ライフサイエンスコーパス: CKD

1 CKD appears to be a condition of soluble klotho deficien

2 CKD stage and hypertension are important determinants of

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

4 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

5 >/= 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

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

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

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

9 14 36 with stage 1 or 2 CKD, 99 with stage 3 CKD, 61 with stage 4 CKD, and 18 with stage 5 CKD.

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

11 2 CKD, 99 with stage 3 CKD, 61 with stage 4 CKD, and 18 with stage 5 CKD.

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

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

14 % of children and 8% of adults had stage 4-5 CKD.

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

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

17 14.4] years), 30072 patients in the stage 5D CKD group (45.0% women; 55.0% men; mean [SD] age, 66.9 [

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

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

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

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

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

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

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

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

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

27 pid metabolism changes that typify advancing CKD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 hyperoxaluric mice from nephrocalcinosis and CKD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 16.6 years, 31.7% of participants developed CKD.

65 9-year follow-up, 404 participants developed CKD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 restore fertility in chronic kidney disease (CKD).

91 ascular morbidity in chronic kidney disease (CKD).

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

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

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

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

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

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

98 or with hypertensive chronic kidney disease (CKD).

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

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

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

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

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

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

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

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

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

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

109 lity sleep are unrecognized risk factors for CKD progression.

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

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

112 can highlight potential new target genes for CKD development.

113 we identified new potential target genes for CKD.

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

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

116 athway as a promising therapeutic target for CKD.

117 cells as attractive therapeutic targets for CKD in humans.

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

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

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

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

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

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

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

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

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

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

128 odium restriction on residual albuminuria in CKD.

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

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

131 may contribute to endothelial dysfunction in CKD.

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

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

134 doubling of serum creatinine or increase in CKD stage.

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

136 LDL may underlie downregulation of KChIP2 in CKD.

137 minimal data on serial FGF23 measurements in CKD.

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

139 ompanied by improved cardiorenal outcomes in CKD.

140 acidosis is associated with poor outcomes in CKD.

141 ight mitigate cardiovascular disease risk in CKD.

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

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

144 e quantity and quality of clinical trials in CKD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 fibrotic macrophage phenotype in UUO-induced CKD.

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

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

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

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

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

165 148 non-CKD patients and 227 patients with CKD were recruited.

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

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

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

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

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

171 progression in individuals with nondiabetic CKD.

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

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

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

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

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

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

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

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

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

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

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

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

184 ity and mortality through the development of CKD.

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

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

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

188 >/=30 ml/min per 1.73 m(2), the incidence of CKD stage 4 or higher after radical (n=9759) or partial

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

190 ation of HCV infection with the incidence of CKD.

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

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

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

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

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

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

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

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

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

200 ded that ECR predicts disease progression of CKD patients.

201 ha has been implicated in the progression of CKD.

202 sposes to the development and progression of CKD.

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

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

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

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

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

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

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

210 resent a therapeutic target in late stage of CKD.

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

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

213 sing therapeutic target for the treatment of CKD.

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

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

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

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

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

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

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

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

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

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

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

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

226 nephropathy frequently leads to progressive CKD.

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

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

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

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

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

232 d to an eGFR category indicating more severe CKD.

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

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

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

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

237 In population studies, CKD etiology is often uncertain.

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

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

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

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

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

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

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

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

246 92 adults with CKD of unknown cause or familial nephropathy or hyperten

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

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

249 any populations and has been associated with CKD progression.

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

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

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

253 h renal disease progression in children with CKD.

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

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

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

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

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

259 varies significantly among individuals with CKD.

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

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

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

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

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

265 mproves depressive symptoms in patients with CKD and MDD.

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

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

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

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

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

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

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

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

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

275 148 non-CKD patients and 227 patients with CKD were recruited.

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

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

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

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

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

281 increased risk of mortality in patients with CKD.

282 farction, and heart failure in patients with CKD.

283 y for myocardial infarction in patients with CKD.

284 d rapid renal deterioration in patients with CKD.

285 onset dialysis in HCV-infected patients with CKD.

286 mortality among dialysis-naive patients with CKD.

287 h changes in renal function in patients with CKD.

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

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

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

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

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

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

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

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

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

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

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

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

300 , and stroke in participants with vs without CKD.