| dc.description.abstract | Smoking increases the production of angiotensin II as an effect of renin secretion stimulated by the efferent sympathetic system through beta-1 adrenergic stimulation of the juxtaglomerular apparatus. Angiotensin II will cause tubular and glomerular injuries through the mechanism of pressure-induced renal injury and ischemia-induced renal injury as a secondary result of intrarenal vasoconstriction and decreased renal blood flow. In addition, there is secondary tubular injury due to angiotensin-induced proteinuria. Angiotensin II activates renal fibroblasts to undergo differentiation into myofibroblasts, stimulates TGF-ß profibrotic cytokines, induces oxidative stress, stimulates chemokines and osteopontin which can cause local inflammation, and stimulates mesangial cell proliferation and hypertrophy. Glomerular capillary hypertension causes an increase in glomerular permeability resulting in an increase in albumin filtration which will further trigger kidney damage through various pathways, including induction of tubular chemokine expression and activation of complement leading to infiltration of inflammatory cells in the interstitium and trigger fibrogenesis. This phenomenon involves endothelial cells and glomerular podocytes and will trigger exacerbation of proteinuria and glomerulosclerosis with the end result in the formation of kidney scar tissue and a decrease in glomerular filtration rate (GFR). | en_US |
