glomerulus
Summary
The glomerulus is the tuft of capillaries in the kidney where blood filtration begins, forming the initial step of urine production. It is surrounded by Bowman's capsule and filters plasma based on size and charge selectivity, producing an ultrafiltrate that enters the nephron tubule. It is a key structure affected in many renal diseases, both nephritic and nephrotic.
Detail
The glomerulus is a network of fenestrated capillaries supplied by the afferent arteriole and drained by the efferent arteriole, both within the renal cortex. It sits within Bowman's capsule, and together with the capsule forms the renal corpuscle. The filtration barrier consists of three layers: (1) fenestrated capillary endothelium (restricts blood cells), (2) glomerular basement membrane (GBM) composed of type IV collagen and heparan sulfate proteoglycans (restricts based on size and negative charge), and (3) podocyte foot processes with slit diaphragms containing nephrin (restricts based on size). This barrier normally allows filtration of water, ions, glucose, and small proteins while retaining albumin and larger proteins and blood cells.
Mesangial cells, located between capillary loops, provide structural support, phagocytic function, and contractile ability to regulate glomerular filtration rate (GFR) by altering capillary surface area. Filtration is driven by Starling forces: glomerular capillary hydrostatic pressure promotes filtration, while Bowman's capsule hydrostatic pressure and glomerular oncotic pressure oppose it. GFR can be estimated clinically using creatinine clearance or biomarkers like cystatin C.
Clinically, glomerular diseases are broadly categorized into nephritic syndromes (characterized by hematuria, RBC casts, hypertension, and mild-moderate proteinuria, e.g., IgA nephropathy, post-streptococcal GN, lupus nephritis, Goodpasture syndrome, ANCA vasculitides) and nephrotic syndromes (characterized by heavy proteinuria >3.5g/day, hypoalbuminemia, edema, hyperlipidemia; e.g., minimal change disease, FSGS, membranous nephropathy, diabetic nephropathy, amyloidosis). Damage can occur due to immune complex deposition, complement activation, autoantibodies (e.g., anti-GBM, anti-PLA2R), metabolic injury (diabetes), or genetic defects (e.g., Alport syndrome affecting type IV collagen). Renal biopsy with light microscopy, immunofluorescence, and electron microscopy is often used to characterize glomerular pathology and guide treatment.
Sources
- Guyton and Hall Textbook of Medical Physiology
- Robbins and Cotran Pathologic Basis of Disease
- First Aid for the USMLE Step 1
- Costanzo Physiology
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