Renal Vascular Anatomy, Physiology and Pathology Kidney Vasculature: Abdominal aorta  renal a.  lobar a.  interlobar a.  arcuate a.  interlobular a.  afferent arteriole  glomerular cap.  efferent arteriole  peritubular cap.  interlobular v.  arcuate v.  interlobar v.  lobar v.  renal v.  IVC Blood Supply to Medulla • Efferent a. of juxtamedullary nephrons • Tubules have high energy demands • Therefore, tubules are sensitive to changes in perfusion Renal Blood Flow • 20% of CO; 1-1.2L/min  Glomerulus fed by AA • GFR is 100-120mL/min • ~144L filtrate/day produced • Urine volume: 1-2L/day (0.5mL/kg/hr) Autoregulation: • Myogenic reflex: arterial SM contracts/ relaxes in response to change in vascular tension. Occurs rapidly. • TGF: see Clinical Approach to Acute Kidney Injury Constrictors Dilators Afferent • ATII (high dose)  PGs Arteriole AA • NE  Kinins • Endothelin  • ADH  Dopamine (low dose) • PG Blockade Efferent Arteriole EA  ATII (low dose)  ANP NO  ATII blockage RAAS Blockers • ACE-inhibitors and ATII-receptor blockers block the action of ATII  ↓intraglomerular pressure • This is beneficial for patients with diseases like diabetic nephropathy where there is glomerular hyperfiltration leading to glomerular sclerosis • However, when hypoperfused, the protective effect of RAAS is blunted  ↓renal perfusion  ↓GFR NSAIDs • COX-2  PGs (e.g. PGE2)  AA vasodilation • COX blockade by NSAIDs  ↓PG production  AA vasoconstriction  ↓renal perfusion and ↓GFR Diuretics • Frusemide is a loop diuretic which blocks the NKCC2 cotransporter in the LoH • NKCC2 is also on MD cells, affecting autoregulation via TGF • Frusemide prevents the production of the medullary osmotic gradient so that salt and fluid can’t be reabsorbed • MD cells cannot sense abnormally high Na in tubular fluid as their NKCC2 channels have also been blocked Vascular Diseases of the Kidney Present as: • Secondary hypertension because of RAAS activation due to hypoperfusion • Renal impairment (↓renal perfusion  ↓GFR)