Glomerulus
Glomerulus renalis
Also known as: glomerular capillaries, glomerular tuft
A tuft of highly permeable, fenestrated capillaries interposed between the afferent and efferent arterioles, where ≈20% of the plasma entering is filtered at high pressure into the glomerular capsule.
Overview
The afferent arteriole divides into ≈5–8 lobules of anastomosing capillary loops that reunite to form the efferent arteriole. Glomerular capillaries differ from other capillaries in three ways: they have large fenestrae (≈70–100 nm) without diaphragms; they sit at a high hydrostatic pressure (≈55–60 mmHg) because they lie between two resistance vessels; and they are supported internally by mesangium and covered externally by podocytes whose filtration slits complete the barrier.
The glomerulus filters ≈125 mL of plasma per minute (both kidneys). The filtrate is essentially protein-free plasma: water, electrolytes, glucose, amino acids, urea and other small solutes (<≈7 kDa) pass freely, while albumin (≈66 kDa, negatively charged) and cells are retained. Glomerular diseases ("glomerulonephritis", "glomerulopathy") are a major cause of CKD and present as nephritic or nephrotic syndromes.
- Location
Within the renal corpuscle, renal cortex.
Anatomy
- Arterial supply
Afferent arteriole in; efferent arteriole out (arteriole–capillary–arteriole arrangement).
- Histology
Fenestrated endothelium with a negatively charged glycocalyx, thick glomerular basement membrane (≈300–350 nm), podocytes with interdigitating foot processes, mesangial cells and matrix between capillaries.
Function
- Plasma ultrafiltration (GFR ≈125 mL/min, ≈180 L/day)
- Retention of plasma proteins and blood cells
- Physiology
NFP ≈10 mmHg (P_GC ≈55 − P_BS ≈15 − π_GC ≈30); filtration fraction ≈20%.
Clinical significance
Glomerulonephritis
Immune-mediated glomerular injury: immune complexes (post-streptococcal, lupus, IgA), anti-GBM antibodies (Goodpasture) or pauci-immune ANCA vasculitis. Inflammation produces nephritic features (haematuria, red-cell casts, hypertension), while podocytopathies produce nephrotic proteinuria.
Diabetic nephropathy
Hyperfiltration, GBM thickening, mesangial expansion and nodular Kimmelstiel–Wilson lesions; first sign is moderately increased albuminuria (30–300 mg/g). The commonest cause of end-stage kidney disease.
Compiled from standard anatomy and physiology references — see the Urinary System sources. For education only; not medical advice.