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|Title:||Mechanism of progression of renal disease: current hemodynamic concepts.||Austin Authors:||Johnston, Colin I;Risvanis, John;Naitoh, M;Tikkanen, Ilkka||Affiliation:||The University of Melbourne, Department of Medicine, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australia||Issue Date:||1-Sep-1998||Publication information:||Journal of Hypertension. Supplement; 16(4): S3-7||Abstract:||Hypertension, a known independent risk factor for end-stage renal failure, damages the kidney in multiple ways. It produces hemodynamic and mechanical stress, which may lead to glomerular endothelial dysfunction. Both of these mechanisms may lead to increased glomerular leakiness, hence proteinuria, which may damage the kidney further. Hypertension may also stimulate the production of vasoactive substances that, in turn, activate the production of cytokines and growth factors, leading to the production of extracellular matrix proteins. Thus, the progression of renal failure is related to both systemic and glomerular hemodynamic changes and to the activation of vasoactive hormones, growth factors and cytokines.To protect the kidney, we need to control or prevent the occurrence of these factors. Therapy with effective antihypertensive agents, such as angiotensin-converting enzyme inhibitors, has been shown to slow the progression of end-stage renal disease.||Gov't Doc #:||9817185||URI:||http://ahro.austin.org.au/austinjspui/handle/1/13626||Journal:||Journal of Hypertension. Supplement||URL:||https://pubmed.ncbi.nlm.nih.gov/9817185||Type:||Journal Article||Subjects:||Animals
Antihypertensive Agents.therapeutic use
Kidney Diseases.physiopathology.prevention & control
|Appears in Collections:||Journal articles|
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