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1 he age-related increase in the prevalence of nephrosclerosis.
2 ed TGF-beta signaling significantly modifies nephrosclerosis.
3 regulation of MMP-14, and the development of nephrosclerosis.
4 prevented renal dysfunction, and attenuated nephrosclerosis.
5 RD among African Americans with hypertensive nephrosclerosis.
6 HIV-associated nephropathy and hypertensive nephrosclerosis.
7 rity (76%) had FSGS and 10% had hypertensive nephrosclerosis.
8 ing diagnoses of impaired renal function and nephrosclerosis-age-associated histologic changes in the
10 increased BP in black men with hypertensive nephrosclerosis and is associated with adverse clinical
11 ldosterone contributes to the development of nephrosclerosis and renal fibrosis in rodent models, but
12 ion) among participants who had hypertensive nephrosclerosis and were enrolled in the African America
15 mild to moderate essential hypertension and nephrosclerosis; angiotensin-converting enzyme because o
16 crostructural level, the histologic signs of nephrosclerosis (arteriosclerosis/arteriolosclerosis, gl
17 ects of tamoxifen in a model of hypertensive nephrosclerosis (chronic inhibition of nitric oxide synt
22 effects in the L-NAME model of hypertensive nephrosclerosis, likely through the inhibition of TGF-be
23 diabetic nephropathy (n = 26), hypertensive nephrosclerosis (n = 7), idiopathic focal segmental glom
24 shion parallel to albuminuria that occurs in nephrosclerosis, several facets of cerebrovascular disea
25 nefit of slowing progression of hypertensive nephrosclerosis was observed with the lower BP goal.
26 in 1094 African Americans with hypertensive nephrosclerosis, which examined the effects of two level
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