Urinary tract obstruction.

摘要: Angiotensin II plays a pivotal role in the progression of renal diseases, including obstructive nephropathy. Increasing levels angiotensin nephropathy upregulate expression several factors: transforming growth factor-beta1 (TGF-beta1), tumor necrosis factor-alpha (TNF-alpha), platelet-derived factor (PDGF), insulin-like (IGF-1), osteopontin, vascular cell adhesion molecule-1 (VCAM-1), nuclear factor-kappaB (NF-kappaB), monocyte chemoattractant peptide-1 (MCP-1), intercellular (ICAM-1), and CD14 among others. Local production TGF-beta, by intrinsic cells or macrophages invading kidney, is key mediator fibrosis. Activation TGF-beta stimulates endothelin production. Endothelin, turn, potent stimulus for fibrogenesis. Oxidative stress, fueled part II, upregulates molecules, compounds cytokines. Sustained leads to apoptosis tubular epithelial cells. Several factors genes involved have been described. Nuclear kappa-B transcriptional regulation present organs, kidney. NF-kappaB activated setting ureteral obstruction. Administration angiotensin-converting enzyme (ACE) inhibitors decreased significantly activation obstructed Studies neonatal rats indicate that chronic obstruction decreases epidermal (EGF). Replacement this reduced vimentin, clusterin, TGF-beta. The administration IGF-1 also lessened interstitial pathology A spectrum urinary tract malformations utility certain markers such as fetal serum beta(2) microglobulin predictor postnatal function bilateral uropathies has number pharmacologic interventions ameliorate increased expansion volume, decrease down-regulate extracellular matrix infiltration interstitium Drugs used include ACE inhibitors, arginine, osteogenic protein-1, Pirferidone, so on. It likely next decade advances genetic manipulations new drug therapies may forestall development fibrosis