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1 th chronic inflammation, including anemia of chronic kidney disease.
2 ibrosis in tissue samples from patients with chronic kidney disease.
3 ne and in human donors of kidney tissue with chronic kidney disease.
4 , increasing age, diabetes, hypertension and chronic kidney disease.
5 naemia and states of FGF23 excess, including chronic kidney disease.
6 n obesity and rheumatoid arthritis, and 2 on chronic kidney disease.
7 sed to diagnose and classify the severity of chronic kidney disease.
8 ith acute kidney injury or those at risk for chronic kidney disease.
9 associated with multiple diseases, including chronic kidney disease.
10 te levels are associated with progression of chronic kidney disease.
11 ce interval: 1.16, 1.74) among patients with chronic kidney disease.
12 ation is essential to prevent progression to chronic kidney disease.
13 erm profibrotic responses that could lead to chronic kidney disease.
14 isk of renal events than in patients without chronic kidney disease.
15 nephropathy has altered the epidemiology of chronic kidney disease.
16 in modulating pruritus in conditions such as chronic kidney disease.
17 ease, stroke, peripheral artery disease, and chronic kidney disease.
18 incomplete or maladaptive kidney repair and chronic kidney disease.
19 ular and total mortality, and progression of chronic kidney disease.
20 er renal IRI, thus preventing progression to chronic kidney disease.
21 nting for ~5% of monogenic disorders causing chronic kidney disease.
22 ed numbers of patients with high CV risk and chronic kidney disease.
23 or follow AKI in a continuum with acute and chronic kidney disease.
24 ment for metabolic acidosis in patients with chronic kidney disease.
25 ndrial energy metabolism may be causative to chronic kidney disease.
26 with type 2 diabetes and moderate-to-severe chronic kidney disease.
27 ut prior heart failure or moderate to severe chronic kidney disease.
28 t baseline was a better predictor of time to chronic kidney disease.
29 glomerular filtration rate in patients with chronic kidney disease.
30 ll-known clinical biomarker for the onset of chronic kidney disease.
31 d predicts accelerated functional decline in chronic kidney disease.
32 hypertension, type 2 diabetes mellitus, and chronic kidney disease.
33 s in two cohorts totaling 3315 patients with chronic kidney disease.
34 tage kidney disease, even at early stages of chronic kidney disease.
35 mediated by the known APOL1 association with chronic kidney disease.
36 which serves as a critical factor leading to chronic kidney disease.
37 on, treatment with ferric carboxymaltose and chronic kidney disease.
38 ncreased risk of developing hypertension and chronic kidney disease.
39 have routinely excluded those with advanced chronic kidney disease.
40 key biomarker for cardiovascular disease and chronic kidney disease.
41 population with type 2 diabetes and advanced chronic kidney disease.
42 ve therapies for the management of acute and chronic kidney disease.
43 diagnosis and prognostication for acute and chronic kidney diseases.
44 ns, sepsis, and ischemia/reperfusion, and in chronic kidney diseases.
45 eir damage contributes to the progression of chronic kidney diseases.
46 ase (1.3 [1.3-1.4]), stroke (2.2 [2.1-2.2]), chronic kidney disease (1.7 [1.7-1.8]), and peripheral a
47 emia (72.1%), diabetes mellitus (31.6%), and chronic kidney disease (28.2%); 20.2% received warfarin
48 disease, 12.8% (n=59), cancer, 11.7% (n=54), chronic kidney disease, 3.9% (n=18) and inflammatory bow
49 disease 1.6 (1.5-1.7), stroke 6.4 (6.3-6.5), chronic kidney disease 4.4 (4.3-4.6), and peripheral art
50 le on-switches in gene therapy for anemia of chronic kidney disease(6), we demonstrated regulated exp
55 e, moderate or severe ischemia, and advanced chronic kidney disease (an estimated glomerular filtrati
58 ture mortality from substance use disorders, chronic kidney disease and acute glomerulonephritis, and
59 Albuminuria acts as a marker of progressive chronic kidney disease and as an indicator for initiatio
61 ract (CAKUTs) represent the leading cause of chronic kidney disease and end-stage kidney disease in c
62 requently reported in patients with advanced chronic kidney disease and is associated with early allo
63 ments are determined in patients with stable chronic kidney disease and may not translate to patients
64 hypertension, obesity, diabetes mellitus and chronic kidney disease and might contribute to disease b
65 e randomly assigned adults with stage 3 or 4 chronic kidney disease and no history of gout who had a
68 and cardiovascular outcomes in patients with chronic kidney disease and type 2 diabetes with optimize
70 weight, the risk of developing or worsening chronic kidney disease and/or atherosclerotic cardiovasc
71 ardiovascular disease (CVD) in patients with chronic kidney diseases and rheumatologic disorders.
72 athies, obesity, hypertension, diabetes, and chronic kidney disease) and yielded additional insights
73 stolic hypertension, -10.1 +/- 20.3 mm Hg in chronic kidney disease, and -10.0 +/- 19.1 mm Hg in atri
74 = 1.2-2.1 for >80 g/day), as were diabetes, chronic kidney disease, and end-stage liver disease (HR
75 ion such as in those with diabetes mellitus, chronic kidney disease, and high risk of future atherosc
77 ients with stable coronary disease, advanced chronic kidney disease, and moderate or severe ischemia,
78 ion in the general population, patients with chronic kidney disease, and patients with heart failure.
81 ociated with PH among patients with advanced chronic kidney disease appears to differ by etiology.
82 rbid conditions, including heart failure and chronic kidney disease, are increasingly prevalent in pa
83 athogenesis of acute kidney injury (AKI) and chronic kidney disease, as well as in abnormal kidney re
86 Identification of people with diabetes and chronic kidney disease at high-risk of early mortality i
87 ngth (per mm; beta = -1.54), and presence of chronic kidney disease (beta = -1.49) were significantly
89 y as a surrogate endpoint for progression of chronic kidney disease, but empirical evidence to suppor
90 Th17 cells play a role in the progression of chronic kidney disease, but the endogenous pathways that
91 relationship between periodontal disease and chronic kidney disease, but there is little evidence to
92 , the use of spironolactone in patients with chronic kidney disease can be restricted by hyperkalaemi
93 te risk equations for outcomes and develop a chronic kidney disease-cardiovascular disease (CKD-CVD)
95 heart failure, peripheral vascular disease, chronic kidney disease, chronic obstructive pulmonary di
96 disease (OR 3.43, 95% CI 1.17 to 10.00), and chronic kidney disease (CKD) (OR 2.81, 95% CI 1.97 to 4.
103 M(2.5)) is associated with increased risk of chronic kidney disease (CKD) and diabetes, a causal driv
109 ic features implicated in the progression of chronic kidney disease (CKD) are interstitial fibrosis a
112 y protease inhibitors pose a similar risk of chronic kidney disease (CKD) as use of older protease in
113 re categorized by the presence or absence of chronic kidney disease (CKD) at baseline (estimated glom
114 d subnetworks that potentially differentiate chronic kidney disease (CKD) by severity or progression.
115 Although often considered a single-entity, chronic kidney disease (CKD) comprises many pathophysiol
119 lance and whether their activities change in chronic kidney disease (CKD) has not yet been elucidated
134 ed with increased mortality and morbidity in chronic kidney disease (CKD) patients, especially in the
135 ophan has been associated with lower risk of chronic kidney disease (CKD) progression, implicating me
136 ssed in the kidney, but its possible role in chronic kidney disease (CKD) remains largely unknown.
139 roke), and safety were analyzed according to chronic kidney disease (CKD) stage estimated from CKD-ep
140 urpose of this study was to assess change in chronic kidney disease (CKD) stage following TAVR, ident
141 exemplify this data integration issue for a chronic kidney disease (CKD) study, comprising complex c
143 r filtration rate (eGFR) in individuals with chronic kidney disease (CKD) to predict the risk of end
144 rare, hereditary cause of kidney stones and chronic kidney disease (CKD) which is characterized by 2
146 y injury (AKI) within 3 months and new-onset chronic kidney disease (CKD) within 1 year following hos
147 atients with heart failure (HF) and advanced chronic kidney disease (CKD), a population underrepresen
148 diabetes duration, retinopathy, nephropathy, chronic kidney disease (CKD), and anaemia as predictors
149 Hyperuricaemia is common among patients with chronic kidney disease (CKD), and increases in severity
150 eous ablation for risk factors for worsening chronic kidney disease (CKD), and otherwise PN; biopsy,
151 in conditions such as diabetes mellitus and chronic kidney disease (CKD), and they may be involved i
152 rare, hereditary cause of kidney stones and chronic kidney disease (CKD), characterized by 2,8-dihyd
155 y virus (HIV) infection have higher risk for chronic kidney disease (CKD), defined by a reduced estim
157 gest new treatments for more common forms of chronic kidney disease (CKD), demonstrating the importan
158 lied to a range of human diseases, including chronic kidney disease (CKD), epilepsy, and amyotrophic
160 he aetiology of cardiometabolic diseases and chronic kidney disease (CKD), in part via metabolism of
161 ally relevant to metabolic diseases, such as chronic kidney disease (CKD), in which dietary approache
163 ted retinopathy and modestly associated with chronic kidney disease (CKD), peripheral artery disease
166 and creatinine is an important biomarker for chronic kidney disease (CKD), we tested the FOLP probe f
167 An estimated glomerular filtration rate by chronic kidney disease (CKD)-EPI-CysC-creatinine <60 mL/
190 ssion models and stratified for diabetes and chronic kidney disease (CKD, defined as estimated glomer
191 intervals: 0.07% overall, 0.2% for stage 5D chronic kidney disease [CKD], 0.5% for stage 5 CKD and n
194 betes in coronary artery disease, stroke and chronic kidney disease, complemented by a systematic rev
195 e aimed to investigate the relations between chronic kidney disease, coronary microvascular dysfuncti
198 and analyze the association between AKI and chronic kidney disease (defined as at least mildly decre
199 tients with atrial fibrillation and advanced chronic kidney disease (defined as creatinine clearance
200 e/incidence of cardiovascular disease (CVD), chronic kidney disease, depression, diabetes, high total
201 specific expression of genes associated with chronic kidney disease, diabetes and hypertension, provi
202 ailure, peripheral arterial disease, asthma, chronic kidney disease, diabetes or COPD in the 12 month
203 and atherosclerosis), comorbidities (anemia, chronic kidney disease, diabetes, and so on), and diseas
204 isk were most sensitive to the prevalence of chronic kidney disease, diabetes, cardiovascular disease
205 ailure, peripheral arterial disease, asthma, chronic kidney disease, diabetes, or COPD in the 12 mont
206 and/or myocardial infarction, heart failure, chronic kidney disease, dialysis, stroke, inpatient admi
207 e, moderate or severe ischemia, and advanced chronic kidney disease did not have substantial or susta
208 ary artery disease among individuals without chronic kidney disease during the 12.5-year follow-up pe
210 ons between PPI use and acute kidney injury, chronic kidney disease, end-stage renal disease, and ele
213 d glomerular filtration rate (eGFR) with the Chronic Kidney Disease Epidemiology Collaboration (CKD-E
214 n Study (CKiD) equation for children and the Chronic Kidney Disease Epidemiology Collaboration (CKD-E
215 ndomization to week 104, calculated with the Chronic Kidney Disease Epidemiology Collaboration creati
216 st error were observed with cystatin C-based chronic kidney disease epidemiology collaboration equati
217 glomerular filtration rate (eGFR) using the Chronic Kidney Disease Epidemiology Collaboration equati
219 mellitus (glycated hemoglobin level, >=7%), chronic kidney disease (estimated glomerular filtration
220 aged 18-85 years with non-dialysis-dependent chronic kidney disease (estimated glomerular filtration
222 t time of LTBI testing (e.g., HIV, diabetes, chronic kidney disease, etc.) were identified from physi
223 tudied in the treatment of heart failure and chronic kidney disease, even in patients without diabete
225 replication in 765,289 participants from the Chronic Kidney Disease Genetics (CKDGen) Consortium.
226 lomerular filtration rate and lowest rate of chronic kidney disease (>=stage 3) from year 1 onwards u
228 hoice of optimal chemotherapy and prognosis, chronic kidney disease has drawn attention in the treatm
229 e on patients with chronic heart failure and chronic kidney disease has identified hypochloremia as a
230 e general population, patients with advanced chronic kidney disease have a >10-fold higher burden of
232 tension, coronary artery disease, arthritis, chronic kidney disease, heart failure, stroke, asthma, c
233 h diabetes (HR, 1.95; 95% CI, 1.06-3.58) and chronic kidney disease (HR, 1.97; 95% CI, 1.05-3.67) eme
234 rrhythmias (HR: 1.62; 95% CI: 1.28 to 2.05), chronic kidney disease (HR: 2.41; 95% CI: 1.54 to 3.78),
235 es and established cardiovascular disease or chronic kidney disease, if kidney function is adequate.
240 618 children and adolescents enrolled in the Chronic Kidney Disease in Children study, an observation
242 fects and represent the most common cause of chronic kidney disease in the first three decades of lif
243 y tract (CAKUT) are the most common cause of chronic kidney disease in the first three decades of lif
244 disease in clinical trials of progression of chronic kidney disease in the setting of increased album
245 increased risk of cardiovascular disease and chronic kidney disease in those with gout, novel associa
248 re urgently needed in patients with advanced chronic kidney disease, including those receiving dialys
249 d frequently occurs in patients with cancer, chronic kidney disease, infection, and many other illnes
250 ron deficiency, which include heart failure, chronic kidney disease, inflammatory bowel disease, pati
260 cal treatments for kidney disease - by 2040, chronic kidney disease is projected to be the fifth lead
262 idney injury and those with risk factors for chronic kidney disease limit conclusions about safety in
265 displays multiple key features of late stage chronic kidney disease-mineral bone disorder (CKD-MBD),
266 therosclerosis, hypertension, heart failure, chronic kidney disease, obesity, and type 2 diabetes mel
267 idities, the most common being hypertension, chronic kidney disease, obstructive sleep apnoea, and me
268 dney repair after acute kidney injury and to chronic kidney disease of varied aetiologies, including
269 scular dysfunction may mediate the effect of chronic kidney disease on abnormal cardiac function and
270 dministrations in patients with stage 4 or 5 chronic kidney disease or undergoing dialysis, the upper
272 aturation (OR, 0.94 [95% CI 0.93-0.96]), and chronic kidney disease (OR, 1.53 [95% CI 1.20-1.95]) wer
273 core of >=8 (p < 0.0001), anemia (p = 0.02), chronic kidney disease (p = 0.003), and higher N-termina
274 ic obstructive pulmonary disease (P = 0.73), chronic kidney disease (P = 0.09), and hearing loss (P =
276 are effective for the treatment of anemia in chronic kidney disease patients and may also be benefici
277 In patients with resistant hypertension and chronic kidney disease, patiromer enabled more patients
278 s of 1-year mortality were old age, anaemia, chronic kidney disease, presence of valvular heart disea
279 CKD to kidney failure was assessed using the Chronic Kidney Disease Prognosis Consortium (CKD-PC) equ
280 dual-level data from eligible cohorts in the Chronic Kidney Disease Prognosis Consortium (CKD-PC) wit
283 delivery approaches for acute kidney injury, chronic kidney disease, renal fibrosis, renovascular hyp
285 cohort of patients with type 2 diabetes and chronic kidney disease, sTNFR1 predicted short-to-medium
287 daily for patients with or without advanced chronic kidney disease, supporting conventional dosing i
290 tcontrast acute kidney injury in adults with chronic kidney disease: the Kompas randomized clinical t
291 atients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral
292 nt diabetes, hypertension, dyslipidemia, and chronic kidney disease were investigated using survival
293 t males, hypertension, diabetes, obesity and chronic kidney disease were most frequent in the COVID-1
294 onstitutional disorders in adults, including chronic kidney disease, which affects more than 1 in 10
295 ular filtration rate (eGFR) in patients with chronic kidney disease who are at risk for progression i
296 testing in an African American patient with chronic kidney disease who is being evaluated for a kidn
297 f renal events in patients with diabetes and chronic kidney disease who were selected to optimise eff
298 scular events in patients with diabetes with chronic kidney disease with or without albuminuria have
300 lar events are prevalent among patients with chronic kidney disease without overt obstructive coronar