glomerular hyperfiltration.

neural imbalance.

asymmetrical renal growth.

compensatory hypertrophy.

established renal tubular fibrosis.

alters renal homeostasis.

causes renal atrophy.

induces interstitial fibrosis.

affects glomerular development.

affects tubular function.

glomerular cysts.

fibromuscular collars.

heterotopic bone formation.

renal atrophy.

excess production of afferent arteriole renin.

renal hyperplasia.

significant obstructive effect.

uncertain prognosis.

vascular recruitment due to obstruction.

artifactual increased tubular uptake.

improve collecting duct function.

reduce renin recruitment in the afferent arteriole.

reduce glomerular sclerosis.

reduce renal apoptosis.

accelerate interstitial fibrosis.

seen only in the setting of obstruction.

a one-way process.

integral to glomerular development.

reflected in the presence of α-smooth muscle actin.

the basis for glomerular sclerosis.

is not related to angiotensin expression.

depends entirely on collagen synthesis.

is independent of transforming growth factor-β activity.

depends on balanced activity of tissue inhibitors of metalloproteinases (TIMPs) and matrix metalloproteinases (MMPs).

depends on normal expression of EGF.

increased growth, fibrosis, and tubular atrophy.

altered growth regulation, renal differentiation, and functional integration.

glomerulosclerosis, interstitial fibrosis, and atrophy.

glomerulosclerosis, renin downregulation, and tubular hypertrophy.

hypoplasia and increased epithelial-mesenchymal transformation.

are mediated by the renin-angiotensin system.

are similar to that seen in postnatally obstructed kidneys.

affect renal interstitial fibrosis.

are minimal in the absence of overt infection.

are the key element in glomerular damage.

is an important regulator of renal growth.

acts predominantly through the angiotensin AT1 receptor.

is unaffected by renal obstruction.

affects epithelial-mesenchymal transformations.

is tightly regulated by EGF.