ライフサイエンスコーパス: kidney disease

1 odocalyxin (PODXL) are associated with human kidney disease.

2 ariable immunodeficiency and glomerulocystic kidney disease.

3 r conservative care in coronary and advanced kidney disease.

4 , greatly increase risk of multiple types of kidney disease.

5 risk factor for the development of diabetic kidney disease.

6 Anemia is a frequent complication of kidney disease.

7 improve the lives of patients suffering from kidney disease.

8 hey may serve as new biomarkers for diabetic kidney disease.

9 proaches for the prevention and treatment of kidney disease.

10 f coronary disease in patients with advanced kidney disease.

11 people living with diabetes and at risk for kidney disease.

12 tment with ferric carboxymaltose and chronic kidney disease.

13 risk of developing hypertension and chronic kidney disease.

14 hought to be involved in the pathogenesis of kidney disease.

15 utinely excluded those with advanced chronic kidney disease.

16 arker for cardiovascular disease and chronic kidney disease.

17 on with type 2 diabetes and advanced chronic kidney disease.

18 while others are associated with proteinuric kidney disease.

19 an normotensive (MNS) rats that also develop kidney disease.

20 pies for the management of acute and chronic kidney disease.

21 induce apoptosis and glomerular dysfunction kidney disease.

22 adverse events and progression to end-stage kidney disease.

23 inhibit progression or promote regression of kidney disease.

24 ic inflammation, including anemia of chronic kidney disease.

25 GFR recovery within 4 weeks, that is, acute kidney disease.

26 tissue, combine to accelerate progression of kidney disease.

27 in tissue samples from patients with chronic kidney disease.

28 ir can also lead to fibrosis and progressive kidney disease.

29 n human donors of kidney tissue with chronic kidney disease.

30 this measure as it applies to patients with kidney disease.

31 sing age, diabetes, hypertension and chronic kidney disease.

32 nd states of FGF23 excess, including chronic kidney disease.

33 y enhanced sKlotho therapeutics for managing kidney disease.

34 icated in the progression and maintenance of kidney disease.

35 ery of mechanisms that trigger and propagate kidney disease.

36 mportant clinical questions in patients with kidney disease.

37 n, stroke), CV death/HHF, and progression of kidney disease.

38 y and rheumatoid arthritis, and 2 on chronic kidney disease.

39 pe 1 diabetes and early-to-moderate diabetic kidney disease.

40 segmental glomerulosclerosis and polycystic kidney disease.

41 ected for either good kidney health or known kidney disease.

42 ibrotic responses that could lead to chronic kidney disease.

43 total mortality, and progression of chronic kidney disease.

44 sociated with autosomal recessive polycystic kidney disease.

45 nsion, type 2 diabetes mellitus, and chronic kidney disease.

46 genetic factors and the urine metabolome in kidney disease.

47 therapeutic potential across the spectrum of kidney disease.

48 of cardiovascular disease and progression of kidney disease.

49 conducted for genes implicated in Mendelian kidney diseases.

50 role in the pathogenesis and progression of kidney diseases.

51 onal Institute of Diabetes and Digestive and Kidney Diseases.

52 onal Institute of Diabetes and Digestive and Kidney Diseases.

53 implantation genetic diagnosis for heritable kidney diseases.

54 s for additional proteinopathies beyond rare kidney diseases.

55 is, and ischemia/reperfusion, and in chronic kidney diseases.

56 anti-inflammatory treatment for vascular and kidney diseases.

57 butes to the pathogenesis and progression of kidney diseases.

58 ge contributes to the progression of chronic kidney diseases.

59 ,5-trisphosphate receptor channel in various kidney diseases.

60 s of kidney cells and across the spectrum of kidney diseases.

61 is and prognostication for acute and chronic kidney diseases.

62 ill be useful for optimising cell therapy in kidney diseases.

63 it play a causal role in the progression of kidney disease?

64 ompared with ICU control group non-end-stage kidney disease (25% vs 41.4%; p = 0.005).

65 .1%), diabetes mellitus (31.6%), and chronic kidney disease (28.2%); 20.2% received warfarin while 79

66 12.8% (n=59), cancer, 11.7% (n=54), chronic kidney disease, 3.9% (n=18) and inflammatory bowel disea

67 1.6 (1.5-1.7), stroke 6.4 (6.3-6.5), chronic kidney disease 4.4 (4.3-4.6), and peripheral artery dise

68 onal Institute of Diabetes and Digestive and Kidney Diseases (5T32DK07352), Natural Sciences and Engi

69 Chronic kidney disease (89% vs 57% P = .0007), diabetes (66% vs

70 t failure, and peripheral arterial disease), kidney disease (a composite of ESKD or halving of the eG

71 eed exists to better understand and stratify kidney disease according to its underlying pathophysiolo

72 CI, 1.21-2.12], P=0.0010) and progression of kidney disease (adjusted HR, 1.51 [95% CI, 1.13 - 2.03],

73 C-2, result in autosomal dominant polycystic kidney disease (ADPKD) and ultimately renal failure.

74 y diagnosis of autosomal dominant polycystic kidney disease (ADPKD) can enable earlier management and

75 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common inherit

76 Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic caus

77 development of autosomal dominant polycystic kidney disease (ADPKD), a debilitating condition for whi

78 ctively, cause autosomal dominant polycystic kidney disease (ADPKD).

79 eteriorates in autosomal dominant polycystic kidney disease (ADPKD).

80 tin 2 leads to autosomal dominant polycystic kidney disease (ADPKD).

81 ), hypertension, hyperlipidemia, and chronic kidney disease (all p < 0.001).

82 r liver disease; 2.04 (95% CI 1.30-3.20) for kidney disease and 8.15 (95% CI 3.59-18.5) for lung absc

83 In patients with chronic kidney disease and a high risk of progression, urate-low

84 The mutual encroachment of underlying kidney disease and cell senescence bring about the concl

85 KUTs) represent the leading cause of chronic kidney disease and end-stage kidney disease in children.

86 human cohorts: the African American Study of Kidney Disease and Hypertension and the Atherosclerosis

87 redict AKI 61.8 (32.5) hours faster than the Kidney Disease and Improving Global Disease Outcomes (KD

88 Roles of autophagy in polycystic kidney disease and kidney cancer have also been describe

89 randomly assigned 777 patients with advanced kidney disease and moderate or severe ischemia on stress

90 ly assigned adults with stage 3 or 4 chronic kidney disease and no history of gout who had a urinary

91 ate during aging, diabetes mellitus, chronic kidney disease and other chronic diseases.

92 identifies asymptomatic patients at risk for kidney disease and reduced survival.

93 to evaluate early biomarkers of proteinuric kidney disease and to test novel therapeutics.

94 elial cells in health, and across a range of kidney diseases and cancer.

95 cal scenarios for interactive association of kidney diseases and cell senescence, both culminating in

96 onal Institute of Diabetes and Digestive and Kidney Diseases and National Heart, Lung, and Blood Inst

97 cular disease (CVD) in patients with chronic kidney diseases and rheumatologic disorders.

98 to the care of patients with immune-mediated kidney diseases and to kidney transplant recipients.

99 obesity, hypertension, diabetes, and chronic kidney disease) and yielded additional insights into the

100 .1 for >80 g/day), as were diabetes, chronic kidney disease, and end-stage liver disease (HR = 1.2, 9

101 es from stressed rats, sera of patients with kidney disease, and fermentation products of metabolical

102 ole in hypertension, cardiovascular disease, kidney disease, and fluid homeostasis.

103 , albuminuria, autosomal dominant polycystic kidney disease, and ischemia/reperfusion-induced acute k

104 elated biomarkers to progression of diabetic kidney disease, and mixed-effects models estimated bioma

105 hen evaluated autoimmune disease parameters, kidney disease, and response to in vivo TLR7/9 pathogeni

106 with PH among patients with advanced chronic kidney disease appears to differ by etiology.

107 he treatment of patients with AAV and severe kidney disease are balanced.

108 Kidney diseases are particularly challenging to tackle b

109 ditions, including heart failure and chronic kidney disease, are increasingly prevalent in patients w

110 patients with autosomal recessive polycystic kidney disease (ARPKD) and long-term clinical outcome an

111 in the POD-ATTAC mouse model of proteinuric kidney disease as well as in kidney epithelial cell line

112 a subgroup of patients with advanced chronic kidney disease at baseline (estimated glomerular filtrat

113 fication of people with diabetes and chronic kidney disease at high-risk of early mortality is a prio

114 ates of the burden of diabetes and burden of kidney disease attributable to PM(2.5) pollution.

115 tional sample of 1000 patients with advanced kidney disease between 2004 and 2014 who were followed u

116 l treatment for most patients with end-stage kidney disease but organ shortage is a major challenge.

117 insight into the aetiology and mechanisms of kidney diseases but raises ethical issues that risk the

118 ein PKD2 cause autosomal dominant polycystic kidney disease, but the function of PKD2 in cilia remain

119 the eight-protein exocyst protein complex to kidney disease, but the underlying mechanism is unclear.

120 ship between periodontal disease and chronic kidney disease, but there is little evidence to assess t

121 Kidney disease can also impact and complicate the treatm

122 In particular, kidney disease can arise from the use of chemotherapeuti

123 equations for outcomes and develop a chronic kidney disease-cardiovascular disease (CKD-CVD) health o

124 Promoting such patient activation in kidney disease care is increasingly being prioritized, a

125 2,8-DHA nephropathy, leading to progressive kidney disease, characterized by crystal deposits, tubul

126 (OR 3.43, 95% CI 1.17 to 10.00), and chronic kidney disease (CKD) (OR 2.81, 95% CI 1.97 to 4.01) had

127 Our primary outcome was chronic kidney disease (CKD) - defined as confirmed decrease in

128 Transition to chronic kidney disease (CKD) after an episode of acute kidney in

129 high proportion of patients develop chronic kidney disease (CKD) after liver transplantation (LT).

130 is associated with increased risk of chronic kidney disease (CKD) and diabetes, a causal driver of CK

131 Associations between chronic kidney disease (CKD) and the gut microbiota have been po

132 -term trials involving patients with chronic kidney disease (CKD) and type 2 diabetes.

133 Persons with chronic kidney disease (CKD) are at high risk of infection.

134 Adults with chronic kidney disease (CKD) are hospitalized more frequently th

135 Patients with chronic kidney disease (CKD) are often 25(OH)D(3) and 1,25(OH)(2

136 orized by the presence or absence of chronic kidney disease (CKD) at baseline (estimated glomerular f

137 Patients with chronic kidney disease (CKD) exhibit reduced exercise capacity,

138 d whether their activities change in chronic kidney disease (CKD) has not yet been elucidated.

139 Patients with chronic kidney disease (CKD) have inability to maintain the norm

140 Chronic kidney disease (CKD) in low-resource settings poses mult

141 It is hypothesized that chronic kidney disease (CKD) induces oxidant stress which contri

142 Chronic kidney disease (CKD) is deemed to be a worldwide health

143 risk factors, and antiretrovirals to chronic kidney disease (CKD) is unknown.

144 s been associated with lower risk of chronic kidney disease (CKD) progression, implicating mechanisms

145 The increasing prevalence of chronic kidney disease (CKD) seriously is threatening human heal

146 f this study was to assess change in chronic kidney disease (CKD) stage following TAVR, identify vari

147 ereditary cause of kidney stones and chronic kidney disease (CKD) which is characterized by 2,8-dihyd

148 with heart failure (HF) and advanced chronic kidney disease (CKD), a population underrepresented in H

149 itions such as diabetes mellitus and chronic kidney disease (CKD), and they may be involved in age-re

150 Chronic kidney disease (CKD), commonly fostering nonrenal compli

151 a range of human diseases, including chronic kidney disease (CKD), epilepsy, and amyotrophic lateral

152 logy of cardiometabolic diseases and chronic kidney disease (CKD), in part via metabolism of ingested

153 evant to metabolic diseases, such as chronic kidney disease (CKD), in which dietary approaches are al

154 nopathy and modestly associated with chronic kidney disease (CKD), peripheral artery disease (PAD) an

155 tinine is an important biomarker for chronic kidney disease (CKD), we tested the FOLP probe for its a

156 imated glomerular filtration rate by chronic kidney disease (CKD)-EPI-CysC-creatinine <60 mL/min/1.73

157 ption, and amelioration of anemia in chronic kidney disease (CKD).

158 rosclerotic disease in patients with chronic kidney disease (CKD).

159 notype strikingly similar to that of chronic kidney disease (CKD).

160 d is commonly found in patients with chronic kidney disease (CKD).

161 r of older LT recipients with pre-LT chronic kidney disease (CKD).

162 PTEN emerged as novel suppressors of chronic kidney disease (CKD).

163 for effective therapy in preventing chronic kidney disease (CKD).

164 failure or death in individuals with chronic kidney disease (CKD).

165 hatemia as in tumoral calcinosis and chronic kidney disease (CKD).

166 nited States-37 million persons-have chronic kidney disease (CKD).

167 T), cardiovascular disease (CVD) and chronic kidney disease (CKD).

168 ase, cancer, liver-, rheumatic-, and chronic kidney disease (CKD).

169 nduced acute kidney injury (AKI) and chronic kidney disease (CKD).

170 y injury [AKI] and atrophy-fibrosis [chronic kidney disease (CKD)] and rejection.

171 dels and stratified for diabetes and chronic kidney disease (CKD, defined as estimated glomerular fil

172 Clearance of 25-hydroxyvitamin D in Chronic Kidney Disease (CLEAR), NCT02937350; Clearance of 25-hyd

173 glomerular tissue of patients with diabetic kidney disease compared with control glomerular tissue.

174 ic backgrounds that may be more resistant to kidney disease compared with humans and, therefore, poor

175 coronary artery disease, stroke and chronic kidney disease, complemented by a systematic review of r

176 ten diagnosed late, and the global burden of kidney disease continues to be underappreciated.

177 ity and mortality in patients with end-stage kidney disease could be partially caused by extensive ca

178 ss the advantages of studying rare monogenic kidney diseases, describe effective patient-derived mode

179 Implications of SerpinB2 in human kidney disease deserve further exploration.

180 cell clearance and complement activation in kidney disease development.

181 c, epigenetic, and developmental elements in kidney disease development.

182 hanges likely mediate the genotype effect on kidney disease development.

183 most sensitive to the prevalence of chronic kidney disease, diabetes, cardiovascular disease, and ch

184 rlying cardiovascular disease, lung disease, kidney disease, diabetes, immunosuppression, and liver d

185 peripheral arterial disease, asthma, chronic kidney disease, diabetes, or COPD in the 12 months befor

186 yocardial infarction, heart failure, chronic kidney disease, dialysis, stroke, inpatient admission),

187 Polycystic kidney disease did not result in different SMR.

188 utcomes in patients with type 2 diabetes and kidney disease (DKD) conventionally define a surrogate e

189 tic predisposition are critical for diabetic kidney disease (DKD) development.

190 Diabetic kidney disease (DKD) is a major complication of diabetes

191 d to development and progression of diabetic kidney disease (DKD).

192 Acute and chronic kidney disease encompasses a complex set of diseases tha

193 consistent reductions in risks for secondary kidney disease end points (albuminuria and a composite o

194 (CKiD) equation for children and the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equa

195 ular filtration rate (eGFR) with the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), Mod

196 were observed with cystatin C-based chronic kidney disease epidemiology collaboration equations.

197 erm outcomes such as mortality and end-stage kidney disease (ESKD) have been rarely reported in this

198 with CKD risk factors and incident end-stage kidney disease (ESKD) in 4,843 participants of the Germa

199 om stage 1 to stage 5 CKD, whereas end-stage kidney disease (ESKD) is defined as permanent kidney fai

200 s (glycated hemoglobin level, >=7%), chronic kidney disease (estimated glomerular filtration rate, 25

201 f LTBI testing (e.g., HIV, diabetes, chronic kidney disease, etc.) were identified from physician cla

202 th a greater risk of progression of diabetic kidney disease, even after adjustment for established cl

203 se of varied aetiologies, including diabetic kidney disease, focal segmental glomerulosclerosis and p

204 in 4,843 participants of the German Chronic Kidney Disease (GCKD) study.

205 lated by Dnmt3a and Dnmt3b were enriched for kidney disease genetic risk loci.

206 r filtration rate and lowest rate of chronic kidney disease (>=stage 3) from year 1 onwards until stu

207 Patients with chronic kidney disease had elevated serum levels of IL-27 and IL

208 Chronic kidney diseases have become a major issue worldwide.

209 coronary artery disease, arthritis, chronic kidney disease, heart failure, stroke, asthma, chronic o

210 onic health problems, such as heart disease, kidney disease, high blood pressure, diabetes, stroke, o

211 -PAD; P-interaction=0.79) and progression of kidney disease (HR, 0.78, PAD; HR, 0.76, no-PAD; P-inter

212 es (HR, 1.95; 95% CI, 1.06-3.58) and chronic kidney disease (HR, 1.97; 95% CI, 1.05-3.67) emerged as

213 as (HR: 1.62; 95% CI: 1.28 to 2.05), chronic kidney disease (HR: 2.41; 95% CI: 1.54 to 3.78), and mul

214 alysis, and total health care costs by eGFR (Kidney Disease Improving Global Outcomes-defined eGFR ca

215 ned as an AKI-stage increase of two or more (Kidney Disease: Improving Global Outcome creatinine-base

216 Kidney Disease: Improving Global Outcomes (KDIGO) and Ac

217 The other factors associated with Kidney Disease: Improving Global Outcomes stage 3 acute

218 w-risk patients and for patients who met the Kidney Disease: Improving Global Outcomes urine output c

219 ficantly worse than for patients who met the Kidney Disease: Improving Global Outcomes urine output c

220 method of screening for the risk of chronic kidney disease in adults.

221 Using data from the Chronic Kidney Disease in Children (CKiD) study, we examined lon

222 The Chronic Kidney Disease in Children Study (CKiD) equation for chi

223 dren and adolescents enrolled in the Chronic Kidney Disease in Children study, an observational cohor

224 ause of chronic kidney disease and end-stage kidney disease in children.

225 The landscape of kidney disease in diabetes has shifted.

226 nificantly increasing the risk of developing kidney disease in humans.

227 ias Barttin) as a genetic modifier of cystic kidney disease in Joubert syndrome, using a Cep290-defic

228 rticle reviews genetic testing for inherited kidney disease in living kidney donors to improve donor

229 ruciferous vegetables and GSTM1 genotypes on kidney disease in mice as well as in human ARIC study pa

230 a, and eventually lead to new definitions of kidney disease in support of precision medicine.

231 rates autoantibody production and autoimmune kidney disease in the Tlr7.1 transgenic mouse model of S

232 d risk of cardiovascular disease and chronic kidney disease in those with gout, novel associations of

233 clinical trials for the treatment of chronic kidney disease in type 2 diabetes.

234 Podocytopathies are kidney diseases in which direct or indirect podocyte inj

235 s, and iii) altered ER Ca(2+) homeostasis in kidney disease, including podocytopathy, diabetic nephro

236 ciency, which include heart failure, chronic kidney disease, inflammatory bowel disease, patient bloo

237 Kidney disease is a global public health concern across

238 Chronic kidney disease is a public health burden and it remains

239 Chronic kidney disease is divided into 5 groups, ranging from st

240 Prevention of kidney disease is highly cost-effective but requires a m

241 nd understanding of the mechanism underlying kidney disease is hindered by the almost exclusive use o

242 As such, kidney disease is often diagnosed late, and the global b

243 While the correlation to kidney disease is robust, there is little consensus conc

244 Although diabetic kidney disease is the leading cause of ESKD in the Unite

245 naling, a therapeutic mainstay of glomerular kidney diseases, is thought to act primarily through reg

246 s for these processes interact and can shape kidney disease, it seems plausible that SerpinB2 might p

247 ctivation has recently emerged as central to kidney disease legislative policy in the United States.

248 jury and those with risk factors for chronic kidney disease limit conclusions about safety in these p

249 Our results support including kidney disease markers in the identification of persons

250 In a large community sample, the addition of kidney disease markers to conventional risk factors impr

251 Understanding the genetic basis of common kidney diseases means having a comprehensive picture of

252 sively investigated the association of 2 key kidney disease measures, estimated glomerular filtration

253 Kidney disease measures, particularly high ACR, were ind

254 the most common being hypertension, chronic kidney disease, obstructive sleep apnoea, and metabolic

255 of CG in a kidney transplant recipient with kidney disease of unknown cause.

256 air after acute kidney injury and to chronic kidney disease of varied aetiologies, including diabetic

257 ysfunction may mediate the effect of chronic kidney disease on abnormal cardiac function and cardiova

258 We excluded patients who had end-stage kidney disease or AKI at admission.

259 ations in patients with stage 4 or 5 chronic kidney disease or undergoing dialysis, the upper bound 9

260 Conversely, chronic kidney disease (OR, 0.53) and invasive mechanical intuba

261 .06; 95% CI: 1.02, 1.10; P = .003), acquired kidney disease (OR: 1.95; 95% CI: 1.004, 3.78; P = .049)

262 In 2015, the Kidney Disease Outcomes Quality Initiative recommended t

263 uctive pulmonary disease (P = 0.73), chronic kidney disease (P = 0.09), and hearing loss (P = 0.31).

264 s that likely mediate the genotype effect on kidney disease pathogenesis.

265 models that are essential for understanding kidney disease pathophysiology.

266 termine the prognostic factors for end-stage kidney disease patients admitted to the ICU.

267 ctive for the treatment of anemia in chronic kidney disease patients and may also be beneficial for t

268 857 incident, adult (18-79 years) end-stage kidney disease patients from 690 dialysis facilities in

269 End-stage kidney disease patients presented frequently severe comp

270 national transplant registry for 35 849 T2DM kidney disease patients who received transplant between

271 ging for chronic diseases such as polycystic kidney disease (PKD), the most common hereditary disease

272 ear mortality were old age, anaemia, chronic kidney disease, presence of valvular heart disease, left

273 importance of albuminuria as a predictor of kidney disease progression and vascular disease has driv

274 role for plasmin (ogen) as a "second hit" in kidney disease progression has yet to have been demonstr

275 nt GSTM1 deletion variant is associated with kidney disease progression in human cohorts: the African

276 We rated less than half of kidney disease quality metrics as highly valid; the othe

277 rd therapy, in adult patients with end-stage kidney disease receiving hemodialysis.

278 approaches for acute kidney injury, chronic kidney disease, renal fibrosis, renovascular hypertensio

279 .67; 95% CI, 1.02, 2.72, P = .04), perceived kidney disease risk following donation (aOR, 1.68; 95% C

280 pment Goal (SDG) has the potential to impact kidney disease risk or improve early diagnosis and treat

281 hin human BSND significantly associates with kidney disease severity in a patient cohort with CEP290

282 nd hospitalisation for heart failure; annual kidney disease stages; and cardiovascular and nonvascula

283 of patients with type 2 diabetes and chronic kidney disease, sTNFR1 predicted short-to-medium term mo

284 associated with high risk of progression of kidney disease, stroke, and peripheral arterial disease.

285 e Biobank Japan dataset (excluding secondary kidney diseases, such as diabetes mellitus) clearly reve

286 or patients with or without advanced chronic kidney disease, supporting conventional dosing in patien

287 obesity, diabetes, hypertension, and chronic kidney disease than white patients.

288 factor H (CFH) are a classic C3G model, with kidney disease that requires several months to progress

289 Applied broadly across multiple inflammatory kidney diseases, these studies promise to enormously exp

290 ined associated with progression of diabetic kidney disease; TNFR-2 had the highest risk (adjusted ha

291 th increased risk of progression of diabetic kidney disease; TNFR-2 had the highest risk after accoun

292 aimed to assess whether adding biomarkers of kidney disease to conventional risk factors improved 10-

293 to assess and address patient activation in kidney disease to facilitate best practices for supporti

294 body-surface area, and evidence of diabetic kidney disease to receive allopurinol or placebo.

295 have a normal lifespan, and fail to develop kidney disease under normal conditions.

296 onal Institute of Diabetes and Digestive and Kidney Diseases, US Department of Agriculture/Agricultur

297 ve and standardize the care of patients with kidney disease who have indication(s) to receive ACR-des

298 vents in patients with diabetes with chronic kidney disease with or without albuminuria have not been

299 In patients with diabetes and chronic kidney disease, with or without albuminuria, sotaglifloz

300 ts are prevalent among patients with chronic kidney disease without overt obstructive coronary artery