ライフサイエンスコーパス: kidney dysfunction

1 rities in metformin prescription in moderate kidney dysfunction.

2 IgR was recently shown to be associated with kidney dysfunction.

3 F508 homozygous patients do not present with kidney dysfunction.

4 ions in CFTR result in little or no apparent kidney dysfunction.

5 n E (apoE) might independently contribute to kidney dysfunction.

6 tein expression to resolve ageing-associated kidney dysfunction.

7 zed by fluid retention, pulmonary edema, and kidney dysfunction.

8 ) were the primary outcomes as indicators of kidney dysfunction.

9 eatinine ratio indicated potential liver and kidney dysfunction.

10 nts who survived, 262 (43.6%) had persistent kidney dysfunction.

11 n studied in a large sample with and without kidney dysfunction.

12 al procedures at risk for AKI and persistent kidney dysfunction.

13 reate a self-perpetuating cycle of heart and kidney dysfunction.

14 so most research has focused on remedies for kidney dysfunction.

15 ch therapies would not be contraindicated by kidney dysfunction.

16 s, few validated biomarkers exist to predict kidney dysfunction.

17 inflammation, and cyst formation, leading to kidney dysfunction.

18 ic knockout of GRK4 decreased injury-induced kidney dysfunction.

19 transplantation-associated post-IRI chronic kidney dysfunction.

20 ecedes nephron loss, fibrosis, and long-term kidney dysfunction.

21 phils from healthy subjects or patients with kidney dysfunction.

22 we characterize a mechanism of tumor-induced kidney dysfunction.

23 on, DNA damage response, tubular damage, and kidney dysfunction.

24 mice also show symptoms of more generalized kidney dysfunction.

25 n critically ill patients is associated with kidney dysfunction.

26 embolism, serious infections and progressive kidney dysfunction.

27 notypes associated with liver, skeletal, and kidney dysfunction.

28 n injury (IRI) can lead to acute and chronic kidney dysfunction.

29 uld slow the progression to higher stages of kidney dysfunction.

30 y be at increased risk for treatment-related kidney dysfunction.

31 fset by greater neurohormonal activation and kidney dysfunction.

32 oral anticoagulants (DOACs) in patients with kidney dysfunction.

33 rd-dose DOACs over warfarin in patients with kidney dysfunction.

34 in patients hospitalized for HF by degree of kidney dysfunction.

35 d ejection fraction experiencing significant kidney dysfunction.

36 ction in glomerular hyperfiltration-mediated kidney dysfunction.

37 oth acute kidney injury (AKI) and persistent kidney dysfunction.

38 litus or hypertension and varying degrees of kidney dysfunction.

39 hocytes in the skin and blood, and liver and kidney dysfunction.

40 rdial edema, phenotypes typically induced by kidney dysfunction.

41 200 mg/m(2), with dose reduction for severe kidney dysfunction.

42 of increased serum retinol in the context of kidney dysfunction.

43 o identify inflammatory processes related to kidney dysfunction.

44 atterning and neonatal death consistent with kidney dysfunction.

45 A miRNA panel was associated with human kidney dysfunction.

46 and venous thromboembolism in patients with kidney dysfunction.

47 and 85 (9.0%) had both retinopathy and early kidney dysfunction.

48 deposition but neither mesangial injury nor kidney dysfunction.

49 mputation, was 14.1% (n = 118) in those with kidney dysfunction, 13.5% (n = 67) in those with heart f

50 is-prone (6%) with the highest proportion of kidney dysfunction (30%) and urinary ketones (6%).

51 ated, 5%) showing the highest proportions of kidney dysfunction (40%) and peripheral artery disease (

52 oporosis, 9.6% [95% CI, 8.0%-11.5%]), renal (kidney dysfunction, 5.0% [95% CI, 4.0%-6.3%]), and hemat

53 ut retain NK cells, showed similar levels of kidney dysfunction 65 days after transplantation (creati

54 107 [31.9%]; OR, 1.54 [95% CI, 1.10-2.16]), kidney dysfunction (87 [34.1%] vs 80 [23.9%]; OR, 1.65 [

55 fied renal failure and reported disorders of kidney dysfunction after adjustment for biological donor

56 ced MRA after a nondiagnostic ultrasound for kidney dysfunction after transplantation.

57 ccinylacetone which induces severe liver and kidney dysfunction along with mutagenic changes and hepa

58 sent in treated HIV infection contributes to kidney dysfunction among HIV-infected men receiving high

59 glomerular filtration rate in assessment of kidney dysfunction among those with ESLD.

60 erved higher incidence and relative rate for kidney dysfunction among treated patients, compared with

61 optosis in acute folate nephropathy and less kidney dysfunction and a lower mortality rate in cisplat

62 Although kidney dysfunction and abnormalities in serum electrolyt

63 to cryptic antigens as novel accelerators of kidney dysfunction and acute or chronic allograft reject

64 iency of either PD-1 ligand also exacerbated kidney dysfunction and acute tubular necrosis after subt

65 ll overexpression of SMN reduced I/R-induced kidney dysfunction and attenuated AKI-to-CKD transition,

66 tients with ESRD, cancer risk is affected by kidney dysfunction and by immunosuppression after transp

67 ain the association between mild to moderate kidney dysfunction and cardiovascular mortality.

68 Early kidney dysfunction and clinical pancreatitis were higher

69 inflammatory markers while decreasing early kidney dysfunction and clinical posttransplant pancreati

70 ular difficulty grasping the significance of kidney dysfunction and connecting this to the symptoms t

71 ers have modified our understanding of acute kidney dysfunction and damage, and their association wit

72 which collectively contribute to age-related kidney dysfunction and disease.

73 s a microvascular complication that leads to kidney dysfunction and ESRD, but the underlying mechanis

74 eruli within 4 days, leading to irreversible kidney dysfunction and failure to thrive.

75 n in 5/6 nephrectomy mice while exacerbating kidney dysfunction and fibrosis.

76 Loss of GRK4 in embryonic zebrafish causes kidney dysfunction and glomerular cysts.

77 Kidney dysfunction and high C-reactive protein (CRP) lev

78 type mice, marked by aggravated proteinuria, kidney dysfunction and histologic lesions.

79 omalizumab, but has adverse effects such as kidney dysfunction and hypertension.

80 Survivors have a greater risk for kidney dysfunction and hypertension.

81 e data indicate strong short-term effects of kidney dysfunction and immunosuppression on cancer incid

82 Knowledge of the relationship between kidney dysfunction and impaired cognition may improve ou

83 Kidney dysfunction and inflammation commonly accompany T

84 or a zoonotic disease known to induce severe kidney dysfunction and inflammation.

85 o offer a new pathway to noninvasively image kidney dysfunction and local injuries at the anatomical

86 Little is known about the association of kidney dysfunction and outcome in acute severe hypertens

87 ice treated with IL-33 developed more severe kidney dysfunction and proteinuria, glomerular sclerosis

88 Identifying early biomarkers of kidney dysfunction and refining assessment methods in th

89 endent association has been observed between kidney dysfunction and the risk of hearing loss, the und

90 ow that Kim-1-deficient mice had more severe kidney dysfunction and tissue damage after bilateral ren

91 systems as a noninvasive means of monitoring kidney dysfunction and treatment.

92 heir TCR repertoire, have significantly less kidney dysfunction and tubular injury after renal IRI co

93 need to understand how brain death leads to kidney dysfunction and, hence, how this can be prevented

94 enal infiltration, (c) reduced the extent of kidney dysfunction, and (d) attenuated proximal tubule d

95 ower body mass index, older age, female sex, kidney dysfunction, and AF rhythm.

96 e, would reduce the incidences of infection, kidney dysfunction, and death is unknown.

97 risk stratification, identification of early kidney dysfunction, and development of interventions to

98 ansplantation, which attenuated proteinuria, kidney dysfunction, and fibrosis compared with control s

99 ailure Assessment, dietary protein [g/kg/d], kidney dysfunction, and glutamine-randomization).

100 KI is characterized by abrupt and reversible kidney dysfunction, and incomplete recovery leads to chr

101 y vasculopathy, lymphoproliferative disease, kidney dysfunction, and infection, each as an ordinal sc

102 in markedly aggravated cyst growth, worsened kidney dysfunction, and shortened life span.

103 became hypertensive, a known risk factor for kidney dysfunction, and showed decreased glomerular filt

104 sozymes and they exhibit low blood pressure, kidney dysfunctions, and male infertility.

105 chanisms involving PRR activity and diabetic kidney dysfunction are unknown.

106 nuria, glomerular injury, podocyte loss, and kidney dysfunction as compared to the mice with diabetes

107 This includes kidney dysfunction as the embryonic kidney (pronephros)

108 present a machine learning model to predict kidney dysfunction, as a proxy for drug induced renal to

109 Kidney dysfunction, as assessed by cystatin C, is associ

110 is, acute hypertension, vascular injury, and kidney dysfunction associated with pathophysiology drive

111 3.18 x 10(-7)) and of experiencing resolving kidney dysfunction at 1 year were 13x higher (P = 2.15 x

112 uptake, target cancerous tissues, and report kidney dysfunction at early stages.

113 79 years) and the prevalence of preadmission kidney dysfunction (baseline eGFR <60 ml/min per 1.73 m(

114 olipids, Krebs and urea cycles, and revealed kidney dysfunction biomarkers.

115 e patients may have reversible components of kidney dysfunction, both HF and renal parameters improvi

116 ampsia is multifactorial, including not only kidney dysfunction but also endothelial dysfunction, as

117 th diabetes typically occurs due to signs of kidney dysfunction but sometimes is due to less serious

118 in forms of immunodeficiency, for example in kidney dysfunction, but may enhance sterile forms of inf

119 e antiretroviral therapy, is associated with kidney dysfunction, but the magnitude of the effect and

120 Tenofovir exposure increased the risk of kidney dysfunction by 63% (HR, 1.63; 95% confidence inte

121 0/yr) was strongly associated with prevalent kidney dysfunction by cystatin C >1.29 g/dl (adjusted OR

122 In unadjusted analysis, kidney dysfunction by either measure was strongly associ

123 Kidney dysfunction can also alter the pharmacokinetics a

124 survive for more than 5 years, time in which kidney dysfunction can develop or progress.

125 nsated heart failure (ADHF), the presence of kidney dysfunction can substantially shape prognosis and

126 Kidney dysfunction causes a myriad of adverse influences

127 scular complications makes the management of kidney dysfunction challenging in these patients.

128 may partially explain their higher burden of kidney dysfunction compared with uninfected men.

129 jury markers, reduced apoptosis and improved kidney dysfunction, concomitant with mitigated histologi

130 Progressive kidney dysfunction defined as a sustained 30% or more de

131 ios (OR) for the association between TDF and kidney dysfunction (defined as eGFR <90 mL/min/1.73 m(2)

132 and eGFR were influenced by the severity of kidney dysfunction: DEHP and BBzP exposure showed negati

133 stage heart failure patients with concurrent kidney dysfunction despite limited evidence supporting i

134 We also compared the risk of persistent kidney dysfunction, dialysis dependence, or death at 60

135 scores, incidence of jaw osteonecrosis, and kidney dysfunction did not differ significantly between

136 ad to hepatorenal syndrome, a severe type of kidney dysfunction driven by circulatory disturbances an

137 ed kidney allografts with various degrees of kidney dysfunction during heart transplantation.

138 blood cells and schistocytes) and transplant kidney dysfunction during the first 2 weeks after transp

139 Finally, 47 of 131 patients experienced kidney dysfunction during the median 15-year follow-up p

140 h eGFR only among the patients with moderate kidney dysfunction (eGFR 30-59 mL/min/1.73 m(2)).

141 addition to elevations in serum creatinine, kidney dysfunction encompasses inadequate maintenance of

142 for kidney replacement therapy or persistent kidney dysfunction, endotracheal intubation, mechanical

143 ntified hundreds of genetic risk regions for kidney dysfunction [estimated glomerular filtration rate

144 HD), periventricular leukomalacia (PVL), and kidney dysfunction; Fer-1 inhibited lipid peroxidation,

145 e toxic gain-of-function variants that cause kidney dysfunction, following a recessive mode of inheri

146 the association with risk of progression to kidney dysfunction from the time of measurement through

147 3(hu/hu) mice display elevated biomarkers of kidney dysfunction, glomerulosclerosis, C3/C5b-9 deposit

148 0 (death, dialysis dependence, or persistent kidney dysfunction [>25% decline in estimated glomerular

149 Yet among patients with advanced kidney dysfunction, guidelines recommend dietary potassi

150 Kidney dysfunction (hazard ratio, 2.28 [95% credible int

151 ently or recently hospitalized with ADHF and kidney dysfunction highlight the importance of improving

152 plant or altered in response to detection of kidney dysfunction, histologic evidence of allograft dam

153 (HR, 1.02; 95% CI, 1.00-1.04; P = .04), and kidney dysfunction (HR, 3.58; 95% CI, 1.35-9.46; P = .01

154 ide (NR) prevented several manifestations of kidney dysfunction (i.e., albuminuria, increased urinary

155 sociation between long-term TDF exposure and kidney dysfunction in a cohort of 1043 human immunodefic

156 vascular hemodynamics recovery, and limiting kidney dysfunction in a vasopressinergic-dependent manne

157 Whether treatment with pravastatin mitigates kidney dysfunction in adult patients with early autosoma

158 ting factors and mechanisms underlying brain-kidney dysfunction in CKD remain poorly understood.

159 nduced by hyperglycemia is the main cause of kidney dysfunction in diabetic nephropathy.

160 entional biomarkers in indicating hepatic or kidney dysfunction in different animal models.

161 osis is an important mediator of progressive kidney dysfunction in DN.

162 Rather, kidney dysfunction in elderly African Americans seems mo

163 This study aimed to assess kidney dysfunction in general surgical patients and exam

164 (BUN) are the primary options for monitoring kidney dysfunction in humans.

165 osuppressant-related factors associated with kidney dysfunction in islet transplant recipients.

166 eNOS deficiency on BP, atherosclerosis, and kidney dysfunction in nnee mice.

167 Early identification of kidney dysfunction in patients with advanced heart failu

168 g recognition of the incidence and impact of kidney dysfunction in recipients of nonrenal solid organ

169 e activation of AMPK to a potential risk for kidney dysfunction in the context of an HFD.

170 ability to determine the actual incidence of kidney dysfunction in the health centers as it was not f

171 Complications of kidney dysfunction include hyperkalemia and metabolic ac

172 s. 4.5 0.5; P < 0.01 vs. low risk) and early kidney dysfunction, including ~8.3 mL/min/1.73 m(2) high

173 ent aly/aly (MAP3K14(aly/aly)) mice had less kidney dysfunction, inflammation, and apoptosis in acute

174 This condition is characterized by kidney dysfunction, inflammation, lipotoxicity, and fibr

175 Kidney dysfunction is a major cause of mortality, but it

176 In conclusion, kidney dysfunction is associated with an increased odds

177 terioration of kidney function or persistent kidney dysfunction is associated with an irreversible lo

178 Kidney dysfunction is associated with bone loss, and pat

179 patients with ESRD, but whether less severe kidney dysfunction is associated with CAC is uncertain.

180 Whether kidney dysfunction is associated with coronary artery ca

181 Whether early kidney dysfunction is associated with small and large ar

182 This study sought to evaluate whether kidney dysfunction is associated with the development of

183 The aim of this study was to examine whether kidney dysfunction is associated with the type of clinic

184 Chronic kidney dysfunction is associated with worse outcomes, bu

185 readily differentiate between the stages of kidney dysfunction is highly desired for improving our f

186 Kidney dysfunction is known to decrease life expectancy

187 Metabolic residue accumulation during kidney dysfunction is known to determine cardiovascular

188 The development of kidney dysfunction is one of the most important after li

189 Significant kidney dysfunction is particularly frequent in patients

190 er from kidney disease, yet the mechanism of kidney dysfunction is poorly understood.

191 nal syndrome as the sole primary etiology of kidney dysfunction is predictive of improvement.

192 Early kidney dysfunction is significantly associated with decr

193 ile chronic kidney disease, due to bilateral kidney dysfunction, is associated with insulin resistanc

194 taracts and glaucoma, mental retardation and kidney dysfunction, is caused by mutations in the OCRL g

195 Kidney dysfunction leads to significant morbidity and mo

196 In rats with HS, RvD1 attenuated the kidney dysfunction, liver injury, and tissue ischemia.

197 sy for cause (n = 58) or without evidence of kidney dysfunction (n = 28).

198 opsy for cause (n=58) or without evidence of kidney dysfunction (n=28).

199 injury (IRI) as assessed by tubular injury, kidney dysfunction, necrosis, apoptosis and inflammatory

200 Studies reporting health assessments, kidney dysfunction, neurological disorders and symptoms,

201 and many disease states, including liver and kidney dysfunction, neurological disorders, and cancer.

202 vents (MAKE30)-a composite of new persistent kidney dysfunction, new initiation of dialysis, and deat

203 Persistent kidney dysfunction occurred in 57 of the 458 patients (1

204 Kidney dysfunction often leads to reluctance to start or

205 ysis to show that genetic variants linked to kidney dysfunction on chromosome 20 target the acyl-CoA

206 health care, but the effects of less severe kidney dysfunction on these outcomes are less well defin

207 s of retinopathy only, 250 (26.5%) had early kidney dysfunction only, and 85 (9.0%) had both retinopa

208 Kidney dysfunction or damage can occur over a longer per

209 can ancestral group were not associated with kidney dysfunction or kidney disease progression.

210 >1000 muM in serum during renal, thyroid and kidney dysfunction or muscle disorder.

211 uartile vs the remaining 3 quartiles), early kidney dysfunction (OR 1.56, 95% CI 1.06-2.28, per stand

212 I, 0.76-1.01), with a decrease in persistent kidney dysfunction (OR, 0.80; 95% CI, 0.69-0.93) and mor

213 mposite primary end point was new infection, kidney dysfunction, or death between days 3 and 15 after

214 The proportion of female sex (P = .009), kidney dysfunction (P = .001), cardiac diseases (P = .00

215 -day follow-up in the outcomes of persistent kidney dysfunction (P = .08), new dialysis dependence (P

216 the longitudinal, noninvasive monitoring of kidney dysfunction progression in preclinical research.

217 ther neutrophils or serum from patients with kidney dysfunction-related HU with or without UA depleti

218 e; however, the molecular mechanisms driving kidney dysfunction remain poorly understood.

219 gold nanoparticles, can noninvasively detect kidney dysfunction, report on the dysfunctional stages,

220 ver, the prognostic biomarker used to report kidney dysfunction (serum creatinine concentration) has

221 um UA of 9-12 mg/dL) related or unrelated to kidney dysfunction significantly diminished neutrophil a

222 ity), incidence of osteonecrosis of the jaw, kidney dysfunction, skeletal morbidity rate (mean number

223 0.80-1.18) and did not significantly vary by kidney dysfunction stage for either of these primary end

224 ction on a protocol biopsy in the absence of kidney dysfunction, subclinical rejection has garnered a

225 AMCKD was characterized by vascular and kidney dysfunction, TGF beta -dependent glomeruloscleros

226 Hepatorenal syndrome (HRS) is a form of kidney dysfunction that characteristically occurs in liv

227 CD2AP is important in kidney dysfunction that is accompanied by inflammation.

228 C seems to identify a "preclinical" state of kidney dysfunction that is not detected with serum creat

229 e newer targeted therapeutics can also cause kidney dysfunction through on and off-target mechanisms.

230 These patients are at risk for kidney dysfunction through the continuum of care for ESL

231 clinical management of patients experiencing kidney dysfunction through the trajectory of advanced he

232 l trials in patients with moderate-to-severe kidney dysfunction to further refine their optimal manag

233 Those with a history of kidney dysfunction, tobacco abuse, and higher ejection f

234 trial, we assigned 11,182 patients with the kidney-dysfunction triad who were being treated at 141 p

235 ease, type 2 diabetes, and hypertension (the kidney-dysfunction triad), the results of large-scale tr

236 y preserved mitochondria but also attenuated kidney dysfunction, tubular damage, interstitial fibrosi

237 was a significant linear interaction between kidney dysfunction type and MELD-Na score.

238 investigated the impact of the inclusion of kidney dysfunction type on the discrimination and calibr

239 In the derivation cohort, kidney dysfunction type was significantly associated wit

240 We defined kidney dysfunction types as follows: acute kidney diseas

241 ty and the potential for objectively defined kidney dysfunction types to enhance the prognostication

242 both severity and recovery of postoperative kidney dysfunction using the pattern of longitudinal cha

243 nal syndrome as the sole primary etiology of kidney dysfunction was 100% specific for native kidney e

244 Kidney dysfunction was a potent predictor of 1-year mort

245 qualitative study of patients with ADHF and kidney dysfunction was conducted at 3 hospitals within a

246 mild nonproliferative retinopathy) and early kidney dysfunction was defined as AER >/=7.5 mug/min.

247 Persistent kidney dysfunction was defined as persistent estimated g

248 he overall incidence and rate of progressive kidney dysfunction was higher in the treated cohort than

249 Their associations with kidney dysfunction were also investigated.

250 Rates of kidney dysfunction were higher among patients treated wi

251 eutic agents are nephrotoxic and can promote kidney dysfunction, which frequently manifests during th

252 ystem and contributing to the progression of kidney dysfunction, which in its turn influences the gut

253 IL11 in TECs leading to SNAI1 expression and kidney dysfunction, which is not seen in Il11 deleted mi

254 d heart failure (HF) often have accompanying kidney dysfunction, which was recently defined as cardio

255 rm mortality was compared in recipients with kidney dysfunction who underwent heart-kidney transplant

256 orage disorder 1b characterized by liver and kidney dysfunction with neutropenia.

257 tual framework for appropriate evaluation of kidney dysfunction within the context of clinical trajec