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1 d there are no clinical signs or symptoms of uremia.
2 not reduce the burden of vascular disease in uremia.
3 on of apoptosis to neutrophil dysfunction in uremia.
4 he clinical course of both liver disease and uremia.
5  pattern that is similar to that observed in uremia.
6 defects in platelet function associated with uremia.
7 y role of IL-6 in macrophage infiltration in uremia.
8 adipose tissue that augments inflammation in uremia.
9 ls in blood, also referred to as azotemia or uremia.
10  28.0 +/- 17.7; P < 0.001) without affecting uremia.
11 early insulin resistance and dyslipidemia in uremia.
12  be a strategy for improving AFV function in uremia.
13 l dysfunction following adenine experimental uremia.
14 gulator of FGF23 production, particularly in uremia.
15 ing sequela of diabetes mellitus and chronic uremia.
16 inflammation and cardiovascular mortality in uremia.
17 stconditioning in 2 rodent models of chronic uremia.
18 dified mice without and with adenine-induced uremia.
19 cause simply feeding more protein aggravates uremia.
20 haracteristic cardiomyopathy associated with uremia.
21  nuclear magnetic resonance at 3 and 6 wk of uremia.
22 me in human drug metabolism, is decreased in uremia.
23 with muscle atrophy from diabetes or chronic uremia.
24  transcription (STAT) signaling as occurs in uremia.
25 ncreases as urea is raised over the range in uremia.
26 ibute directly to the carbonylation found in uremia.
27  nephropathy has become the leading cause of uremia.
28 UT-A protein whose abundance is increased by uremia.
29 ardial and hepatic calcifications induced by uremia.
30  that increased TGF-beta1, a complication of uremia, activates Notch in endothelial cells of AVFs, le
31 sease (ESRD) patients cannot be explained by uremia alone.
32                                    Worsening uremia also renders CKD patients vulnerable to potential
33 s a mechanism linking inflammation, smoking, uremia and coronary artery disease pathogenesis.
34 tonomic neuropathy arises in the presence of uremia and diabetes, with severe dysfunction seen when t
35          kat2J/kat2J mice develop anemia and uremia and die before 1 yr of age.
36 e-might represent a mechanistic link between uremia and dysfunctional primary hemostasis in patients
37 ice and the radial arteries of patients with uremia and hyperphosphatemia.
38 tion as a potential mechanistic link between uremia and platelet dysfunction in ESKD, we used liquid
39 lyses should therefore prevent both clinical uremia and the later, often lethal sequelae.
40 ncreased significantly after 3 days of acute uremia and this increment was prevented by thyroparathyr
41 ially vasculopathic, especially in diabetes, uremia, and aging, in which AGEs classically accumulate.
42 oad, hyperkalemia, metabolic acidosis, overt uremia, and even progressive azotemia in the absence of
43 overload, hyponatremia, metabolic alkalosis, uremia, and hyperglycemia, than those patients who did n
44 of diabetes, dyslipidemia, oxidative stress, uremia, and hyperphosphatemia, "osteoblast-like" cells f
45 ted because they exhibited less proteinuria, uremia, and inflammatory infiltration.
46 xic metabolite that is elevated in diabetes, uremia, and sepsis, which are diseases that increase the
47 CVD and provide unique insight into specific uremia- and PD-induced pathomechanisms of CVD.
48  and nontraditional risk factors, as well as uremia- and transplant-related factors, affect 2 process
49              With trauma, sepsis, cancer, or uremia, animals or patients experience accelerated degra
50           Clinical manifestations related to uremia are managed through a combination of residual kid
51  malnutrition with atherosclerotic events in uremia are unclear.
52                                        Acute uremia (ARF) causes metabolic defects in glucose and pro
53  is the first study in humans characterizing uremia as a state in which hepatic CYP3A4 activity is ac
54 imarily organic in nature and are related to uremia as well as the other comorbid conditions that fre
55 elanocortin signaling in the pathogenesis of uremia-associated cachexia and demonstrate the potential
56 I-12i would also be effective in attenuating uremia-associated cachexia in a mouse model.
57                We tested the hypothesis that uremia-associated cachexia is caused by leptin signaling
58  such as leptin may be an important cause of uremia-associated cachexia via signaling through the cen
59 e melanocortin-4 receptor (MC4-R) attenuates uremia-associated cachexia.
60 crobiota and reducing progression of CKD and uremia-associated complications.
61 otyping were performed with a large group of uremia-associated parathyroid tumors.
62 ly include both conventional and dialysis or uremia-associated risk factors.
63 chromosome 11 occurred in only one of the 46 uremia-associated tumors (2%); the tumor also contained
64                  Therefore, we conclude that uremia associates with intestinal dysbiosis, intestinal
65 lar calcification persists after reversal of uremia, because of a lack of active resorption of apatit
66 uelae: hematuria, anemia, dysuria, stunting, uremia, bladder cancer, urosepsis, and human immunodefic
67  effect on the cardiac remodeling process in uremia, but because high levels of GH have adverse cardi
68  decreased glomerular filtration (leading to uremia), compromised glomerular integrity (leading to pr
69                                              Uremia contributed partially to peritoneal inflammatory
70 each, were begun before clinical evidence of uremia developed in each patient and/or before the nonpr
71                                              Uremia did not affect secretory IgA release into the ile
72                       AKI and the associated uremia did not seem to affect extrarenal HO-1 gene activ
73             Persistent signs and symptoms of uremia (eg, nausea, fatigue) and volume overload (eg, dy
74 bnormalities cause cardiovascular disease in uremia; few observational studies in humans have explore
75 isk factor; however, the mechanisms by which uremia harms the endothelium are still unclear.
76 ntribution of adipose tissue inflammation in uremia has not been characterized.
77 pruritus of cholestasis, but not pruritus of uremia, Hodgkin's disease, or atopic dermatitis.
78 racteristics of overhydration, hyponatremia, uremia, hyperglycemia, and alkalosis.
79                          Different levels of uremia, hyperphosphatemia, and aortic calcification were
80                                              Uremia impairs the atheroprotective properties of HDL, b
81 nd UT-A protein abundance is up-regulated in uremia in both liver and heart.
82 (3) UT-A protein abundance is upregulated in uremia in both liver and heart; and (4) UT-B is expresse
83              Here, we used adenine to induce uremia in both Npt2b-deficient and wild-type mice.
84  calcium and magnesium in brain during acute uremia in dogs.
85 nst the catabolism of a low-protein diet and uremia in patients with renal failure.
86                Because of adverse effects of uremia in the innate and adaptive immune systems, we hyp
87                                        Also, uremia in vitamin D2-treated TPTX dogs failed to increas
88                                              Uremia, in the absence of renal injury, induced the NGAL
89                                              Uremia increases the abundance of this 49-kD UT-A protei
90 a, streptozotocin-induced diabetes mellitus, uremia induced by subtotal nephrectomy, and from pair-fe
91 may represent an independent risk factor for uremia-induced atherosclerosis.
92 th ESRD, supporting a mechanistic link among uremia, inflammation, and atherosclerosis.
93                                              Uremia is a complex metabolic state marked by derangemen
94                                      Because uremia is accompanied by hypertension, the effects of hy
95  of the parathyroid by both hypocalcemia and uremia is dependent upon intact dicer function and miRNA
96 jury in the pathogenesis of complications of uremia is incompletely defined, although diminished bioe
97 ure), suggesting that renal ischemia but not uremia is necessary for the apoptosis observed.
98  to the same kidney, revealing that systemic uremia is not necessary for protection.
99 he pathogenesis of cachexia in patients with uremia is unknown.
100 terorganismal communication, suggesting that uremia is, at least in part, a disorder of RSS.
101 he neurological abnormalities noted in acute uremia may be related in part to the rise in the Ca cont
102 iseases, leading to suggestions that chronic uremia may cause intestinal dysbiosis that contributes t
103 at the posttranslational regulation of TF in uremia may have a causative role in the increased ST ris
104 ent studies have popularized the notion that uremia may induce pathological changes in the gut microb
105                          One complication of uremia, metabolic acidosis, stimulates the degradation o
106                                We posit that uremia modulates TF in the local vessel wall to induce p
107          The results indicate that (a) acute uremia of 3 days is associated with a marked rise of Ca
108 ted peptide reversed the cachexic effects of uremia on appetite, weight gain, body composition, and m
109                   We evaluated the effect of uremia on CYP3A and transporter expression in vitro by i
110 d investigations into the effects of chronic uremia on myocardial infarct size and the protective eff
111 re anuric and developed clinical symptoms of uremia on POD 1.
112 C4-RKO mice resisted the cachexic effects of uremia on weight gain, body composition, and metabolic r
113                           In adenine-induced uremia, only a modest increase in serum FGF23 levels occ
114 ents but not in those with diabetes, disuse, uremia or fasting.
115                                              Uremia or humoral factors are not responsible for the pr
116 t and whether their abundance was altered by uremia or hypertension or in human heart failure.
117 6-kDa protein is upregulated in rat heart in uremia or models of hypertension; and (3) the rat result
118 conventional cardiovascular risk factors and uremia- or dialysis-related variables with PVD.
119 ad impaired PTH secretion after experimental uremia- or folic acid-induced AKI.
120              We separated plasma LDL from 90 uremia patients undergoing hemodialysis into 5 subfracti
121                                              Uremia per se mildly reduced miR-133b levels only.
122 and (b) these alterations are not related to uremia, per se, but are dependent on the presence of exc
123                                           If uremia prevents suppression of essential amino acid or p
124                                              Uremia promotes changes in adipocytes and macrophages en
125 KD are also exposed to other nontraditional, uremia-related cardiovascular disease risk factors, incl
126 extremely high prevalence of traditional and uremia-related cardiovascular risk factors.
127 e Charlson comorbidity index (CCI) and other uremia-related comorbidities, not included in the CCI, w
128  on the epidemiology of both traditional and uremia-related CVD and focus on postulated mechanisms of
129 iated with the recognition and management of uremia-related CVD in developed and developing nations.
130 extremely high prevalence of traditional and uremia-related CVD risk factors.
131 ling and metabolic changes driven by soluble uremia-related factors.
132 factors for CV disease, both traditional and uremia-related, are present in children before they even
133       Together, IS and AHR have potential as uremia-specific biomarkers and targets that may be lever
134 rs (eg, diabetes mellitus and hypertension), uremia-specific factors that arise from accumulating tox
135  to identify 49 HDL-associated proteins in a uremia-specific pattern.
136                  Regarding function of these uremia-specific proteins, only SAA mimicked ESRD-HDL by
137 due to emerging conditions such as hemolytic uremia syndrome.
138 l settings of atherosclerosis, diabetes, and uremia that promote arteriosclerotic calcification-elici
139 d to both acute and chronic hypocalcemia and uremia, the major stimuli for PTH secretion.
140                                              Uremia (U) was induced in female dilute brown agouti/2 m
141 portin knockout experiment in the setting of uremia, using an adenine nephropathy model, where three
142                                              Uremia was imposed on LDL receptor null mice (a model of
143                                              Uremia was induced by 5/6 nephrectomy in adult female mi
144                                              Uremia was induced in male Sprague-Dawley rats via a two
145 ses of coma such as diabetic ketoacidosis or uremia were excluded.
146 d increased oxidative stress associated with uremia, which may contribute to the improved survival af
147 sm induced by either chronic hypocalcemia or uremia, which was measured by increased phosphorylation
148   We also studied the independent effects of uremia without concomitant kidney injury by performing b
149 trophy (10 to 14%; P < 0.05) was observed in uremia without evidence of dysfunction or changes in myo

 
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