 3.5 (95% CI, 1.5-5.5) and 7.8 (95% CI, 2

153 In matching samples of 24 patients with CKD from the C-PROBE study, circulating GDF-15 levels si

154 reclassified 7.7% (50 of 653) of those with CKD G3aA1 by eGFRcreat to eGFR >/= 60 ml/min/1.73 m2.

155 onfirm the diagnosis in people classified as CKD G3aA1 by eGFRcreat.

156 h assumed cost savings, to participants with CKD G3aA1 increased the cost of monitoring by pound23 pe

157 om 2003 to 2013, 2319002 patients in the non-CKD group (34.7% women; 65.3% men; mean [SD] age, 64.2 [

158 14.4] years), 30072 patients in the stage 5D CKD group (45.0% women; 55.0% men; mean [SD] age, 66.9 [

159 as markedly lower compared with the stage 5D CKD group (AOR, 0.37; 95% CI, 0.33-0.43; P < .001) but s

160 P < .001) but similar compared with the non-CKD group (AOR, 1.14; 95% CI, 0.99-1.31; P = .08).

161 renal transplant recipients vs the stage 5D CKD group or the non-CKD group.

162 ipients vs the stage 5D CKD group or the non-CKD group.

163 r filtration rate, and 3 (4%) had persistent CKD > stage 2.

164 Of 4 patients with chronic kidney disease (CKD) > stage 2 at short-term follow-up, 1 had a normaliz

165 International acute kidney injury and CKD guidelines were reportedly accessible in 52 (45%) an

166 t colocalization with variants identified in CKD GWASs, indicating that MANBA is a potential target g

167 Patients with later stages of CKD had lower renal elasticity values, indicating stiffe

168 Chronic kidney disease (CKD) has a prevalence of approximately 13% and is most f

169 of HIF activation in chronic kidney disease (CKD) has been widely evaluated, the results have been in

170 We hypothesized that subjects with CKD have increased arterial and cellular inflammation, r

171 ople at high predicted risk for both CVD and CKD have substantially greater risks for both CVD and CK

172 tudy indicate that a subset of children with CKD have unsuspected genomic disorders that predispose t

173 fected patients with chronic kidney disease (CKD) have rarely been studied because they rarely accept

174 lar disease risk factors among patients with CKD; however, the changes in the C statistic are small.

175 erapy had a 30% decreased risk of developing CKD (HR, 0.70; 95% CI, 0.55-0.88).

176 tablished treatment options in patients with CKD; improve management of symptoms and complications of

177 CKD; establish better diagnostic methods in CKD; improve understanding of the natural course of CKD;

178 in the evaluation and care of patients with CKD in additional settings is warranted.

179 Data from the CKD in Children Study Chronic Kidney Disease in Children

180 inary tract (CAKUT) are the leading cause of CKD in children, featuring a broad variety of malformati

181 anomalies, and constitute the main cause of CKD in children.

182 were used to compare the risk of developing CKD in HCV patients compared with non-HCV patients and t

183 cells as attractive therapeutic targets for CKD in humans.

184 0), are associated with an increased risk of CKD in individuals of recent African ancestry.

185 unilateral ureter obstruction (UUO) model of CKD in mice.

186 y tract (CAKUT) are the most common cause of CKD in the first three decades of life.

187 higher quartiles had a greater incidence of CKD in the fully adjusted model (odds ratio for fourth v

188 d risk in people with CKD, its use to define CKD in this manner has not been evaluated in primary car

189 assessed the risk of chronic kidney disease (CKD) in chronic hepatitis C virus (HCV)-infected patient

190 GFR decline >3 ml/min per year) and incident CKD (incident eGFR <60 ml/min per 1.73 m(2) and >1 ml/mi

191 r year decline in eGFR), but not of incident CKD (incident rate ratio, 0.90 [95% confidence interval,

192 d with significantly higher risk of incident CKD, incident CKD or mortality, and rapid eGFR decline.

193 Hg; control-RDN, -15 +/- 1 mm Hg; p < 0.05; CKD-intact, -11 +/- 3 mm Hg; CKD-RDN, -19 +/- 9 mm Hg; p

194 ) or sham procedures (control-intact, n = 6; CKD-intact, n = 7).

195 The relevance of UMOD for CKD is clear, because the encoded protein, uromodulin (T

196 ion over provision of care only for advanced CKD is still evolving in many countries.

197 Chronic kidney disease (CKD) is a complex gene-environmental disease affecting c

198 Chronic kidney disease (CKD) is defined by reduced estimated glomerular filtrati

199 eing a marker of GFR and risk in people with CKD, its use to define CKD in this manner has not been e

200 eurocognitive function in some children with CKD may be attributable to genetic lesions that affect b

201 o mineral bone disorder associated with CKD (CKD-MBD) could help the medical community to better unde

202 ake in the arterial wall in 14 patients with CKD (mean+/-SD age: 59+/-5 years, mean+/-SD eGFR: 37+/-1

203 In CKD mice, activation of HIF-2alpha at the beginning of C

204 Since CKD mimics a form of accelerated cardiovascular aging, w

205 d with hyperphosphatemia in a mouse model of CKD-mineral bone disorder and alphaKL-null mice.

206 educed hyperphosphatemia in a mouse model of CKD-mineral bone disorder, and it reduced hyperphosphate

207 s in part due to lack of clinically relevant CKD models in non-human primates.

208 For chronic kidney disease (CKD) monitoring in primary care, serum creatinine with e

209 ted States are at greater risk of developing CKD, MPGN, and cryoglobulinemia.

210 In patients with CKD, not only renal but also, nonrenal clearance of drug

211 -up of 8 years, 228 (6.4%) cases of incident CKD occurred in participants.

212 tions in a substantial number of adults with CKD of many causes.

213 92 adults with CKD of unknown cause or familial nephropathy or hyperten

214 e, we investigated the effect of preexisting CKD on cardiac function in mice with sepsis and whether

215 Currently, the description of the CKD onset and progression at the molecular level is stil

216 without evidence of effect modifications by CKD or deleterious effect on the main kidney outcome.

217 Patients with CKD or ESRD had greater in-hospital mortality, hospital

218 ompare in-hospital outcomes of patients with CKD or ESRD with those patients with no CKD/ESRD.

219 bin C trait did not associate with prevalent CKD or ESRD.

220 cantly higher risk of incident CKD, incident CKD or mortality, and rapid eGFR decline.

221 ney disease (CKD), the composite of incident CKD or mortality, and rapid rate of eGFR decline (slopes

222 id not associate with progression to stage 3 CKD or renal death.

223 ts (6 trials), patients who had stage 3 to 5 CKD or were receiving dialysis (3 trials), or postmenopa

224 o identify patients in the non-CKD, stage 5D CKD, or prior renal transplant groups.

225 differ between participants with and without CKD (P values for interactions >/=0.30).

226 ng of the key molecular events that modulate CKD pathogenesis.

227 atients; the differences level off when only CKD patients affected by glomerulonephritis or systemic

228 148 non-CKD patients and 227 patients with CKD were recruited.

229 sociate with renal fibrosis in biopsies from CKD patients and show concordant DNA methylation changes

230 are comparable with those of nontransplanted CKD patients with similar levels of kidney function impa

231 ded that ECR predicts disease progression of CKD patients.

232 low-up revealed 27% reduction in the risk of CKD per 1-SD decrease in mean asleep systolic BP, indepe

233 levels were associated with a higher risk of CKD progression after adjustment for traditional risk fa

234 -based eGFR in risk prediction equations for CKD progression and all-cause mortality and investigated

235 discrimination in risk prediction models for CKD progression and all-cause mortality compared to simi

236 tion, muscle catabolism, and higher risks of CKD progression and mortality.

237 elop novel therapeutic interventions to slow CKD progression and reduce CKD complications; and increa

238 of habitual sleep duration and quality with CKD progression in 431 Chronic Renal Insufficiency Cohor

239 in the kidney, significantly associated with CKD progression in individuals with nondiabetic CKD.

240 A hallmark of CKD progression is renal fibrosis characterized by exces

241 siderably and accurate information regarding CKD progression may improve clinical decisions.

242 lood pressure and albuminuria, and prevented CKD progression more effectively than eplerenone.

243 The primary end point of CKD progression was a composite of 50% eGFR loss, eGFR l

244 stand better the contribution of genetics to CKD progression, we performed a genome-wide association

245 lity sleep are unrecognized risk factors for CKD progression.

246 be an amenable target for the prevention of CKD progression.

247 any populations and has been associated with CKD progression.

248 significantly attenuated in control-RDN and CKD-RDN animals.

249 hypertension and improved renal function in CKD-RDN sheep (p < 0.0001 for 2 and 5 months vs. pre-RDN

250 m Hg; p < 0.05; CKD-intact, -11 +/- 3 mm Hg; CKD-RDN, -19 +/- 9 mm Hg; p < 0.001).

251 Sheep underwent RDN (control-RDN, n = 8; CKD-RDN, n = 7) or sham procedures (control-intact, n =

252 surveillance; tackle major risk factors for CKD; reduce acute kidney injury-a special risk factor fo

253 during aging and in chronic kidney disease (CKD), regardless of cause.

254 evelop a molecule-centric database featuring CKD-related experiments from available literature public

255 apeutic targets for intervention to suppress CKD-related systemic inflammation and its consequences.

256 The patient with chronic kidney disease (CKD) represents an extreme model for arteriosclerosis, v

257 Patients with CKD requiring dialysis have a higher risk of sepsis and

258 ted Poisson models to assess whether CVD and CKD risk group effects were multiplicative.

259 CKD event rates by predicted 5-year CVD and CKD risk groups (</=1%, >1%-5%, >5%) and fitted Poisson

260 Participants' CVD and CKD risk groups had multiplicative predictive effects, w

261 This suggests that CVD and CKD risk in HIV-positive persons should be assessed toge

262 red meat consumption over years may increase CKD risk, whereas white meat and dairy proteins appear t

263 By 12 weeks after TAC, mice developed CKD secondary to CHF associated with elevated renal GPCR

264 Development of CKD secondary to chronic heart failure (CHF), known as c

265 cardiovascular mortality in individuals with CKD seems to diminish as eGFR declines.

266 ase (IKK) reduces the cardiac dysfunction in CKD sepsis.

267 In hypertensive CKD sheep, RDN reduced blood pressure and improved basal

268 Screening for CKD should be considered before and during long-term, hi

269 to improve health outcomes for patients with CKD should prioritize HF in addition to CHD prevention.

270 activation of HIF-2alpha at the beginning of CKD significantly aggravated renal fibrosis, whereas it

271 er than 90 have worse outcomes compared with CKD stage 1 patients; the differences level off when onl

272 tcome was poor; among the 14 women, four had CKD stage 1-4, five had received a renal allograft, and

273 tor (suPAR) levels strongly predict incident CKD stage 3 in adults.

274 ignificantly lower relative risk of incident CKD stage 4 or higher (hazard ratio, 0.34; 95% confidenc

275 >/=30 ml/min per 1.73 m(2), the incidence of CKD stage 4 or higher after radical (n=9759) or partial

276 CKD stage and hypertension are important determinants of

277 ell as age, serum albumin concentration, and CKD stage at onset affected ESRD risk.

278 doubling of serum creatinine or increase in CKD stage.

279 n, were used to identify patients in the non-CKD, stage 5D CKD, or prior renal transplant groups.

280 rossover trial, 45 patients with nondiabetic CKD stages 1-3 and albuminuria >300 mg/24 h despite rami

281 renal biopsies from patients with different CKD stages revealed significant correlation of HIF-targe

282 Patients with CKD suffer from food aversion, anorexia, and malnutritio

283 International Society of Nephrology hosted a CKD summit of more than 85 people with diverse expertise

284 ce framework based on ten themes: strengthen CKD surveillance; tackle major risk factors for CKD; red

285 -related inflammasome activation can promote CKD symptoms via infiltration of M1 macrophages.

286 life is substantially lower for people with CKD than for the general population, and falls as GFR de

287 of HF with incident chronic kidney disease (CKD), the composite of incident CKD or mortality, and ra

288 In two mouse models of CKD, the decline in renal function associated with the a

289 c milieu in patients with moderate to severe CKD through a pilot, randomized, 2x2 factorial design tr

290 igenome-wide association studies of eGFR and CKD using whole-blood DNA methylation of 2264 ARIC Study

291 Incidence of CKD was 69.0/1000 patient-years in HF patients versus 14

292 Among 3 diverse community-based cohorts, CKD was associated with an increased risk of HF that was

293 ssociated with younger age at diagnosis, and CKD was observed in all phenotypes.

294 148 non-CKD patients and 227 patients with CKD were recruited.

295 ity of patients with chronic kidney disease (CKD) were investigated to find out whether oral disease

296 with stage 3, 4, or 5 non-dialysis-dependent CKD, who were enrolled at 3 US medical centers.

297 1) examined adults with type 2 diabetes and CKD (with estimated glomerular filtration rate less than

298 higher incidence of chronic kidney disease (CKD) with intensive systolic blood pressure (SBP) loweri

299 it people who are at risk for or affected by CKD worldwide.

300 t high (>5%) predicted risk for both CVD and CKD would be at even greater risk for CVD and CKD events