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Renal Autoregulation and GFR

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Renal Autoregulation and GFR
Photo by Robina Weermeijer / Unsplash

Take home messages

  • Renal metabolic demand is determined by blood flow
  • Autoregulation occurs via the myogenic reponse and tubuloglomerular feedback, plus some other bits and bobs we don't really understand
  • The units on the graph don't matter, as long as there's a plateau from around 75mmHg to 160mmHg ish

The blood supply to the kidney

The kidneys receive a quarter of the cardiac output, which is approximately:

  • 1.25 litres per minute or
  • 400 - 500ml/100g/minute

Over 90% of this supply is to the cortex, with only around 5% reaching the medulla, hence the medulla's profound sensitivity to hypoperfusion in shock states (why all really sick people get an AKI).

Why such low flow to the medulla?

  • To maintain a steady urea concentration gradient, which drives all of the water-reabsorbing machinery in the Loop of Henle and Collecting duct
  • If the blood flow were any higher, simple biophysics determines it would wash away all of that hard-earned urea

Weirdly, the hardest working bit of the kidney needs to be in a constant state of near-hypoxia in order for its machinery to actually work.

The kidneys are special

We knew that already, but tell us again why?

Because unlike any other organ, the metabolic demand of the kidney is determined in large part by the blood flow that it receives - not the other way around.

This may sound completely nonsensical, but if you think about it, the kidney's job is mostly maintaining concentration gradients and reabsorbing ions such as sodium, and these ions only need absorbing if they're being supplied and filtered by the glomerulus in the first place.

  • Muscle tissue's job is to move as much as it is told to do so, and it just has to hope it receives enough fuel and oxygen to facilitate this
  • The kidneys however are like factory workers on a production line, told to clean up whatever comes along the conveyor belt - if there's less blood supplied, there's less work to do

The very high renal blood flow that we see is actually to allow efficient filtration in the glomerulus, rather than being due to the kidneys having a particularly high metabolic demand (the renal oxygen extraction is pretty low at around 10-15% on a good day).

This means that renal oxygen extraction remains amazingly constant over a wide range of renal blood flow values

The blood is supplied via the renal artery which supplies two capillary networks

    • A high pressure glomerular network
    • A low pressure peritubular network
Image credit

What is the course of blood vessels through the kidneys?

  • Aorta
  • Renal artery
  • Segmental artery
  • Interlobar artery
  • Arcuate artery
  • Cortical radial artery
  • Afferent arteriole
  • Glomerulus
  • Efferent arteriole
  • Peritubular capillary
  • Vasa recta
  • Veins
  • Renal vein
  • IVC

Around 30 vasa recta branch off from each efferent arteriole

Autoregulation

The kidneys are not unique in their ability to regulate their own blood flow, but they have their own special graph that you need to be able to draw in the exam.

When drawing this graph, the most important part is a relatively flat line between pressures of around 75mmHg and 160mmHg

💡
Renal blood flow is stable for mean arterial blood pressures between 75 and 160 mmHg.
You can also add in GFR if you're feeling fancy

How does it work?

As with many magical aspects of physiology, we don't fully understand, however we suspect it may involve three mechanisms.

Myogenic response

  • The afferent arteriole has stretch receptors embedded within the muscle of the vessel wall
  • If it is stretched, magical mechanisms involving things like stretch-sensitive calcium channels make it contract, reducing the diameter of the lumen and increasing the resistance of the vessel
  • Ohm's law dictates that flow will therefore be adjusted nicely

This is responsible for around 50% of the autoregulatory power of the kidney and is clearly not unique to renal tissue.

Tuboglomerular feedback

  • As blood flow to the kidney increases, more blood is filtered and more sodium passes along the tubule to the macula densa
  • Increased sodium detected at the macula densa causes afferent arteriolar constriction
  • Probably using adenosine and ATP
  • This reduces flow and completes the negative feedback loop

This is unique to the kidney.

Humoral and autonomic influence

  • Vasoconstrictors such as angiotensin II and endothelin constrict the efferent arteriole, reducing renal blood flow but maintaining GFR
  • Vasodilators such as prostaglandins, bradykinin and other amino acids do the opposite
  • Sympathetic tone contributes to arteriole contraction - with slightly more afferent than efferent contraction - meaning sympathetic stimulation reduces renal blood flow slightly

This box exists largely to explain the fact that if you take away tubuloglomerular feedback and myogenic response, you still somehow get some autoregulation of blood flow.

In the exam they're looking for knowledge about the previous two mechanisms, so don't worry too much about this bit.

Tell me about GFR

Glomerular filtration rate is a process of ultrafiltration and occurs at around 125ml/min

💡
Ultrafiltration uses pressure or concentration gradient and a semipermeable membrane that will only permit molecules smaller than a certain size through.

This works out at around 180 litres per day, and the main determining factor is particle size

  • Molecules over 70 000 daltons are not filtered
  • Molecules below 7000 daltons are freely filtered
  • Negatively charged molecules are repelled by the basement membrane and therefore have a reduced filtration fraction

Glomerular filtration and tubular reabsorption of fluid and solutes can be altered by the kidneys to maintain homeostasis and remove waste products and drugs.

The principle is the same as of Starling’s forces

Starling's forces in a conventional blood vessel bed
💡
GFR = Kf (PG − PB − πG)

Where:

      • Kf = glomerular ultrafiltration coefficient
      • PG = Glomerular hydrostatic pressure
      • PB = Bowman’s capsule hydrostatic pressure
      • Ï€G = Glomerular oncotic pressure

There are other forces at play, such as the viscosity of the fluid, friction to the flow of the fluid and interstitial pressure causing compression of renal tubules, however these are generally ignored.

Syllabus

  • PB_BK_49 Structure and function, renal circulation
  • PB_BK_50 Blood flow and glomerular filtration, plasma clearance and tubulo-glomerular feedback
  • PB_BK_51 Tubular function and urine formation; transport processes
  • PB_BK_52 Assessment of renal function

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References and Further Reading

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