ライフサイエンスコーパス: kidney disease

1 th diabetes mellitus and 50 with nondiabetic kidney disease).

2 isk and slows the progression of proteinuric kidney disease.

3 periods compared with those without chronic kidney disease.

4 ions toward mitochondrial fitness and cystic kidney disease.

5 ificantly more likely to have severe chronic kidney disease.

6 and those with diabetes mellitus or chronic kidney disease.

7 , respiratory disease, stroke, diabetes, and kidney disease.

8 lack of animal models exhibiting progressive kidney disease.

9 may serve as therapeutic targets in diabetic kidney disease.

10 renal inflammation and fibrosis in diabetic kidney disease.

11 nd podocyte dysfunction leads to proteinuric kidney disease.

12 rotein causing autosomal dominant polycystic kidney disease.

13 ablished cardiovascular disease, and chronic kidney disease.

14 urely than they are to progress to end stage kidney disease.

15 s of diabetes, muscular dystrophy, and acute kidney disease.

16 mpairment and progressive and/or immunologic kidney disease.

17 and their persistence in progressive chronic kidney disease.

18 es to extraskeletal complications in chronic kidney disease.

19 get for the treatment of fibrosis in chronic kidney disease.

20 ere more likely to have progression of their kidney disease.

21 ns of possibly high relevance to IgAN and/or kidney disease.

22 n of acute kidney injury to advanced chronic kidney disease.

23 a major point in patients with severe acute kidney disease.

24 iated with increased cancer risk and chronic kidney disease.

25 horus intake is a modifiable risk factor for kidney disease.

26 otency for glucose lowering in patients with kidney disease.

27 l role in hereditary and sporadic glomerular kidney disease.

28 risk for developing hypertension and chronic kidney disease.

29 itochondrial dysfunction in APOL1-associated kidney disease.

30 r frequency influencing the risk of diabetic kidney disease.

31 o-inflammatory, prognostic marker in chronic kidney disease.

32 t in a rat model of hypertensive proteinuric kidney disease.

33 bnormalities including patients with chronic kidney disease.

34 leading to high plasma suPAR and proteinuric kidney disease.

35 10(-4)) associated with the risk of diabetic kidney disease.

36 with an increased risk of developing chronic kidney disease.

37 iovascular risk factors, stroke, and chronic kidney disease.

38 replacement therapy for those with end-stage kidney disease.

39 BTBR Lep(ob) mice exhibited diabetic kidney disease.

40 sease (ADPKD) constitutes the most inherited kidney disease.

41 herapeutic strategy in progressive, fibrotic kidney disease.

42 V genotype 1 infection and stage 4-5 chronic kidney disease.

43 mice are needed to develop new therapies for kidney disease.

44 s (P=3.0x10(-6)) in pathogenesis of diabetic kidney disease.

45 ncreatic neoplasia, and 1 case of polycystic kidney disease.

46 tabolic reprograming and fibrogenesis during kidney disease.

47 of new treatments for patients with fibrotic kidney disease.

48 s a common underlying process of progressive kidney diseases.

49 to one of six GN subtypes or two comparator kidney diseases.

50 be valuable for the treatment of progressive kidney diseases.

51 erapeutic strategies for chronic progressive kidney diseases.

52 increase susceptibility to some progressive kidney diseases.

53 t for better understanding and management of kidney diseases.

54 apoptosis and renal interstitial fibrosis in kidney diseases.

55 and durable loss of renal function [chronic kidney disease]).

56 Chronic kidney disease (10.4% vs. 5.6%; aOR, 1.49 [CI, 1.24 to 1

57 use of autosomal dominant tubulointerstitial kidney disease, a condition that leads to CKD and ESRD.

58 ing with IgAN, autosomal dominant polycystic kidney disease (ADPKD) and diabetic nephropathy associat

59 Autosomal dominant polycystic kidney disease (ADPKD) constitutes the most inherited ki

60 Autosomal dominant polycystic kidney disease (ADPKD) is caused by inactivating mutatio

61 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 or

62 Autosomal dominant polycystic kidney disease (ADPKD) is characterized by innumerous fl

63 Autosomal dominant polycystic kidney disease (ADPKD) is driven by mutations in PKD1 an

64 Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inherited diso

65 patients with autosomal dominant polycystic kidney disease (ADPKD) remains untested.

66 pathy (DN) and autosomal-dominant polycystic kidney disease (ADPKD) served as "external" non-GN compa

67 nifestation of autosomal dominant polycystic kidney disease (ADPKD).

68 athogenesis of autosomal dominant polycystic kidney disease (ADPKD).

69 ted disorders, autosomal dominant polycystic kidney diseases (ADPKD), a significant cause of ESRD, an

70 se recent data demonstrate increased risk of kidney disease after donation, including a small increas

71 the pathogenesis of hypertension, polycystic kidney disease, AKI, and CKD.

72 ned risk of developing chronic and end-stage kidney disease, an association that is largely attribute

73 F23) increase early during acute and chronic kidney disease and are associated with adverse outcomes.

74 (RHD) are major causes of pediatric chronic kidney disease and are highly genetically heterogeneous.

75 ver, no T2D mouse model of combined diabetic kidney disease and atherosclerosis exists.

76 Diabetic kidney disease and atherosclerotic disease are major cau

77 ciated with certain risk factors for chronic kidney disease and certain kidney-biopsy findings.

78 Patients had stage 4 or 5 chronic kidney disease and either had received no previous treat

79 All factors, except preexisting kidney disease and failed ventilator liberation, were me

80 sponse in patients with stage 4 or 5 chronic kidney disease and HCV infection.

81 ctive study of 899 African American Study of Kidney Disease and Hypertension (AASK) and 761 Modificat

82 ts enrolled in the African American Study of Kidney Disease and Hypertension (AASK) Cohort Study who

83 replicated in the African American Study of Kidney Disease and Hypertension cohort (discovery P=5.42

84 determine whether African American Study of Kidney Disease and Hypertension nephropathy (AASK-N) is

85 inical outcomes in African American Study of Kidney Disease and Hypertension participants (n=1044).

86 odocyte injury is an early event in diabetic kidney disease and is a hallmark of glomerulopathy.

87 ve-to include patients with advanced chronic kidney disease and kidney transplant recipients.

88 Kidney fibrosis is a hallmark of chronic kidney disease and leads to extracellular matrix accumul

89 s eicosanoid are also elevated in polycystic kidney disease and may contribute to cyst formation.

90 ure was associated with an increased risk of kidney disease and osteoporosis/fracture, this risk did

91 African Americans develop chronic kidney disease and pulmonary hypertension (PH) at dispro

92 lymphoproliferation, and significant chronic kidney disease and requiring long-term immunosuppressive

93 a consequence of diseases such as leukemia, kidney disease and sarcoidosis.

94 d despite strong correlation between chronic kidney disease and survival.

95 events and death among patients with chronic kidney disease and the general population.

96 injury is a major determinant of proteinuric kidney disease and the identification of potential thera

97 fit in effectiveness in patients with severe kidney disease and worse effectiveness with no benefit i

98 ase (AD) associated with their long-standing kidney disease and/or neurotoxic immunosuppressant agent

99 hich intravital FLIM can be applied to study kidney diseases and metabolism.

100 icroRNAs could be developed as biomarkers of kidney diseases and might be involved in disease mechani

101 have uncovered a strong association between kidney diseases and two sequence variants of the APOL1 g

102 exclusively enrolling patients with chronic kidney disease), and at least 50 peripheral artery disea

103 pus erythematosus, recent pneumonia, chronic kidney disease, and active cancer, but confounding by dr

104 inflammation and increased risk of diabetes, kidney disease, and cardiovascular disease.

105 -cardiac variables (body-mass index, chronic kidney disease, and chronic obstructive pulmonary diseas

106 proved and timely detection of (progressive) kidney disease, and could provide new therapeutic opport

107 rom bone marrow failure syndromes to chronic kidney disease, and from nutritional deficiencies to inf

108 hypertension, leg ulcers, priapism, chronic kidney disease, and large-artery ischemic stroke.

109 s progressive retinal dystrophy, fibrocystic kidney disease, and liver fibrosis.

110 e, heart failure, diabetes mellitus, chronic kidney disease, anemia, coagulopathy, obesity, major ble

111 The Chronic Kidney Disease Antidepressant Sertraline Trial (CAST) wa

112 In particular, patients with chronic kidney disease are at high risk for adverse events after

113 Most forms of chronic, progressive kidney disease are characterized by fibrosis whereby the

114 Progressive kidney diseases are often associated with scarring of th

115 Autosomal recessive polycystic kidney disease (ARPKD) is an important childhood nephrop

116 r cells, ciliopathies such as the polycystic kidney disease, as well as in the genetic diseases short

117 In multivariable adjusted analyses, kidney disease associated with increased odds of odor id

118 Furthermore, autosomal dominant polycystic kidney disease-associated TRPP2 mutant T448K significant

119 atients treated, 2250 patients had prevalent kidney disease at baseline, of whom 67% had a diagnosis

120 The current view of diabetic kidney disease, based on meticulously acquired ultrastru

121 onal Institute of Diabetes and Digestive and Kidney Diseases brought together clinicians and basic sc

122 (FGF23) increase during the early stages of kidney disease, but the underlying mechanism remains inc

123 those seen in autosomal dominant polycystic kidney disease, but without clinically relevant kidney c

124 ificant predictors for ADHF included chronic kidney disease, cardiovascular disease, age>/=75 years,

125 hrotic syndrome (SRNS) causes 15% of chronic kidney disease cases.

126 coupled receptors (GPCRs) and the polycystic kidney disease-causing polycystin 1/2 complex.

127 es in the recipients' draining liquid at the Kidney Disease Center, The First Affiliated Hospital, Co

128 n monoxide (CO) and risk of incident chronic kidney disease, chronic kidney disease progression, and

129 morbidities (cardiovascular disease, chronic kidney disease, chronic lung disease, liver disease, and

130 Of 4 patients with chronic kidney disease (CKD) > stage 2 at short-term follow-up,

131 to subgroups of those with stage 1-2 chronic kidney disease (CKD) (estimated glomerular filtration ra

132 DD) is prevalent among patients with chronic kidney disease (CKD) and is associated with morbidity an

133 Complex human traits such as chronic kidney disease (CKD) are a major health and financial bu

134 es in renal function in an all-cause chronic kidney disease (CKD) cohort.

135 Chronic kidney disease (CKD) has a prevalence of approximately 1

136 ough the effect of HIF activation in chronic kidney disease (CKD) has been widely evaluated, the resu

137 C virus (HCV)-infected patients with chronic kidney disease (CKD) have rarely been studied because th

138 We assessed the risk of chronic kidney disease (CKD) in chronic hepatitis C virus (HCV)-

139 eptor (suPAR) independently predicts chronic kidney disease (CKD) incidence and progression.

140 Complications of chronic kidney disease (CKD) include weak bones and increased fr

141 Chronic kidney disease (CKD) is a complex gene-environmental dis

142 Chronic kidney disease (CKD) is a prevalent cause of morbidity a

143 Chronic kidney disease (CKD) is defined by reduced estimated glo

144 For chronic kidney disease (CKD) monitoring in primary care, serum c

145 The patient with chronic kidney disease (CKD) represents an extreme model for art

146 To reduce over-diagnosis of chronic kidney disease (CKD) resulting from the inaccuracy of cr

147 elated to mortality of patients with chronic kidney disease (CKD) were investigated to find out wheth

148 of the reported higher incidence of chronic kidney disease (CKD) with intensive systolic blood press

149 s, but less likely to have stage 3-5 chronic kidney disease (CKD), alcohol or drug abuse or dependenc

150 are highly elevated in patients with chronic kidney disease (CKD), and it is likely that FGF23 direct

151 ce of type 2 diabetes mellitus (DM), chronic kidney disease (CKD), and treated hypertension (HTN) by

152 antagonists slow the progression of chronic kidney disease (CKD), but their use is limited by hyperk

153 pe 2 diabetes and moderate to severe chronic kidney disease (CKD), congestive heart failure (CHF), or

154 s may be advantageous in adults with chronic kidney disease (CKD), in whom the cause of kidney failur

155 ffecting kidneys during aging and in chronic kidney disease (CKD), regardless of cause.

156 the association of HF with incident chronic kidney disease (CKD), the composite of incident CKD or m

157 disease process, often progresses to chronic kidney disease (CKD), with no available effective prophy

158 individuals are at increased risk of chronic kidney disease (CKD).

159 y may be associated with the risk of chronic kidney disease (CKD).

160 re of a variety of organs, including chronic kidney disease (CKD).

161 pathogenic process in progression of chronic kidney disease (CKD).

162 of renal elasticity in patients with chronic kidney disease (CKD).

163 esive plan to address the problem of chronic kidney disease (CKD).

164 lent in dialysis-naive patients with chronic kidney disease (CKD).

165 nsion (control) or with hypertensive chronic kidney disease (CKD).

166 urvival of MALA induced in mice with chronic kidney disease (CKD).

167 tation (KT) may restore fertility in chronic kidney disease (CKD).

168 ted with cardiovascular morbidity in chronic kidney disease (CKD).

169 y associated with the progression of chronic kidney diseases (CKD) by producing renal tubulointerstit

170 ression of ShcA in several human proteinuric kidney diseases compared with normal conditions.

171 NTERPRETATION: Even mild-to-moderate chronic kidney disease conferred increased risk of incident peri

172 ption; n=105) with outcomes in women without kidney disease (controls; n=24,640).

173 I was associated with development of chronic kidney disease, conversion to chronic dialysis, hospital

174 l-cause mortality in patients with prevalent kidney disease (defined as eGFR <60 mL.min(-1).1.73 m(-2

175 uring Ang II-induced hypertension attenuated kidney disease development in MYH9(E1841K/E1841K) mice.

176 more often from atrial fibrillation, chronic kidney disease, diabetes mellitus, and dyslipidemia, and

177 ication for incident or progressive diabetic kidney disease (DKD) in persons with type 2 diabetes.

178 developing therapeutics to prevent diabetic kidney disease (DKD) is limited by a lack of animal mode

179 Pathogenetic markers of diabetic kidney disease (DKD) progression to ESRD are lacking.

180 ent feature of damaged podocytes in diabetic kidney disease (DKD).

181 eight, maternal education, seizure disorder, kidney disease duration, and genetically defined ancestr

182 an 60 mL/min per 1.73 m(2), incident chronic kidney disease, eGFR decline of 30% or more, and end-sta

183 ated with increased risk of incident chronic kidney disease, eGFR decline, and end-stage renal diseas

184 primary event in the development of diabetic kidney disease either.

185 V genotype 1 infection and stage 4-5 chronic kidney disease enrolled at 68 centres worldwide to eithe

186 Body surface area (BSA)-adjusted chronic kidney disease epidemiology (CKD-EPI) was the most accur

187 Using Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equa

188 and specificity of ultrasound for diagnosing kidney disease, especially when these agents are conjuga

189 African Americans participants with chronic kidney disease (estimated glomerular filtration rate <60

190 oint associations of two measures of chronic kidney disease (estimated glomerular filtration rate [eG

191 r requirement, thrombocytopenia, preexisting kidney disease, failed ventilator liberation, and acute

192 ry data was able to predict advanced chronic kidney disease following hospitalization with acute kidn

193 In two other models of progressive kidney disease, global Mif deletion or MIF inhibition al

194 Older patients and those with kidney disease had higher gastrointestinal bleeding rate

195 Patients with chronic kidney disease had higher rates of both hyperkalemia and

196 Kidney disease has been linked to dysregulated signaling

197 ification of genetic factors associated with kidney disease has the potential to provide critical ins

198 with both HCV infection and advanced chronic kidney disease have limited treatment options.

199 In conclusion, patients with kidney disease have olfactory deficits that may influenc

200 2 allografts from rapid recurrence of native kidney disease) have a high risk of further recurrence a

201 r, more likely to have hypertension, chronic kidney disease, HF, coronary heart disease, and stroke.

202 ance of the microbiome in the development of kidney disease, however, is largely unknown.

203 c cAMP signaling is pathologic in polycystic kidney disease; however, its spatiotemporal actions are

204 between fine particulate matter and risk of kidney disease; however, the association between ambient

205 TAVR (HR, 1.21; 95% CI, 1.05-1.39), chronic kidney disease (HR, 1.20; 95% CI, 1.04-1.39), chronic lu

206 e session, allergy for cephalosporins, known kidney disease, immunosuppressant use, or pregnancy.

207 developed acute kidney injury, as defined by Kidney Disease Improving Global Outcome criteria (change

208 n of patients who developed AKI according to Kidney Disease Improving Global Outcomes (KDIGO) criteri

209 Clinical guidelines recommend using Kidney Disease Improving Global Outcomes (KDIGO) criteri

210 By implementing the Kidney Disease Improving Global Outcomes criteria, AKI w

211 eak serum creatinine and staged according to Kidney Disease Improving Global Outcomes criteria.

212 studied 16,968 critically ill patients with Kidney Disease Improving Global Outcomes stage 2 or 3 AK

213 We used the Kidney Disease: Improving Global Outcomes criteria to de

214 phrectomized rats) that develops progressive kidney disease in association with TGF-beta overexpressi

215 APOL1 G1 and G2 variants facilitate kidney disease in blacks.

216 Data from the CKD in Children Study Chronic Kidney Disease in Children (CKiD) Study indicate that a

217 cribes the incidence and causes of end-stage kidney disease in children on long-term dialysis, and hi

218 ontributing to initiation and progression of kidney disease in diabetes.

219 L1 (APOL1) risk variants are associated with kidney disease in hypertensive AAs.

220 h account for much of the increased risk for kidney disease in sub-Saharan African ancestry populatio

221 vels of endothelin-1 indicate future risk of kidney disease in the general population.

222 riants in the APOL1 gene are associated with kidney diseases in African ancestral populations; yet, t

223 re pathological hallmarks of a wide range of kidney diseases, including diabetic nephropathy.

224 5-AG) are associated with advanced stages of kidney disease independent of kidney function and glycem

225 ted with type 2 diabetes (T2D), and diabetic kidney disease is a major cardiovascular risk factor.

226 Treatment for end-stage kidney disease is a major economic challenge and a publi

227 Some evidence suggests that chronic kidney disease is a risk factor for lower-extremity peri

228 Chronic kidney disease is a significant complication after liver

229 Kidney disease is a substantial worldwide clinical and p

230 Diabetic kidney disease is among the most frequent complications

231 sures that slows down and delays age-related kidney disease is caloric restriction.

232 Autosomal dominant polycystic kidney disease is caused by mutations in the genes encod

233 he olfaction-nutrition axis in patients with kidney disease is limited.

234 ABSTRACT: Chronic kidney disease is strongly associated with a decrease in

235 suPAR associated with future and progressing kidney disease is unclear, but is likely extra-renal, as

236 is, a common pathological feature of chronic kidney diseases, is often associated with apoptosis in r

237 festation of JBTS is a juvenile-onset cystic kidney disease, known as nephronophthisis, typically pro

238 onal Institute of Diabetes and Digestive and Kidney Diseases-led consortium to optimize approaches fo

239 Patients with previous VTE, chronic kidney disease, liver disease, cancer, and thrombophilia

240 Patients with previous VTE, chronic kidney disease, liver disease, cancer, and thrombophilia

241 e to reduce the dose in patients with severe kidney disease may increase bleeding risk, whereas dose

242 Both chronic kidney disease measures were independently associated wi

243 We investigated the modifications of chronic kidney disease-mineral and bone disorder with a special

244 The management of chronic kidney disease-mineral and bone disorders has recently c

245 ay a pivotal role in inflammation in a mouse kidney disease model.

246 ies of human kidney development, modeling of kidney diseases, nephrotoxicity and kidney regeneration.

247 erosis, hypertension, heart failure, chronic kidney disease, obesity, and type 2 diabetes mellitus.

248 1 had significantly higher odds of diabetic kidney disease (odds ratio [OR], 2.58; 95% CI, 1.39-4.81

249 Patients with underlying kidney disease or abnormal serum creatinine levels on ho

250 ication (OR = 1.45; CI, 1.27-1.65), diabetic kidney disease (OR = 1.31; CI, 1.08-1.59), prior foot ex

251 nsion (OR, 1.95; 95% CI, 1.03-3.70), chronic kidney disease (OR, 2.05; 95% CI, 1.15-3.64), creatinine

252 established cardiovascular disease, chronic kidney disease, or both.

253 re (HF) admission or mortality among chronic kidney disease patients, including patients with non-end

254 ist for patients with symptomatic polycystic kidney disease (PCKD).

255 or a wider range of cross-sectional diabetic kidney disease phenotypes.

256 hypoglycemia (HI) and congenital polycystic kidney disease (PKD) are rare, genetically heterogeneous

257 sruption has been associated with polycystic kidney disease (PKD) genes, the majority of which encode

258 Polycystic kidney disease (PKD) is a life-threatening disorder, com

259 Proliferative kidney disease (PKD) is a major threat to wild and farme

260 ominantly with the second Ig-like polycystic kidney disease (PKD) repeat domain (PKD2) present in the

261 Polycystic kidney diseases (PKDs) are genetic disorders that can ca

262 utic target for the treatment of proteinuric kidney disease.Podocytes are essential components of the

263 of the general population and to the chronic kidney disease population, the risk was lowest in the ge

264 eneral population and highest in the chronic kidney disease population.

265 nternational cohorts included in the Chronic Kidney Disease Prognosis Consortium (baseline measuremen

266 of incident chronic kidney disease, chronic kidney disease progression, and end-stage renal disease

267 ar K(+) loss and cytotoxicity does not drive kidney disease progression.

268 ge in patient-reported overall health on the Kidney Disease Quality of Life Survey (median score, 0 i

269 ogenous renoprotective factor in progressive kidney diseases, raising the possibility of pharmacologi

270 view of the events underlying progression of kidney disease reflected in the urine.

271 ar diseases, the role of such alterations in kidney diseases remains largely unknown.

272 were kidney events (a composite of end-stage kidney disease, renal death, development of an estimated

273 term and developed slowly progressive cystic kidney disease, renal fibrosis, and hydronephrosis.

274 Data were analyzed according to kidney diseases, renal function (staging according to CK

275 onal Institute of Diabetes and Digestive and Kidney Diseases Repository and included in our analyses:

276 National Institute of Diabetes and Digestive Kidney Diseases repository and tested for seven markers

277 ial infarction (MI) in patients with chronic kidney disease requiring long-term dialysis (stage 5D CK

278 ted glomerular filtration rate and end stage kidney disease requiring renal replacement therapy.

279 Diabetic kidney disease, retinopathy, peripheral neuropathy, card

280 protein-L1 (APOL1) variants with a recessive kidney disease risk, named G1 and G2, occur at high freq

281 ic diagnosis of calciphylaxis without severe kidney disease (serum creatinine level >3 mg/dL; glomeru

282 Kidney disease severity varies considerably and accurate

283 re prevalent among patients who have chronic kidney disease than among those who do not have the dise

284 the development and progression of diabetic kidney disease than placebo.

285 tein in urine (proteinuria) is a hallmark of kidney disease that typically occurs in conjunction with

286 of evidence showing the pandemic of chronic kidney disease, the impact of pre-operative kidney funct

287 In end-stage chronic kidney disease, the option of organ transplantation is l

288 Uromodulin-associated kidney disease (UAKD) is caused by mutations in the urom

289 d persistence of otherwise detrimental APOL1 kidney disease variants.

290 The C-statistic for incident chronic kidney disease was 0.636 for ADA fasting glucose concent

291 Chronic kidney disease was defined as estimated glomerular filtr

292 Advanced chronic kidney disease was defined by a sustained reduction in e

293 e secondary to autosomal dominant polycystic kidney disease was referred to a quaternary care center

294 d fibrocystin (also implicated in polycystic kidney disease), we demonstrate these motifs to be suffi

295 e the contribution of the E1841K mutation in kidney disease, we studied the effects of the E1841K mut

296 All-cause death and incident chronic kidney disease were secondary outcomes.

297 Patients with chronic kidney disease who also have HCV infection are at higher

298 + mice developed spontaneous and progressive kidney disease with organ failure over 24 weeks.

299 ge renal disease than those who have chronic kidney disease without HCV infection.

300 years, prior cardiovascular disease, chronic kidney disease, women, black race, and 3 levels of basel