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Physiology · Renal, fluids and acid–base

Glomerular filtration: the barrier and its determinants !

  • Mechanism
  • Exam priority: high

The kidneys filter about 180 litres of plasma a day. How much they filter depends on pressures in the glomerulus and the tone of its two arterioles.

Updated 2026-11-01

Also called: Glomerular filtration rate, GFR

See it in 3D: Kidneys · Vessels inside the kidney

What it is

Glomerular filtration is the movement of cell-free, nearly protein-free plasma from the glomerular capillary into Bowman's capsule. Starling forces drive it, and the tone of the afferent (inflow) and efferent (outflow) arterioles regulates it. It is the first step in urine formation and the best overall measure of kidney function.

How it works, step by step

  1. Plasma enters through the afferent arteriole into a capillary with high hydrostatic pressure (≈ 60 mmHg), far above other capillaries.
  2. That pressure pushes fluid through the fenestrated endothelium, the basement membrane and the slits between podocytes.
  3. Bowman's capsule pressure (≈ 18 mmHg) and plasma oncotic pressure (≈ 32 mmHg on average) oppose it.
  4. Net filtration pressure (≈ 10 mmHg) times the filtration coefficient (Kf) gives GFR.
  5. Along the capillary, protein becomes concentrated, oncotic pressure rises and filtration slows toward the efferent end.
  6. The tone of the two arterioles sets glomerular pressure, so the kidney adjusts GFR without changing arterial pressure.

The nephron: segments, transporters and diuretics

The nephron: segments, transporters and diuretics CortexOuter medullaInner medulla3006009001200mOsm/kgUrineGlomerulusProximal tubuleDistal tubuleThin descendingThin ascendingThick ascendingCollecting ductJuxtaglomerularapparatusNHE3 · SGLT2Filters ≈ 180 L/dayAQP1Passive NaClNKCC2 · ROMKParacellular Ca²⁺, Mg²⁺NCC · Ca²⁺ (PTH)ENaC · ROMK/BKAQP2 (ADH)α: H⁺-ATPase · β: pendrin

Glomerulus and Bowman capsule Filters ≈ 180 L/day · GFR ≈ 125 mL/min

Glomerulus and Bowman capsule

  • What it does: Filters plasma: ≈ 180 L/day (GFR ≈ 125 mL/min), filtration fraction ≈ 20%. The barrier (fenestrated endothelium, negatively charged basement membrane and podocytes with slit diaphragms) lets water and small solutes through, not cells or most proteins.
  • Transporters: No transporters: Starling forces drive it (capillary hydrostatic pressure for; capsule pressure and plasma oncotic pressure against).
  • Hormones: Ang II constricts the efferent arteriole more (holds GFR up); prostaglandins dilate the afferent; autoregulation (myogenic and tubuloglomerular feedback) keeps GFR steady.
  • Drugs: NSAIDs (afferent constriction) and ACE inhibitors or ARBs (efferent dilation) can lower GFR.
  • Disorders: Nephritic syndrome (hematuria, inflammation) and nephrotic syndrome (proteinuria > 3.5 g/day, podocyte injury).
  • Glomerulus and arterioles
  • Proximal tubule
  • Thin descending limb
  • Thin ascending limb
  • Thick ascending limb
  • Distal convoluted tubule
  • Collecting tubule and duct
  • Juxtaglomerular apparatus (macula densa)
  • Cortex
  • Medulla
  • Interstitial osmolality (≈ 300 → 1200 mOsm/kg)
Illustrative schematic drawn by Durgical (a long-loop juxtamedullary nephron); proportions and percentages are approximate and not for clinical decisions.

Equations

Glomerular filtration (Starling)GFR = Kf × [(PGC − PBS) − (πGC − πBS)]
Kf
filtration coefficient (permeability × area)
PGC
glomerular capillary hydrostatic pressure
PBS
Bowman's space hydrostatic pressure
πGC
glomerular plasma oncotic pressure
πBS
filtrate oncotic pressure (≈ 0)

Every cause of a change in GFR acts on one of these terms.

Filtration fractionFF = GFR / RPF
RPF
renal plasma flow (≈ 625 mL/min)

Rises when the efferent constricts (angiotensin II) and the blood leaving the glomerulus is more concentrated in protein.

Reference values (young adult)

ParameterValueNote
GFR≈ 125 mL/min≈ 180 L/day; falls with age
Renal plasma flow≈ 625 mL/min
Filtration fraction≈ 0.2 (20%)
Glomerular capillary pressure≈ 60 mmHg
Net filtration pressure≈ 10 mmHg

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

What happens to GFR

ChangeStarling termGFRRenal flow
Afferent constriction (NSAIDs, sympathetic)↓ P_GC↓↓
Efferent constriction (angiotensin II)↑ P_GC↑ (modest)↓
Efferent dilation (ACE inhibitors, ARBs)↓ P_GC↓↑
Ureteral or stone obstruction↑ P_BS↓≈
Hypoalbuminemia↓ π_GC↑ (slight)≈
Nephron loss (CKD)↓ K_f↓↓

Clinical notes

  • Prerenal acute kidney injury: hypovolemia plus an NSAID plus an ACE inhibitor/ARB removes afferent dilation and efferent constriction at once (the 'triple whammy' when a diuretic is added).
  • Nephrotic syndrome: podocyte injury lets albumin through (proteinuria > 3.5 g/day) with edema and hypoalbuminemia.
  • Creatinine rises little until about half of GFR is lost, so a 'normal' creatinine does not rule out reduced GFR.

Test yourself

Think of the answer, then tap the question to see it.

Why can an ACE inhibitor raise creatinine in a patient with bilateral renal artery stenosis?

With low inflow pressure, GFR depends on angiotensin II constricting the efferent. Blocking it dilates the efferent, glomerular pressure falls and GFR drops.

What happens to GFR and filtration fraction if only the efferent arteriole constricts?

Glomerular capillary pressure rises, so GFR increases (modestly) while plasma flow falls, and the filtration fraction rises.

Why is an NSAID dangerous in a dehydrated patient?

In hypovolemia, prostaglandins keep the afferent arteriole dilated. The NSAID blocks them, the afferent constricts, glomerular pressure falls and acute kidney injury can follow.

Which Starling force changes first in a ureteral obstruction?

Bowman's space hydrostatic pressure: retained urine raises it, it opposes filtration and GFR falls.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 25.5 Physiology of Urine Formation (OpenStax (Rice University), 2022); Acute Kidney Injury (StatPearls (NCBI Bookshelf), 2024); Chronic Kidney Disease (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 27). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.