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1 tribute to accelerated microcalcification in chronic renal disease.
2 evalent in patients with atherosclerosis and chronic renal disease.
3 eases such as hepatitis, liver cirrhosis and chronic renal disease.
4 ation, coronary heart disease, diabetes, and chronic renal disease.
5 exists between atrial fibrillation (AF) and chronic renal disease.
6 addressed the potential benefits of IL-10 in chronic renal disease.
7 and improves renal function in this model of chronic renal disease.
8 he increased synthesis of fibronectin during chronic renal disease.
9 enal injury in a variety of animal models of chronic renal disease.
10 herapy in organ remodeling diseases, such as chronic renal disease.
11 kg + 5 x 20 mg/kg) over 12 wk induced severe chronic renal disease.
12 laying a critical role in the progression of chronic renal disease.
13 , ischemic heart disease, and progression of chronic renal disease.
14 ascular disease event rates in patients with chronic renal disease.
15 ore rapid rate of progression of nondiabetic chronic renal disease.
16 of gender on the progression of nondiabetic chronic renal disease.
17 protein restriction slows the progression of chronic renal disease.
18 hypertension, congestive heart failure, and chronic renal disease.
19 esigned to slow or arrest the progression of chronic renal disease.
20 e effect of low-protein diets in humans with chronic renal disease.
21 and renal vasculopathy prior to the onset of chronic renal disease.
22 ients with EN but not in patients with other chronic renal diseases.
23 central role in the onset and progression of chronic renal diseases.
24 o be common endpoint result of many forms of chronic renal diseases.
25 be necessary for halting the progression of chronic renal diseases.
26 ions for inhibiting the RAS in patients with chronic renal diseases.
27 volved in molecular pathways of acquired and chronic renal diseases.
28 y and mortality as well as increased risk of chronic renal disease, a finding that is especially rele
29 erulonephritis, both leading causes of human chronic renal disease, affecting 10% of the world popula
30 indirectly contributes to the progression of chronic renal disease and is an important factor in the
31 cells is associated with the development of chronic renal disease and may promote fibrogenesis by in
33 , prior MI, prior CVD, rheumatoid arthritis, chronic renal disease, and chronic obstructive pulmonary
34 n renal tubular epithelia in mouse models of chronic renal diseases, and such induction was spatially
35 thought to play a role in the progression of chronic renal disease, but clinical trials to date have
36 between analgesic use and increased risk of chronic renal disease, but few cohort studies have exami
38 eliorates renal fibrosis in animal models of chronic renal disease by promoting extracellular matrix
40 ve demonstrated that 50% of individuals with chronic renal disease (CRD) die of cardiovascular causes
41 (NO) deficiency occurs and may contribute to chronic renal disease (CRD), the status of the NO system
42 6 human renal biopsy samples from a range of chronic renal diseases (CRD) to determine changes in tTg
44 de additional protection from progression of chronic renal disease; however, there have been few long
45 9), diabetes (HR, 5.2; 95% CI, 5.0-5.6), and chronic renal disease (HR, 1.7; 95% CI, 1.5-1.9) occurre
51 suggest that the beneficial effect of HGF in chronic renal disease is attributable, at least in part,
52 c treatment of dyslipidemia in children with chronic renal disease is controversial because conclusiv
53 and suggests that predisposition to develop chronic renal disease may include an in utero origin.
54 ngs in children with dilated cardiomyopathy, chronic renal disease, obesity, type I diabetes, juvenil
56 deficiency was present in one third, ACI or chronic renal disease or both was present in one third,
57 t predictors of any GDMT included absence of chronic renal disease or nonsustained ventricular tachyc
59 d therapeutic intervention for patients with chronic renal disease, regardless of whether systemic hy
60 er cancer (SMR = 2.5; 95% CI: 1.6, 3.7), and chronic renal disease (SMR = 2.0; 95% CI: 1.5, 2.8).
61 llitus (SMR = 1.90, 95% CI: 1.35, 2.61), and chronic renal disease (SMR = 3.11, 95% CI: 1.66, 5.32).
62 nes plays a major role in the development of chronic renal diseases such as diabetic nephropathy.
63 t cells is a key event in the progression of chronic renal diseases that leads to end-stage renal fai
64 levels in serum were measured by ELISA, and chronic renal disease was induced by a 5/6 nephrectomy (
65 ic systemic fibrosis (NSF) in the setting of chronic renal disease with associated gadolinium exposur
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