Glomerular filtration barrier: charge selectivity and albumin
The barrier that filters blood in the glomerulus largely holds albumin back by size and charge, the main charge barrier thought to be its basement membrane (a thin protein meshwork).
Remember
The negatively charged basement membrane repels negatively charged albumin and helps keep it in the blood. Pressure drives filtration but does not decide which proteins cross.
Memory aid
windows, wall, sieve
Remember the layers in the order blood meets them: the windows (fenestrae), the charged wall (basement membrane) and the sieve (podocyte slits).
Blood in the glomerulus is filtered through three layers in turn. The first is the fenestrated endothelium (the capillary lining, perforated by small windows called fenestrae), which holds back blood cells and the largest proteins. The second is the basement membrane (a thin protein meshwork lying between the capillary and the podocytes). Last come the podocytes (cells whose finger-like foot processes leave narrow gaps called filtration slits).
The windows and the slits act mainly as sieves, and a sieve works by size. The basement membrane is thought to block medium-to-large proteins by size too. Albumin, the main plasma protein, is kept in the blood by charge as well. The basement membrane is thought to carry a net negative charge, attributed to its anionic (negatively charged) proteoglycans, which are proteins with long sugar-based chains attached. Albumin is negatively charged too, and like charges push each other apart, so the membrane repels it.
The result is an ultrafiltrate, meaning plasma water and small solutes such as glucose with almost no protein, which enters Bowman’s space (the cup-shaped space around the glomerulus). The barrier largely holds albumin back, and a small amount can still cross.
Hydrostatic pressure (the pressure of blood against the capillary wall) drives fluid and small solutes across the barrier, but it does not decide which molecules cross.
When the charge barrier is damaged, albumin escapes into the urine, a state called albuminuria. If too much albumin is lost in the urine, oncotic pressure (the pull that plasma proteins exert on water) falls and fluid can leak into the tissues, producing oedema (swelling).
Key facts
- Order of layers
- blood meets the windows (fenestrae), then the negatively charged basement membrane, then the podocyte sieve.
- Charge barrier
- the basement membrane is thought to carry a net negative charge that repels negatively charged albumin and helps keep it in the blood.
- Size barrier
- the fenestrae and filtration slits hold back blood cells and the largest proteins, and the basement membrane is thought to block medium-to-large proteins by size too.
- Pressure
- hydrostatic pressure drives fluid out of the capillary but does not decide which molecules cross.
- If the charge is lost
- albumin would cross more easily, even when pressure and pore size are unchanged.
- Why albumin loss matters
- if too much albumin is lost in the urine, blood oncotic pressure falls and this can lead to oedema.
Exam traps
- Hydrostatic pressure in the capillaries drives fluid across the barrier, but it does not select which molecules cross, so it cannot explain why albumin is held back.
- The podocyte slits are a real part of the barrier, but they act as a sieve by size, whereas the main charge-based repulsion of negatively charged albumin comes from the charged basement membrane.
- The fenestrae let water and small solutes through and hold back blood cells and the largest proteins, but they are not the main barrier to negatively charged albumin, because the main structure adding charge-based repulsion is the basement membrane.
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