Afferent vs efferent arteriole: GFR, RPF and filtration fraction
Two resistors set the pressure in the glomerulus. Learn the 2×2 table of afferent and efferent constriction and dilation, and use it to explain NSAID and ACE inhibitor kidney injury.
Chapters (8)
Predict the change in GFR, renal plasma flow and filtration fraction with afferent or efferent arteriolar constriction or dilation, for example with NSAIDs and ACE inhibitors.
The short version
- Afferent changes move GFR and RPF in the same direction, so filtration fraction stays about the same.
- Efferent changes move GFR and RPF in opposite directions, so filtration fraction changes.
- Filtration fraction is GFR divided by RPF, normally about 0.20.
- NSAIDs block prostaglandins and so constrict the afferent arteriole: GFR and RPF fall.
- ACE inhibitors and ARBs remove angiotensin II, so the efferent arteriole dilates: GFR falls, RPF rises and filtration fraction falls.
One tiny vessel, one creatinine jump
A man with long-standing high blood pressure starts an ACE inhibitor. Ten days later his creatinine has climbed from 1.0 to 2.2 mg/dL. The drug did that by relaxing one tiny vessel in the kidney.
This lesson covers the afferent vs efferent arteriole question: how each vessel changes GFR, renal plasma flow (RPF) and filtration fraction.[1][2]
What sets GFR: the afferent and efferent arterioles
The arterioles change GFR mainly by changing the hydrostatic pressure inside the glomerular capillary. Two resistors set that pressure: the afferent arteriole before the glomerulus, and the efferent arteriole after it.[1][2]
- Tighten the afferent arteriole and pressure in the glomerulus falls, so less flows in and less is pushed through.
- Tighten the efferent arteriole and pressure in the glomerulus rises, so more is pushed through, but less flows in overall.
GFR, RPF and filtration fraction
Normal GFR is about 125 mL/min. Renal plasma flow (RPF) is the plasma entering the kidneys, about 625 mL/min in this lesson. Textbooks give about 600–700.
the share of incoming plasma that is filtered; normally about 0.20 (125 / 625).[2][6]
The 2×2 table: afferent vs efferent, constriction vs dilation
| Constriction | Dilation | |
|---|---|---|
| Afferent | GFR ↓, RPF ↓, FF about unchanged | GFR ↑, RPF ↑, FF about unchanged |
| Efferent | GFR ↑ modestly (↓ if severe), RPF ↓, FF ↑ | GFR ↓, RPF ↑, FF ↓ |
With afferent constriction, pressure falls, GFR falls and RPF falls with it. Both drop together, so filtration fraction stays about the same. Afferent dilation does the opposite.[1][2] The filtration fraction rows follow from FF = GFR / RPF: when numerator and denominator move together FF holds, when they move apart FF changes.
With efferent constriction, pressure builds, so GFR rises modestly, but blood is dammed back and RPF falls. GFR up and RPF down means filtration fraction rises. Squeeze too hard and the flow loss wins, so GFR falls as well. Efferent dilation reverses this: pressure falls, GFR falls, RPF rises and filtration fraction falls.[1][2]
Angiotensin II, sympathetic drive and a worked example
Angiotensin II preferentially constricts the efferent arteriole, defending GFR.[3] Strong sympathetic drive constricts mainly the afferent arteriole, so GFR and RPF both fall.
- Normal: GFR 125, RPF 625, FF = 125 / 625 = 0.20
- Efferent constriction: GFR rises to 135, RPF drops to 500
- FF = 135 / 500 = 0.27, so filtration fraction is up
Prostaglandins, NSAIDs, ACE inhibitors and renal artery stenosis
Prostaglandins dilate the afferent arteriole, and they matter most when angiotensin II and sympathetic tone are high. An NSAID blocks them, so the afferent arteriole constricts and GFR and RPF fall. Volume depletion, heart failure and cirrhosis make this dangerous.[4][5]
An ACE inhibitor or an ARB removes angiotensin II, so the efferent arteriole dilates: GFR falls, RPF rises and filtration fraction falls.[1][3]
With a narrowed renal artery in both kidneys, or in a solitary functioning kidney, GFR leans on that efferent tone. Take it away and creatinine jumps, which could be the man in the opening case.[3]
Practice question
Original · USMLE styleA 71-year-old man with heart failure and osteoarthritis comes to the physician because of fatigue and decreased urine output for 4 days. His medications are lisinopril, furosemide, and, for the past week, ibuprofen 800 mg three times daily for knee pain. Temperature is 36.8 C (98.2 F), pulse is 98/min, respirations are 16/min, and blood pressure is 102/64 mm Hg. Mucous membranes are dry. Serum creatinine is 1.8 mg/dL; it was 1.1 mg/dL 3 months ago. Three months ago he took part in a renal physiology research study; measurements then and now are shown.
| Glomerular filtration rate, 3 months ago | 90 mL/min |
|---|---|
| Glomerular filtration rate, now | 54 mL/min |
| Renal plasma flow, 3 months ago | 450 mL/min |
| Renal plasma flow, now | 270 mL/min |
Common questions
How do afferent and efferent arterioles affect GFR?
Afferent constriction and efferent dilation lower GFR. Afferent dilation and efferent constriction (modest) raise it, because the arterioles set the pressure inside the glomerular capillary.
What is filtration fraction and what is its normal value?
Filtration fraction is GFR divided by RPF, the share of incoming plasma that is filtered. It is normally about 0.20.
Why do NSAIDs lower GFR?
NSAIDs block prostaglandins, which dilate the afferent arteriole. The afferent arteriole constricts, so GFR and RPF fall, most dangerously in volume depletion, heart failure and cirrhosis.
Why can an ACE inhibitor raise creatinine?
An ACE inhibitor removes angiotensin II, so the efferent arteriole dilates and GFR falls. With narrowed renal arteries in both kidneys, or in a solitary functioning kidney, GFR leans on that efferent tone and creatinine can jump.
Transcript
Read the full narration, by chapter584 words
0:00A creatinine jump after an ACE inhibitor
A man with long-standing high blood pressure starts an ACE inhibitor. Ten days later, his creatinine has climbed from 1.0 to 2.2 milligrams per decilitre. The drug did that by relaxing one tiny vessel in the kidney. Today: how the afferent and efferent arterioles change GFR, renal plasma flow, and filtration fraction.
0:25What sets the GFR: the afferent and efferent arterioles
Last time, GFR depended on the hydrostatic pressure inside the glomerular capillary. Two resistors set that pressure: the afferent arteriole before the glomerulus, and the efferent arteriole after it. Tighten the afferent arteriole, and pressure in the glomerulus falls, so less flows in and less is pushed through. Tighten the efferent arteriole, and pressure in the glomerulus rises, so more is pushed through, but less flows in overall.
0:54GFR, RPF and filtration fraction
Normal GFR is about 125 mL per minute. Renal plasma flow, RPF, is the plasma entering the kidneys, about 625. Filtration fraction is GFR divided by RPF, the share of incoming plasma that is filtered. Normally about 0.2.
1:16The 2x2 table: afferent vs efferent, constriction vs dilation
Afferent constriction: pressure falls, GFR falls, and RPF falls with it. Both drop together, so filtration fraction stays about the same. Afferent dilation does the opposite: GFR up, RPF up, filtration fraction about unchanged. Efferent constriction: pressure builds, so GFR rises modestly, but blood is dammed back, so RPF falls. GFR up and RPF down means filtration fraction rises. Squeeze too hard and the flow loss wins, so GFR falls as well. Efferent dilation: pressure falls, GFR falls, RPF rises, and filtration fraction falls. The rule: the afferent moves GFR and RPF together. The efferent moves them in opposite directions.
2:11Angiotensin II, a worked example and sympathetic drive
Let's run it. Angiotensin II preferentially constricts the efferent arteriole, defending GFR. Say GFR becomes 135 and RPF drops to 500. One 35 over 500 is 0.27: filtration fraction is up. Strong sympathetic drive constricts mainly the afferent arteriole, so GFR and RPF both fall. Prostaglandins dilate the afferent arteriole, and they matter most when angiotensin II and sympathetic tone are high.
2:47Prostaglandins, NSAIDs, ACE inhibitors and renal artery stenosis
An NSAID blocks them, so the afferent arteriole constricts: GFR and RPF fall. Volume depletion, heart failure and cirrhosis make this dangerous. An ACE inhibitor or an ARB removes angiotensin II, so the efferent arteriole dilates: GFR falls, RPF rises, filtration fraction falls. With a narrowed renal artery in both kidneys, or in a solitary functioning kidney, GFR leans on that efferent tone. Take it away, and creatinine jumps. That could be our man.
3:25Practice question
Your turn. A 71-year-old man with heart failure takes lisinopril, furosemide, and, for knee pain, ibuprofen. He is dry, with low urine output, and his creatinine has risen sharply. In an earlier study, GFR was 90, RPF 450. Now GFR is 54, and RPF is 270. Which change in arteriolar resistance best explains this? A, afferent dilation. B, efferent constriction. C, efferent dilation. D, afferent constriction. E, a lower filtration coefficient. Pause here and decide. Both values fell by 40%, so filtration fraction stayed at 0.2. A is out: afferent dilation raises GFR and RPF. B is out: efferent constriction would raise filtration fraction. C is out: the lisinopril would drop GFR, but RPF would rise, not fall. E is out: a lower filtration coefficient cuts GFR, but plasma entering stays the same. So the answer is D: afferent constriction, from the ibuprofen.
4:46High-yield recap and next lesson
Three things to keep. One: afferent changes move GFR and RPF together; efferent changes move them apart. Two: NSAI Ds constrict the afferent; ACE inhibitors dilate the efferent. Three: filtration fraction is GFR over RPF, normally about 0.2. Next up: renal clearance, which measures GFR and RPF.
Sources
Numbers in the text, e.g. [1], point here- Boundless Anatomy and Physiology, 24.3C Regulation of Glomerular Filtration Rate. LibreTexts. med.libretexts.org/Bookshelves/Anatomy_and_Physiology/Anatomy_and_Physiology_(Boundless)/24:__Urinary_System/24.3:_Physiology_of_the_Kidneys/24.3C:_Regulation_of_Glomerular_Filtration_Rate
- LITFL Primary Exam, 2018A Q09 (afferent and efferent arteriolar tone, filtration fraction). partone.litfl.com/exams/2018A/2018A09.html
- Textor SC. Renal Arterial Disease and Hypertension: ACE inhibitors, ARBs and GFR dependence on angiotensin II. Clin J Am Soc Nephrol 2014. pmc.ncbi.nlm.nih.gov/articles/PMC4046729
- Whelton A. Nephrotoxicity of nonsteroidal anti-inflammatory drugs: physiologic foundations and clinical implications. Am J Med 1999;106(5B):13S-24S. pubmed.ncbi.nlm.nih.gov/10390124/
- Whelton A, Hamilton CW. Nonsteroidal anti-inflammatory drugs: effects on kidney function. J Clin Pharmacol 1991. pubmed.ncbi.nlm.nih.gov/1894754/
- Filtration fraction. Wikipedia (definition and the usual value of about 20%). en.wikipedia.org/wiki/Filtration_fraction
Textbooks give a normal RPF of about 600-700 mL/min; the lesson uses 625 so that FF = 125 / 625 = 0.20. Example values are illustrative.
The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.
Image credits. All video diagrams are original; no third-party artwork is used in the video. Example values are illustrative. Thumbnail plate (nephron): Servier Medical Art (smart.servier.com), CC BY 4.0, adapted (recoloured, resized).
Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-REN-024.
For exam study only, not medical advice. Read the medical disclaimer.
In this series
Playlist on YouTube- EP 01GFR and Starling forces at the glomerulus5:25
- EP 02Afferent vs efferent arteriole: GFR, RPF and filtration fraction5:16
- EP 03Renal clearance: inulin, creatinine and PAH5:20
- EP 04Glucose transport maximum, splay and SGLT24:55
- EP 05Countercurrent multiplier: how the kidney concentrates urine5:02
- EP 06Aldosterone and ADH in the distal nephron5:20
- EP 07Diuretics by nephron segment: loop, thiazide and more5:53
- EP 08RAAS explained: renin, angiotensin II and aldosterone5:23