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Renal blood supply

• Renal arteries (from the aorta) → segmental arteries → interlobar arteries →

arcuate arteries → interlobular arteries → afferent arterioles → glomeruli
→ efferent arterioles → vasa recta and peritubular capillaries → renal
veins (merge into the inferior vena cava)
Renal blood flow
• Renal blood flow (RBF): the blood volume that flows through the kidney per
unit time
• Normal: ∼ 20% of cardiac output, 1.2 L/Min
• Renal plasma flow (RPF): the volume of plasma that flows through the kidney
per unit time
• RPF = RBF × (1 - Hct)
• Para-aminohippuric acid (PAH): nearly 100% of PAH that enters the
kidney is also excreted (completely filtrated and secreted) →
clearance rate is used to estimate RPF
• Effective renal plasma flow (eRPF) = (urine concentration of PAH) ×
(urine flow rate / plasma concentration of PAH)
Regulation of renal blood flow
The kidney has multiple mechanisms to regulate its own blood flow, and thus, the
rate of glomerular filtration if fluctuations in systemic blood pressure occur.
Myogenic autoregulation (Bayliss effect)
• Description: renal arteries maintain a constant blood pressure (between 80–
180 mm Hg)
• Description: renal hypoperfusion (particularly renal medulla) → stimulate
prostaglandin synthesis → vasodilation of renal vessels → increased renal
Tubuloglomerular feedback
• Description: feedback system between the tubules and glomeruli that adjusts
the GFR according to the resorption capacity of the tubules
• Mechanism: macula densa (of the juxtaglomerular apparatus) monitors the
NaCl concentration in the DCT
• Hypotonic urine (↓ Intraluminal Cl- concentration) → vasodilation of
afferent arterioles → ↑ GFR → ↑ Cl- intraluminal concentration
• Hypertonic urine (↑ Intraluminal Cl- concentration) → vasoconstriction of
afferent arterioles → ↓ capillary pressure → ↓ GFR → ↑ Intraluminal
Cl- concentration
Renin-angiotensin-aldosterone system (RAAS)
• Description: hormonal system that regulates arterial blood pressure and
sodium concentration
• Mechanism: renal hypoperfusion (e.g., hypotension, hypovolemia),
hyponatremia or increased sympathetic tone → kidneys release renin
(produced in the juxtaglomerular apparatus) → renin converts
angiotensinogen (produced in the liver) to angiotensin I → conversion of
angiotensin I to angiotensin II through angiotensin-converting enzyme
(ACE, mostly produced in the lungs) → Angiotensin II acts as a strong
vasoconstrictor and induces the secretion of aldosterone by the adrenal
cortex → aldosterone increases renal reabsorption of sodium (and water)
and augments the excretion of potassium and protons → ↑ extracellular
fluid, ↑ blood pressure, ↓ K+, ↑ pH
• Effects
• Systemic: ↑ arterial blood pressure
• Renal: maintains GFR during renal hypoperfusion

ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II.

Angiotensin receptor blockers inhibit the effect of angiotensin II. Both drug
classes are used to treat arterial hypertension.
• Natriuretic peptides
• Atrial natriuretic peptide (ANP): volume overload → dilation of atria →
secretion of ANP by myocytes
• Brain natriuretic peptide (BNP): volume overload → dilation of ventricles
→ secretion of ANP by myocytes
• Inhibits epithelial Na2+ transporter in the collecting duct →
increased water secretion → lowering the central venous
• Inhibits secretion of aldosterone, renin, ADH, and ACTH
• Antidiuretic hormone (ADH)
• Increases contraction of smooth muscle in blood vessels via V1 receptor
→ increased blood pressure → increased kidney perfusion
• Increases free water reabsorption in the collecting duct (stimulation of
adenylate cyclase → ↑ cAMP → incorporation of aquaporins in the
luminal membrane of collecting ducts)
• Increases urea resorption (↑ incorporation of urea transporters in the
collecting duct)
Autonomic regulation
• Mechanism
• Noradrenaline → binds to α1 receptors → vasoconstriction of arterioles
→ ↑ resistance → ↓ renal blood flow
• Dopamine → binds to D1 receptors → vasodilatation of arterioles → ↓
resistance → ↑ renal blood flow
Hypovolemic shock with severe hypotension activates the sympathetic nervous
system. Subsequently, the hypovolemia and noradrenaline-induced
vasoconstriction result in low renal blood flow → low GFR → low urine production
→ acute renal injury
Measurement of renal function
This section focuses on the basics of glomerular filtration and tubular secretion.
For more information on kidney function tests, see Diagnostic evaluation of the
kidney and urinary tract.
• Definition: the volume of plasma that is cleared of a substance X per unit time
• Clearance of X (mL/min) = (Urine concentration of X (mg/mL) × (Urine flow rate
(mL/min)) / Plasma concentration of X (mg/mL)

Glomerular filtration rate

• Definition: the rate at which fluid is filtered by the kidneys
• Normal GFR
• ♂ 95–145 mL/min/1.73m2
• ♀ 75–125 mL/min/1.73m2
• After the age of 29, a physiological decrease in the GFR of about 10
mL/min/1.73m2 occurs every 10 years.
• GFR depends on the effective filtration pressure
• (PGC – PBS) – (πGC – πBS)]
• GC = glomerular capillary, BS = Bowman space, P = hydrostatic pressure, π =
osmotic pressure
• πBS normally equals 0
• Normal effective filtration pressure is 13 mm Hg
• Glomerular filtration is driven by the difference between hydrostatic and
osmotic pressure
• Starling equation for the glomerulus : GFR: Jv = Kf × [(PGC – PBS) –
σ(πGC – πBS)]
• Jv = net fluid flow
• Kf = filtration constant
• σ = Staverman reflection coefficient sigma
GFR is directly proportional to the renal plasma flow!