|  | Conditions & Treatments | Kidney Disease

Kidney Blood Supply: Arteries, Veins & Nephron Circulation

The kidneys receive 20-25% of cardiac output (~1.2 L/min) despite being <0.5% of body weight—reflecting their high metabolic and filtration demands.

Arterial Supply

  1. Renal arteries branch from abdominal aorta at L1-L2.
  2. Segmental arteries (5 typically): superior, anterosuperior, anteroinferior, inferior, posterior. End arteries—no anastomoses → infarct risk if occluded.
  3. Interlobar arteries penetrate renal capsule, travel between pyramids.
  4. Arcuate arteries arch at corticomedullary junction.
  5. Interlobular arteries ascend into cortex.
  6. Afferent arterioles → glomerulus (filtration).
  7. Efferent arterioles → peritubular capillaries (cortical nephrons) OR vasa recta (juxtamedullary nephrons).

Venous Drainage

  • Peritubular capillaries/vasa recta → interlobular veins → arcuate veins → interlobar veins → renal vein → IVC.
  • Left renal vein longer; passes anterior to aorta, receives left gonadal, adrenal, lumbar veins.
  • Right renal vein shorter; direct to IVC.

Nephron Blood Supply & Filtration

  • Glomerular capillaries: High-pressure (P_GC ~45 mmHg) fenestrated endothelium + basement membrane + podocytes = filtration barrier.
  • Filtration fraction: ~20% of renal plasma flow becomes filtrate (180 L/day).
  • Peritubular capillaries: Low-pressure, high-surface-area reabsorption (proximal tubule 65%, loop, distal, collecting duct).
  • Vasa recta: Countercurrent exchanger maintaining medullary osmotic gradient for urine concentration.

Regulation of Renal Blood Flow (RBF) & GFR

  • Autoregulation (myogenic + tubuloglomerular feedback): Maintains constant RBF/GFR over MAP 80-180 mmHg.
  • Neural: Sympathetic (α1) → afferent/efferent constriction → ↓RBF (exercise, hemorrhage, stress).
  • Hormonal:
    • RAAS: Ang II → efferent > afferent constriction → maintains GFR despite ↓RBF.
    • ANP/BNP: Dilate afferent, constrict efferent → ↑GFR, ↓reabsorption.
    • Prostaglandins (PGE2, PGI2): Vasodilatory; protective in hypovolemia/NSAID use.
    • Endothelin: Potent vasoconstrictor.

Clinical Correlates

  • Renal artery stenosis → flash pulmonary edema, refractory hypertension, renal atrophy.
  • Contrast nephropathy: vasoconstriction + direct toxicity.
  • ACEi/ARB: efferent dilation → ↓GFR (expected rise in Cr ≤30%); contraindicated in bilateral RAS.
  • Shock: sympathetic/RAAS activation → cortical ischemia, medullary preservation → ATN.

Renal hemodynamics are exquisitely regulated—balancing filtration, reabsorption, and oxygen delivery.

Kidney Disease - Related Articles