Physiology chapters
Glomerular filtration
The nephron and the steps of urine formation, the layers and charge of the filtration membrane, the pressures that drive filtration, the filtration fraction, and how angiotensin II and the arterioles control GFR.
- Urine forms in three steps: glomerular filtration, tubular reabsorption and tubular secretion; normal GFR is about 125 mL/min (180 L/day).
- The filtration membrane (fenestrated endothelium, basement membrane, podocytes) blocks cells and most proteins; its negative charge repels albumin.
- Net filtration pressure (about 10 mmHg) = glomerular hydrostatic pressure − Bowman's capsule pressure − glomerular oncotic pressure; angiotensin II constricts mainly the efferent arteriole and helps keep GFR up.
On this page
Overview
The kidneys clean the blood, control water and salt balance, help control blood pressure and acid-base balance, and make hormones (erythropoietin, renin, active vitamin D).
Each kidney has about one million nephrons. Urine formation starts with filtration of plasma at the glomerulus.
The nephron
A nephron has two parts:
- Glomerulus: a tuft of capillaries inside Bowman's capsule, where plasma is filtered.
- Tubule: proximal tubule → loop of Henle → distal tubule → collecting duct, where the filtrate is modified.
| Type | Share | Features |
|---|---|---|
| Cortical nephrons | About 70–80% | Glomeruli in the outer cortex; short loops of Henle; surrounded by peritubular capillaries |
| Juxtamedullary nephrons | About 20–30% | Glomeruli near the medulla; long loops deep into the medulla; supplied by the vasa recta; key for concentrating urine |
The juxtaglomerular apparatus is where the distal tubule touches its own glomerulus. It includes the macula densa (sensing NaCl in the tubule) and the juxtaglomerular cells in the afferent arteriole (making renin).
Steps in urine formation
- Glomerular filtration: plasma (without cells and most proteins) passes into Bowman's capsule.
- Tubular reabsorption: useful substances and most water return to the blood.
- Tubular secretion: some substances move from the blood into the tubule.
Amount excreted = filtered − reabsorbed + secreted.
Glucose and amino acids are filtered and almost completely reabsorbed. Creatinine is filtered and not reabsorbed (a little secreted). Para-aminohippuric acid (PAH) is filtered and strongly secreted.
Renal blood flow
The kidneys receive about 20–25% of cardiac output (about 1,100–1,250 mL/min), far more than their size needs, because blood flow drives filtration.
The blood passes through two capillary beds in series: the high-pressure glomerular capillaries (filtration) and the low-pressure peritubular capillaries (reabsorption), separated by the efferent arteriole.
The filtration membrane
Three layers:
- Fenestrated capillary endothelium: large pores; stops cells.
- Basement membrane: a mesh of collagen and negatively charged proteoglycans.
- Podocytes of Bowman's capsule: their foot processes leave filtration slits covered by a slit diaphragm.
What gets through depends on:
- Size: small molecules pass freely; molecules about the size of albumin are mostly held back.
- Charge: negatively charged molecules are repelled by the negative charge of the membrane.
Albumin is small enough to pass partly, but it is negatively charged and is repelled by the negative charges of the membrane. Loss of these charges (minimal change disease) causes proteinuria.
Forces of filtration
| Force | Approx. value | Effect |
|---|---|---|
| Glomerular capillary hydrostatic pressure | About 60 mmHg | Favours filtration |
| Bowman's capsule hydrostatic pressure | About 18 mmHg | Opposes |
| Glomerular capillary oncotic pressure | About 32 mmHg (average) | Opposes |
| Bowman's capsule oncotic pressure | About 0 | - |
Net filtration pressure = 60 − 18 − 32 = about 10 mmHg.
GFR = net filtration pressure × filtration coefficient (Kf). Kf is very high in glomeruli because the membrane is thin and its area large.
Normal GFR is about 125 mL/min, or 180 L/day. Because the plasma volume is about 3 L, the whole plasma is filtered about 60 times a day.
Filtration fraction
Filtration fraction = GFR ÷ renal plasma flow ≈ 125 ÷ 650 ≈ 0.2 (20%).
As blood moves along the glomerulus and plasma is filtered, protein becomes more concentrated, so oncotic pressure rises along the capillary.
Factors that change GFR
| Change | Effect on GFR |
|---|---|
| Afferent arteriole constriction | Falls (less pressure in the glomerulus); renal blood flow falls |
| Afferent arteriole dilation | Rises |
| Efferent arteriole constriction (moderate) | Rises (blood backs up into the glomerulus); renal blood flow falls; filtration fraction rises |
| Severe efferent constriction | Falls (oncotic pressure rises too much) |
| Raised Bowman's pressure (urinary obstruction) | Falls |
| Raised plasma oncotic pressure (dehydration) | Falls |
| Reduced Kf (glomerular disease, diabetes, hypertension) | Falls |
Constricting the efferent arteriole raises GFR (moderately) while lowering renal blood flow. Constricting the afferent arteriole lowers both.
Angiotensin II
When blood pressure or volume falls, renin is released and angiotensin II is formed.
Angiotensin II constricts efferent arterioles more than afferent arterioles. This keeps glomerular pressure and GFR up while renal blood flow is reduced. It also increases sodium reabsorption and aldosterone release.
ACE inhibitors and angiotensin receptor blockers dilate the efferent arteriole and can reduce GFR, especially with bilateral renal artery stenosis, where GFR depends on angiotensin II.
Prostaglandins dilate the afferent arteriole. NSAIDs block them and can lower GFR in people with poor kidney perfusion.
Autoregulation
GFR and renal blood flow stay fairly constant when mean arterial pressure varies between about 75 and 160 mmHg. Two mechanisms:
- Myogenic response: when pressure rises, the afferent arteriole wall is stretched and constricts.
- Tubuloglomerular feedback: if GFR rises, more NaCl reaches the macula densa, which signals the afferent arteriole to constrict (and less renin to be released), bringing GFR back down. If GFR falls, the opposite happens.
Clinical relevance
Acute kidney injury from low perfusion
How it happens: dehydration, bleeding or shock lower glomerular pressure; NSAIDs and ACE inhibitors make it worse.
What you see: falling urine output and rising creatinine.
Nephrotic syndrome
How it happens: damage to the filtration barrier (podocytes and charge).
What you see: heavy proteinuria, low albumin, oedema and high cholesterol.
Expect: renal blood flow as a share of cardiac output, normal GFR and filtration fraction, the layers and charge barrier of the membrane, the Starling forces and net filtration pressure, the effect of afferent vs efferent constriction, the action of angiotensin II, and the two mechanisms of autoregulation.
Quick revision
- Kidneys receive 20–25% of cardiac output.
- GFR about 125 mL/min (180 L/day); filtration fraction about 20%.
- Net filtration pressure about 10 mmHg (60 − 18 − 32).
- Membrane: fenestrated endothelium, negatively charged basement membrane, podocytes.
- Afferent constriction: GFR falls. Efferent constriction: GFR rises, FF rises.
- Angiotensin II constricts efferent more than afferent.
- Autoregulation: myogenic + tubuloglomerular feedback (macula densa).
Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).
FAQ
What is the normal glomerular filtration rate?
About 125 mL/min, or about 180 litres a day.
What is the filtration fraction?
The proportion of renal plasma flow that is filtered at the glomerulus, normally about 20%.
Why is albumin normally kept out of the filtrate?
Its size is near the limit of the pores and its negative charge is repelled by the negative charges of the glomerular membrane.
How does angiotensin II affect GFR?
It constricts the efferent arteriole more than the afferent, helping to maintain GFR when blood pressure falls.