Renal blood flow and GFR

Vivian Imbriotis | Jan. 2, 2026

$$RBF = \frac{MAP - \text{Renal venous pressure}}{R_{\text{afferent}} + R_{\text{efferent}}}$$

$$RPF = RBF \cdot (1 - \text{haematocrit})$$

$$GFR = RPF \cdot \text{filtration fraction}$$


The kidneys receive 25% of the cardiac output, RBF = 1.25L/min

Of this, 0.55 is plasma, RPF = 700mL/min

Of that plasma, the filtration fraction is typically 20%, so GFR = 130mL/min

20% of cardiac output = 1.1L/min

If HCT is 0.45, then RPF is 0.6L/min, and about 20% (filtration fraction) is filtered (GFR = 0.12L/min)

90% of the unfiltered blood then flows through glomeruli -> peritubular capillaries (cortex) -> renal veins

10% flows from glomeruli -> vasa recta (medulla) -> renal veins


Local regulation is by:

1.      Myogenic autoregulation: myogenic reflex minimizes changes in GFR that occur with changes in BP by maintaining almost-constant RBF for MAP 80-180. Stretch of arteriole \(\to\) reflex constriction.

2.      Tubuloglomerular feedback: Increased flow and decreased filtrate osmolality is sensed by macula densa cells \(\to\) mesangial cell constriction and afferent arteriolar constriction which increases renal resistance


Systemic regulation is by

  1. The sympathetic nervous system. Catecholamines constrict efferent > afferent arterioles, reducing RBF and GFR
  2. Angiotensin II, which constricts efferent >> afferent arterioles, reducing RBF but maintaining GFR


Other determinants are:

  1. MAP outside of the autoregulatory range
  2. Renal venous pressure (e.g. in renal venous thrombosis)
  3. Viscosity e.g. in polycythaemia

20% of cardiac output = 1.1L/min

If HCT is 0.45, then RPF is 0.6L/min, and about 20% (filtration fraction) is filtered (GFR = 120mL/min)

$$\text{GFR} = \text{hydraulic permeability} \cdot SA \cdot \text{net filtration pressure}$$

$$\text{GFR} = K_f (P_{\text{plasma}} - \pi_{\text{plasma}} - P_{\text{filtrate}})$$

The \(P_{\text{plasma}}\) is decreased by afferent arteriolar constriction, and increased by efferent arteriolar constriction.

\(\pi_{\text{plasma}}\) is increased by low RBF and decreased by hypoalbuminaemia.

Surface area is decreased by mesangial cell constriction or loss of glomeruli in renal disease.


Regulation is therefore by

1.      Myogenic autoregulation: myogenic reflex minimizes changes in GFR that occur with changes in BP by maintaining almost-constant RBF for MAP 80-180.

2.      Tubuloglomerular feedback: Increased flow and decreased filtrate osmolality is sensed by macula densa cells \(\to\) mesangial cell constriction \(\downarrow SA\) and afferent arteriolar constriction \(\downarrow P_{\text(plasma)}\)

3.      Circulating catecholeamines and angiotensin II (constrict efferent > afferent arteriole, which decreases GFR but LESS THAN they decrease renal blood flow)

4.       Increased systemic blood pressure outside of autoregulatory range (“pressure diuresis”)