CorpusHuman Anatomy
UrinaryMembrane

Glomerular filtration barrier

Also known as: filtration membrane, filtration barrier, glomerular basement membrane, GBM, slit diaphragm

The three-layer sieve between glomerular blood and Bowman space — fenestrated endothelium, glomerular basement membrane and podocyte slit diaphragms — that is highly permeable to water and small solutes but restricts proteins by size and negative charge.

Overview

GBM thickness≈300–350 nm
Freely filteredRadius <≈1.8 nm (<≈7 kDa)
Normal urinary albumin<30 mg/day

1. Fenestrated capillary endothelium — pores ≈70–100 nm stop blood cells; its negatively charged glycocalyx repels anionic proteins.

2. Glomerular basement membrane (GBM) — ≈300–350 nm thick, formed by fusion of endothelial and podocyte basal laminae; a meshwork of type IV collagen (α3, α4, α5 chains), laminin, nidogen and negatively charged heparan sulfate proteoglycans.

3. Podocyte filtration slits — ≈25–40 nm gaps between interdigitating foot processes bridged by the slit diaphragm (nephrin, NEPH1, podocin, CD2AP), the final size-selective layer.

Selectivity: molecules with an effective radius <≈1.8 nm (≈<7 kDa, e.g. inulin, glucose, urea) are freely filtered; those >≈4 nm are excluded; at a given size, cationic molecules pass more easily than anionic ones. Albumin (≈66–69 kDa, radius ≈3.5 nm, negatively charged) is almost completely retained — the small amount filtered is reabsorbed by PCT endocytosis (megalin–cubilin), so normal urine contains <30 mg albumin/day.

Location

Wall of the glomerular capillaries within the renal corpuscle.

Parts & subdivisions

  1. Fenestrated endothelium
    Large pores; anionic glycocalyx.
  2. Glomerular basement membrane
    Type IV collagen, laminin, heparan sulfate; main charge barrier.
  3. Nephrin–podocin zipper; final size barrier.

Function

  • Permit high-volume filtration of water and small solutes
  • Retain plasma proteins and cells (size and charge selectivity)

Clinical significance

Alport syndrome

Mutations in type IV collagen α3/α4/α5 (usually X-linked COL4A5) produce a split, "basket-weave" GBM with haematuria, progressive kidney failure, sensorineural deafness and eye defects (anterior lenticonus). "Can't see, can't pee, can't hear a bee."

Anti-GBM (Goodpasture) disease

Autoantibodies against the NC1 domain of the α3 chain of type IV collagen in glomerular and alveolar basement membranes → rapidly progressive GN with pulmonary haemorrhage; linear IgG deposition on immunofluorescence.

Loss of charge or slit integrity

Podocyte injury (minimal change disease, FSGS) or mutations in nephrin (congenital nephrotic syndrome, Finnish type) cause nephrotic-range proteinuria.

Compiled from standard anatomy and physiology references — see the Urinary System sources. For education only; not medical advice.