ライフサイエンスコーパス: renal disease

1 pathy (DN) is the leading cause of end-stage renal disease.

2 o chronic kidney disease ending in end stage renal disease.

3 and suggest a possible strategy for treating renal disease.

4 ccelerated development of autoantibodies and renal disease.

5 diabetes mellitus are the leading causes of renal disease.

6 We enrolled adults with end-stage renal disease.

7 T2 inhibition in the progression of diabetic renal disease.

8 ients, including patients with non-end-stage renal disease.

9 donors are at an increased risk of end-stage renal disease.

10 underlying pathophysiologic process as their renal disease.

11 nd an increased risk of developing End Stage Renal Disease.

12 dness, Leber congenital amaurosis (LCA), and renal disease.

13 ng causes of death in patients with advanced renal disease.

14 and as a composite endpoint, progression of renal disease.

15 ed kidney cysts and progression to end-stage renal disease.

16 odiamide, should be avoided in patients with renal disease.

17 choice for patients with terminal end-stage renal disease.

18 ron number is implicated in hypertension and renal disease.

19 the utility of this technique for studies of renal disease.

20 proof of causality of these risk alleles for renal disease.

21 dies have focused on patients with end-stage renal disease.

22 diatric chronic kidney disease and end-stage renal disease.

23 autoantibody production, and mild lupus-like renal disease.

24 e basis to evaluate vascular therapeutics in renal disease.

25 e perspective of chronic cardiometabolic and renal disease.

26 cyte biology and a new therapeutic target in renal disease.

27 pidemia, drug dependence or tobacco use, and renal disease.

28 between atrial fibrillation (AF) and chronic renal disease.

29 B7-1, could be a novel therapy for diabetic renal disease.

30 , ICU stay less than 24 hours, and end-stage renal disease.

31 ng progression of the condition to end-stage renal disease.

32 e novo chronic kidney disease, and end-stage renal disease.

33 ety of human diseases, including progressive renal disease.

34 ary disease, peripheral vascular disease, or renal disease.

35 rhythm complexity in patients with end-stage renal disease.

36 henotype of severe retinopathy and end-stage renal disease.

37 tes the development of chronic and end-stage renal disease.

38 ypertension associated with obesity and with renal disease.

39 ferred treatment for patients with end-stage renal disease.

40 hed in many patients with cardiovascular and renal disease.

41 h more patients in the combination group had renal disease.

42 ill enable improvements in MSC therapies for renal disease.

43 st follow-up; no patient developed end-stage renal disease.

44 exudates in center subfield, and absence of renal disease.

45 ts with chronic kidney disease and end-stage renal disease.

46 ation early after the diagnosis of end-stage renal disease.

47 ed hemoglobin A1c, statin use, and end-stage renal disease.

48 n increased risk of posttransplant end-stage renal disease.

49 , self-limiting nephritis to fatal end-stage renal disease.

50 D1 mutations are associated with more severe renal disease.

51 tion, autoantibody formation, and lupus-like renal disease.

52 ependent contributions of these disorders to renal disease.

53 enesis, has been suggested as a biomarker of renal disease.

54 uced risk of future progression to end-stage renal disease.

55 , eGFR decline of 30% or more, and end-stage renal disease.

56 el, end-stage renal disease, or death due to renal disease.

57 kidney disease, eGFR decline, and end-stage renal disease.

58 s) of induction and the role of periostin in renal disease.

59 n is a lifesaving intervention for end-stage renal disease.

60 is is associated with cancer progression and renal disease.

61 L users in order to delay the progression of renal disease.

62 , and metabolic derangements associated with renal disease.

63 , obesity, and a family history of end-stage renal disease.

64 nd endogenous fructose as mediators of acute renal disease.

65 velopment and progression of cardiometabolic/renal disease.

66 l cells will lead progressively to end-stage renal disease.

67 -intensive populations such as patients with renal disease.

68 diagnosis and intervention for patients with renal disease.

69 neither family A nor family B men had overt renal disease.

70 s new drug targets to treat APOL1-associated renal diseases.

71 d with that in controls and nonfibrillary GN renal diseases.

72 s with cardiovascular diseases, diabetes, or renal diseases.

73 ex-specific differences in susceptibility to renal diseases.

74 terest as potential diagnostic biomarkers in renal diseases.

75 rogression of immune- and nonimmune-mediated renal diseases.

76 es of these genes in kidney cell biology and renal diseases.

77 TGF-beta signaling, including biomarkers of renal diseases.

78 t alleles are at elevated risk of developing renal diseases.

79 ant therapeutic applications in inflammatory renal diseases.

80 diabetes mellitus (11.0% versus 17.0%), and renal disease (1.8% versus 5.8%; P<0.01 for all comparis

81 ar filtration rates (Modification of Diet in Renal Disease 4) were significantly higher in the respon

82 nd all-cause mortality (8.7%) than end-stage renal disease (4.0%).

83 lar filtration rate (Modification of Diet in Renal Disease-4) <30 mL/min per 1.73 m), acute rejection

84 Six (0.2%) developed end-stage renal disease 5 to 17 years after donation, (2.7/10 000

85 rtality as well as increased risk of chronic renal disease, a finding that is especially relevant amo

86 required to educate patients with end-stage renal disease about all treatment options, including kid

87 -1.26), and a 98% higher hazard of end-stage renal disease (adjusted hazard ratio = 1.98, 95% CI 1.81

88 morbidity, including continued high rates of renal disease, ageing-related disability, and cancers.

89 Secondary outcomes were end-stage renal disease and acute kidney injury.

90 st a new approach to phosphate management in renal disease and associated mineral disorders.

91 ociated with an increased risk for end-stage renal disease and cardiovascular events.

92 ble and six-variable Modification of Diet in Renal Disease and chronic kidney disease epidemiology wi

93 oke, associations between retinal emboli and renal disease and function remain unclear.

94 (ERalpha)-deficient mice are protected from renal disease and have prolonged survival compared with

95 that mutations of NUP genes cause a distinct renal disease and identify aberrant SMAD signaling as a

96 e from the development of autoantibodies and renal disease and increased the frequency of immunoregul

97 pment and progression of cardiometabolic and renal disease and is associated with increased cardiovas

98 d be aware that GAP can occur without NSF or renal disease and is associated with the use of radiolog

99 c kidney disease, as patients with end-stage renal disease and kidney transplant recipients.

100 candidates to delay progression to end-stage renal disease and limit or abrogate cardiovascular morbi

101 nsformed the life of patients with end-stage renal disease and other chronic kidney disorders by retu

102 -to-microvascular alterations in progressive renal disease and provide a platform that may serve as t

103 al immunoglobulin (MIg) in the occurrence of renal disease and raises the issue of the therapeutic ma

104 teinuria and frequently results in end-stage renal disease and recurrence after kidney transplantatio

105 its in patients with SLE were independent of renal disease and were best detected with SDOCT.

106 the relationship between cardiovascular and renal diseases and the African-American population durin

107 unction (abbreviated modification of diet in renal disease) and chronic graft histopathology (Banff).

108 of renal-replacement therapy, or death from renal disease) and incident albuminuria.

109 atheters, diabetes mellitus, AIDS, end-stage renal disease, and cirrhosis), need for intensive care,

110 nce of diabetes, prior stroke, hypertension, renal disease, and congestive heart failure than white m

111 underlying pathophysiologic process as their renal disease, and neither had vision loss.

112 spect of the care of patients with end-stage renal disease, and phosphate binders are usually needed.

113 phropathy (DN) is a major cause of end-stage renal disease, and therapeutic options for preventing it

114 human nephrogenesis, modeling and diagnosing renal diseases, and drug discovery.

115 involved in the pathogenesis of cardiac and renal diseases, and in the progression of tumour growth

116 ies (cardiovascular, respiratory, liver, and renal diseases, and non-AIDS defining cancers because of

117 , and assess relevant risk factors including renal disease, antiphospholipid antibody, and anti-Ro/SS

118 ts with chronic kidney disease and end-stage renal disease are at 5- to 10-fold higher risk for devel

119 , the mechanisms underlying APOL1-associated renal diseases are unknown.

120 to 4-fold higher in patients with end-stage renal disease as compared with individuals with normal r

121 al fluids, which is upregulated in leukemia, renal diseases as well as in a number of inflammatory ga

122 ely, these data demonstrate that the risk of renal disease associated with APOL1 is probably not rela

123 patients with Bardet-Biedl syndrome-related renal disease attending the United Kingdom national Bard

124 identified all adult patients with end-stage renal disease attributed to 1 of 6 GN subtypes who initi

125 Abnormalities in FH are associated with the renal diseases atypical hemolytic uremic syndrome and de

126 erate personalized in vivo models of genetic renal diseases bearing patient-specific mutations.

127 The number of patients with end-stage renal disease being relisted for a second kidney transpl

128 d with: (1) baseline modification of diet in renal disease (beta = 0.51 +/- 0.05; P < 0.0001); (2) du

129 es of hyperlipidemia, diabetes, smoking, and renal disease but higher Society of Thoracic Surgeons Pr

130 tial therapeutic target for the treatment of renal diseases but also controls the function of other c

131 n is the best treatment option for end-stage renal disease, but allograft loss remains a significant

132 ve births and are a major cause of end-stage renal disease, but their genetic aetiology is not well u

133 D1 and PKD2 populations, men had more severe renal disease, but women had larger liver cyst volumes.

134 Notch3 may be involved in the progression of renal disease by promoting migratory and proinflammatory

135 The complement-mediated renal diseases C3 glomerulopathy (C3G) and atypical hemo

136 Renal disease can also profoundly affect the colonic mic

137 Progression to end-stage renal disease can be slowed by appropriate medical manag

138 However, the progression of renal diseases can be delayed by angiotensin II blockers

139 hropathy responsible for 4%-10% of end-stage renal disease cases.

140 ylation is altered in human and experimental renal diseases characterized by pathologic foot process

141 atients with various comorbidities including renal disease, chronic obstructive pulmonary disease, at

142 itus or peripheral vascular disease, primary renal disease classification, and angiotensin converting

143 hich has been observed in the progression of renal disease, contributes to GN progression.

144 ng adults aged 45-64 years instead, rates of renal disease could persist more than other complication

145 Chronic renal disease (CRD) accelerates the development of ather

146 The autoimmune renal disease deficient for complement factor H-related

147 ecreased autoantibody levels, and attenuated renal disease, despite evidence of concurrently enhanced

148 ched for age, body mass index, hypertension, renal disease, diabetes mellitus, and AS severity.

149 ublic insurance or no insurance at end-stage renal disease diagnosis, more regional acute care hospit

150 ar events or mortality) and renal (end-stage renal disease: dialysis, transplantation, and/or >60% es

151 The combination of cardiac and renal disease driven by metabolic risk factors, referred

152 oncentration and/or progression to end-stage renal disease) during follow-up in both cohorts.

153 recessive mutations in FAT1 cause a distinct renal disease entity in four families with a combination

154 sing the appropriate Modification of Diet in Renal Disease equation depending on the prevailing metho

155 a link between apical polarity proteins and renal diseases, especially renal cyst diseases.

156 accounting for the progression to end-stage renal disease (ESRD) after discharge.

157 Kidney donors can develop end-stage renal disease (ESRD) after donation, but the outcomes of

158 amined the association of incident end-stage renal disease (ESRD) after liver transplantation (LT) an

159 Obesity and end-stage renal disease (ESRD) are on the increase worldwide.

160 editerranean fever (FMF) who reach end-stage renal disease (ESRD) due to reactive amyloidosis A (AA)

161 on between serum 1,5-AG levels and end-stage renal disease (ESRD) from baseline (1990-1992) through 2

162 h the risk of rapid progression to end-stage renal disease (ESRD) in a cohort of proteinuric patients

163 tality, cardiovascular events, and end-stage renal disease (ESRD) in a large cohort of U.S. veterans.

164 rvival advantage for patients with end-stage renal disease (ESRD) over dialysis, regardless of body m

165 with dialysis, nearly one third of end-stage renal disease (ESRD) patients are not educated about kid

166 end-stage liver disease (ESLD) and end-stage renal disease (ESRD) patients awaiting transplant.

167 n of herpes zoster (HZ) vaccine in end-stage renal disease (ESRD) patients might be insufficient, con

168 ncy incidence has been reported in end-stage renal disease (ESRD) patients, especially of female sex.

169 atitis C virus (HCV) infection and end-stage renal disease (ESRD) remains controversial without consi

170 ther groups (P = 0.06) and time to end stage renal disease (ESRD) was longer in this group (P = 0.03)

171 ses of myocardial infarction (MI), end-stage renal disease (ESRD), and non-AIDS-defining cancer (NADC

172 ts with CKD, especially those with end-stage renal disease (ESRD), are controversial.

173 f black race, are at high-risk for end-stage renal disease (ESRD), but contributing factors are evolv

174 Outcomes included progression to end stage renal disease (ESRD), length of stay, and mortality.

175 ship of BMI with macroalbuminuria, end-stage renal disease (ESRD), or DKD defined as presence of macr

176 ease that is an important cause of end-stage renal disease (ESRD), which requires transplantation or

177 virus (HIV)-infected patients with end-stage renal disease (ESRD).

178 om chronic kidney disease (CKD) to end-stage renal disease (ESRD).

179 KI or impede progression to CKD or end-stage renal disease (ESRD).

180 ng for individual risk factors for end-stage renal disease (ESRD).

181 and one-third of patients develop end-stage renal disease (ESRD).

182 omy increases the risk of eventual end-stage renal disease (ESRD).

183 h chronic kidney disease (CKD) and end-stage renal disease (ESRD).

184 was associated with development of end-stage renal disease (ESRD).

185 n increased risk of progression to end-stage renal disease (ESRD).

186 , major cardiovascular outcome-and end-stage renal disease [ESRD], doubling of serum creatinine, and

187 function (defined as Modification of Diet in Renal Disease-estimated glomerular filtration rate <60 m

188 Galectin-3 has been linked to incident renal disease, experimental renal fibrosis, and nephropa

189 , preferably, or the Modification of Diet in Renal Disease formula should be used for the evaluation

190 calculated using the Modification of Diet in Renal Disease formula.

191 r application of the Modification of Diet in Renal Disease formula.

192 x- and four-variable Modification of Diet in Renal Disease formulas were available from a subset (n =

193 Children with renal disease had highly variable and often markedly ske

194 nstrate that hURECs from a JBTS patient with renal disease have elongated and disorganized primary ci

195 In conclusion, children with renal disease have exceptional heterogeneity in the T ce

196 usion, although many patients with end stage renal disease have received transplants through the paid

197 , once believed to be safe for patients with renal disease, have been strongly associated with nephro

198 ated with greater frequency in patients with renal disease, heart failure, and with use of certain me

199 cipients' age, cause and length of end-stage renal disease, hemoglobin, albumin, selected comorbiditi

200 fection is common in patients with end-stage renal disease, highly efficacious, well-tolerated, direc

201 t predictors of MACE were cardiogenic shock, renal disease, history of peripheral vascular disease, m

202 sex (HR, 1.21; 95% CI, 1.12-1.31), end-stage renal disease (HR, 1.66; 95% CI, 1.41-1.95), severe chro

203 lso associated with development of end-stage renal disease (HR, 2.40; 95% CI, 0.76-7.58) and acute ki

204 llow-up of donors has demonstrated end-stage renal disease in 0.6% at 25 years.

205 ition that leads to impairment and end-stage renal disease in 20-40% of patients within 10-20 years.

206 t Ab-mediated inflammatory kidney injury and renal disease in a mouse nephrotoxic serum nephritis mod

207 of the Fn14 receptor significantly improves renal disease in a spontaneous lupus nephritis model thr

208 ibition with rapamycin partially ameliorated renal disease in B6.Pdss2(kd/kd) mice with complexes I-I

209 the largest reported cohort of patients with renal disease in Bardet-Biedl syndrome and identifies ri

210 itute the most important cause for end-stage renal disease in children and adolescents.

211 longer survival, the prevalence of end-stage renal disease in HIV is increasing.

212 ted expression of APOL1-G1 could precipitate renal disease in humans.

213 stem (RAS) blockade, can slow progression of renal disease in patients with type 2 diabetes and stage

214 Current biomarkers of renal disease in systemic vasculitis lack predictive val

215 n the aHUS cohort and, vice versa, a lack of renal disease in the AMD cohort.

216 We localized the main drivers of renal disease in the DiGeorge syndrome to a 370-kb regio

217 he most common cause of hereditary end-stage renal disease in the first three decades of life.

218 All patients with end-stage renal disease in the United States without prior renal r

219 tive analysis of all patients with end-stage renal disease in the US Renal Data System who initiated

220 Surprisingly, renal disease in this model is complement and FcR indepe

221 osuppressive therapy, persons with end-stage renal disease (including hemodialysis patients), blood a

222 adults with chronic liver disease, end-stage renal disease (including hemodialysis patients), or HIV

223 ement regulatory proteins can lead to severe renal diseases, including atypical hemolytic uremic synd

224 n has a beneficial effect in early stages of renal disease induced by 3dUUO.

225 lysis via fistula in patients with end-stage renal disease irrespective of race/ethnicity.

226 Because the role of biTregs in inflammatory renal disease is also unknown, we studied these cells in

227 bility of T cell maturation in children with renal disease is available.

228 Renal disease is growing in prevalence and has striking

229 ic kidney disease progression, and end-stage renal disease is not clear.

230 Renal disease is prevented in both active and passive im

231 biomarker for patients having or at risk for renal disease, is described in this work.

232 n, especially its association with end-stage renal disease, may be less than many have surmised.

233 We assessed the Modification of Diet in Renal Disease (MDRD) performance to predict serum creati

234 nsion (AASK) and 761 Modification of Diet in Renal Disease (MDRD) Trial participants previously rando

235 participants in the Modification of Diet in Renal Disease (MDRD) trial.

236 as eGFR based on the Modification of Diet in Renal Disease (MDRD4) Study and the chronic kidney disea

237 ticular, administration of Bis-T-23 in these renal disease models restored the normal ultrastructure

238 proven to have protective effects in several renal disease models.

239 For the risk of progression of renal disease, no significant differences were detected

240 ations, otherwise known as nail patella-like renal disease (NPLRD).

241 d spectrum of BBS phenotypes spans diabetes, renal disease, obesity, sleep apnea, cardiovascular dise

242 A 74-year-old woman with end-stage renal disease on maintenance hemodialysis presented to t

243 tors of any GDMT included absence of chronic renal disease or nonsustained ventricular tachycardia, l

244 onephrosis (hereafter called acetate-induced renal disease, or C2RD).

245 ing of the serum creatinine level, end-stage renal disease, or death due to renal disease.

246 , such as those with cardiovascular disease, renal disease, or diabetes.

247 all enrolled patients had vascular disease, renal disease, or diabetes.

248 ined doubling of serum creatinine, end-stage renal disease, or renal death.

249 Other major factors are concomitant renal disease, or use of tamoxifen.

250 with glimepiride, slowed the progression of renal disease over 2 years in patients with type 2 diabe

251 Medicare-linked data on waitlisted end-stage renal disease patients between 2005 and 2009 with contin

252 Sixty-seven consecutive end-stage renal disease patients underwent live-donor robotic KT a

253 used in chronic kidney disease and end-stage renal disease patients with hyperphosphatemia.

254 tation is an attractive option for end-stage renal disease patients with type 1 diabetes.

255 iving-donor kidney transplants for end-stage renal disease patients with willing but incompatible liv

256 entering dialysis program: age, sex, primary renal disease, period of dialysis onset, and cardiovascu

257 During the end-stage renal disease phase at the time of transplant, cinacalce

258 End-stage renal disease (PR = 1.41; 95% CI: 1.21-1.63; P = 0.001),

259 hanisms should reveal options for preventing renal disease progression after AKI.

260 er elevated suPAR levels are associated with renal disease progression in children with CKD.

261 est absolute excess risks of death were from renal disease (rate ratio, 20.1; 95% CI, 17.2 to 23.4),

262 oordination strategies for all patients with renal disease, realign incentives for all clinical stake

263 plant recipients with aHUS-related end-stage renal disease received eculizumab: 10 from day 0 and 2 a

264 Renal disease recurrence was scored using the histopatho

265 ng the biologic outcomes on the evolution of renal disease remain mostly unknown.

266 hypoxia in the initiation and progression of renal disease remains rudimentary.

267 c kidney disease, and some develop end-stage renal disease, requiring renal replacement therapy.

268 A 50-year-old woman with end-stage renal disease secondary to autosomal dominant polycystic

269 In HNF1B patients who reach end-stage renal disease, single kidney transplantation (SKT) or co

270 d in a striking acceleration in the onset of renal disease, SLO germinal center formation, and autore

271 ents with both type 1 diabetes and end-stage renal disease, SPK recipients had similar progression of

272 estimated using the Modification of Diet in Renal Disease study (MDRD) equation for recruitment (but

273 hythmic and Cardiovascular Risk in End Stage Renal Disease Study.

274 Further adjustment for hepatitis C, renal disease, substance abuse, and hemoglobin level (HR

275 of all patients who underwent CEA in the US Renal Disease System-Medicare-matched database between J

276 jection, Cyp4a14KO male mice developed worse renal disease than streptozotocin-treated wild-type mice

277 at higher risk for progression to end-stage renal disease than those who have chronic kidney disease

278 physiological responses within pulmonary and renal diseases that are still poorly controlled by curre

279 AKUT as a feature (syndromic CAKUT) or cause renal diseases that may manifest as phenocopies of CAKUT

280 In patients with end-stage renal disease, the prevalence of acquired risk factors f

281 than 65 years of age), such as in end-stage renal disease, this therapy has not been optimized for o

282 The median time from diagnosis of renal disease to referral was 60 months (range, 2-444 mo

283 In most patients who develop end-stage renal disease, transplantation is the renal replacement

284 ngoing Time to Reduce Mortality in End Stage Renal Disease Trial, a large cluster-randomized, pragmat

285 ryoglobulinemia, chronic kidney or end-stage renal disease, type 2 diabetes, B-cell lymphoma, lichen

286 Patients with end-stage renal disease use the emergency department (ED) at a 6-f

287 es mellitus, previous myocardial infarction, renal disease, ventilatory support, use of circulatory s

288 An increased risk of end-stage renal disease was associated with an IQR increase in con

289 In children, renal disease was often detected within the first year o

290 At diagnosis, renal disease was severe, with nephrotic-range proteinur

291 However, compared with placebo, end-stage renal disease was significantly less likely after dual t

292 rious associations of lymphangiogenesis with renal disease, we here tested the hypothesis that VitD h

293 (doubling of serum creatinine and end-stage renal disease) when used as an adjunct to angiotensin-co

294 free and antibiotic-treated mice ameliorated renal disease, whereas expansion of these cells upon Cit

295 agonist anti-Ox40 mAbs potently exacerbated renal disease, which was accompanied by activation of ki

296 For patients with end-stage renal disease who are not candidates for fistula, dialys

297 that morbidly obese patients with end-stage renal disease who undergo LSG to improve transplant cand

298 mic fibrosis (NSF) in the setting of chronic renal disease with associated gadolinium exposure.

299 ese key players mediating the comorbidity of renal disease with body composition and obesity.

300 ropathy (DN) is the major cause of end-stage renal disease worldwide.