Sentence examples for obstructive kidney from inspiring English sources

Wu, C. F. et al. Transforming growth factor β-1 stimulates profibrotic epithelial signaling to activate pericyte-myofibroblast transition in obstructive kidney fibrosis.

Chronic and obstructive kidney diseases were excluded.

Work in experimental models of kidney disease including protein overload injury, proliferative glomerulonephritis, and obstructive kidney disease suggests that increased PAI-1 expression is associated with interstitial fibrosis, and reduction in PAI-1 expression (via drug therapy or recombinant techniques) is associated with attenuation of renal fibrotic injury [46] [50].

Greater awareness of this issue may help clarify the mechanisms underlying the development of proteinuria in the context of obstructive kidney diseases.

These findings not only confirm the development of renal inflammation and fibrosis in the current investigation but also provide further support to the view of TGF- β1-mediated fibrogenesis in obstructive kidney disease.

Given the fact that similar changes are observed in 99mTc-MAG3 renogram in human patients with renal obstruction [ 26, 27], combination of this imaging technique with mouse UUO models should provide an effective assay for evaluating treatment protocols of this disease or screening new pharmacological agents as well as for elucidating pathophysiological mechanisms of obstructive kidney disease.

Astragali Radix and Angelicae Sinensis Radix increased the production of NO in obstructive kidneys via enhancement of endothelial NOS activity (Meng et al., 2007).

As shown in Figure 2, there was only occasional immunostaining of TGF-β1 in the tubular cells of the sham-operated kidneys but diffuse staining in the obstructive kidneys, especially the proximal tubular cells and infiltrating monocyte/macrophage.

The patient, born in 1964, was diagnosed as affected by obstructive chronic kidney disease (CKD) with crystalluria at the age of 28.

It does not suggest that findings of non-obstructive hydronephrosis, kidney size, and cortical echogenicity and thickness are not useful in determining the presence of chronic kidney disease in the setting of renal insufficiency.

Non-diabetic ESKD cases in our sample set correspond to the union of H-ESKD patients as described in the companion paper (28) with FSGS, HIVAN and ESKD patients, exclusive of the following etiologies: congenital, obstructive, cancer-related kidney diseases or known monogenic forms of kidney disease (e.g. autosomal dominant polycystic kidney disease, Alport syndrome).