Macrovascular and microvascular disease Atherosclerosis • Most common cause of renal artery stenosis • Atherosclerotic plaque at the ostia • Risk factors same for CVD: smoking, HT, Dyslipidaemia, DM, FHx • >70% of stenosis is haemodynamically significant  ↓Renal blood flow  RAAS activation  secondary HT  Treatment: o Stenting o Control of CVD risk factors o RAAS blockade to rectify HT Fibromuscular Dysplasia • Mostly affects young women • Can also affect other vessels including carotids • Presents with secondary HT • Strong of pears appearance on angiogram • Treated with angioplasty not stent Large Vessel Vasculitis: Takayasu’s vasculitis Microvascular Disease Hypertensive/benign Nephrosclerosis • Chronic HT  narrowed preglomerular arteries and AA  glomerular ischaemia • Remaining nephrons develop preglomerular vasodilation to preserve glomerular filtration  glomerular HT and hyperfiltration Diabetic Nephropathy • Hyperglycaemia and AGEs  glomerular HT and hyperfiltration • Kimmelstiel-Wilson nodules form from microaneurysms of glomerular cap. • DM also results in microvascular diseases in: retinopathy, nephropathy, peripheral and autonomic neuropathy Atheroembolic Renal Disease • Embolization of cholesterol crystals from atherosclerotic plaques in large arteries • Precipitated by procedures such as coronary angiograms, can occur spontaneously or can occur after the introduction of anticoagulant e.g. Warfarin • Crystals may or may not occlude vessel lumen but produce inflammatory response over weeks to months • Presents as worsening renal function, HT, livedo reticularis, distal emboli Thrombotic Microangiopathies • Affects the glomerular capillaries • Endothelial dysfunction  microvascular thrombi formation o Thrombotic thrombocytopaenic purpura (TTP) o ADAMTS13 deficiency (plasma metalloprotease that cleaves vWF) o Produced widespread microthrombi including in the brain • Haemolytic-Uraemic Syndrome (HUS) o Complement system activation  microthrombi formation • Antiphospholipid Antibody syndrome o Antiphospholipid antibodies  hypercoagulable state  second hit/infection  microthrombi formation • Scleroderma renal crisis o Endothelial dysfunction  microthrombi and HT Small Vessel Vasculitis • Vasculitis of the glomerular cap.  glomerular necrosis  nephritic syndrome • ANCA associated vasculitis, cryoglobulinaemic vasculitis, IgA vasculitis Medium Vessel Vasculitis: polyarteritis nodosa Crescent GN/Focal Necrotising GN