Potential pathomechanisms of smoking-induced renal injury

• Increased sympathetic nerve activity.
• Increase in BP and heart rate.
• Decreased fall in nighttime BP.
• Increase in renal vascular resistance leading to a decrease in GFR and renal plasma flow.
• Increase in intraglomerular capillary pressure.
• Aggravation of hyperfiltration in patients with diabetic nephropathy.
• Atherosclerosis of renal arteries and myointimal hyperplasia of the intrarenal arteries and arterioles.
• Endothelin-1–mediated and/or angiotensin II-mediated proliferation and matrix accumulation of vascular smooth muscle cells, endothelial cells, and mesangial cells.
• Tubulotoxic effects with alteration of tubular function.
• Toxic effects on endothelial cells.
    • alteration of the prostaglandin/thromboxane metabolism.
    • oxidative stress through generation of reactive oxygen species.
    • NO depletion.
    • impairment of endothelial cell-dependent vascular dilation.
    • increased adhesion of monocytes to the endothelium.
    • carbon monoxide–induced hypoxia.
• Increased clotting of platelets.
• Impaired lipoprotein and glycosaminoglycan metabolism.
• Modulation of the immune response.
• Vasopressin-mediated antidiuresis.
• Insulin resistance.