Glomerular Filtration Rate Determinants
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Direct answer
Glomerular filtration rate — normally about 125 mL/min, or 180 L filtered per day of which over 99% is reabsorbed — is determined by the product of the filtration coefficient (Kf) and the net filtration pressure, which is glomerular capillary hydrostatic pressure (about 60 mmHg) minus Bowman's capsule pressure (about 18 mmHg) minus the capillary oncotic pressure (about 32 mmHg, rising along the capillary), giving roughly 10 mmHg of net drive. Afferent and efferent arteriolar tone steer both GFR and renal plasma flow: afferent constriction lowers both, while mild efferent constriction (low-dose angiotensin II) raises GFR; GFR is measured classically by inulin clearance and estimated clinically from creatinine-based equations.
What you must remember
- The numbers: GFR about 125 mL/min (women about 110), 180 L/day; urine output only 1-1.5 L/day, so more than 99% of filtrate is reabsorbed.
- Net filtration pressure arithmetic: 60 (capillary hydrostatic) − 18 (Bowman's hydrostatic) − 32 (mean oncotic) ≈ 10 mmHg; Kf is roughly 12.5 mL/min/mmHg.
- Oncotic pressure rises along the glomerulus: because about 20% of plasma water filters (filtration fraction), capillary protein concentration climbs, so filtration actually stops near the efferent end when filtration fraction is high.
- Arteriolar rules: afferent constriction (sympathetic, endothelin, adenosine) drops GFR and RPF; efferent constriction (angiotensin II at low levels) raises GFR while dropping RPF — hence filtration fraction rises; high-dose angiotensin II constricts enough to drop GFR too.
- Renal plasma flow's permissive role: high flow washes off the rising oncotic pressure and sustains GFR; low flow (hypovolaemia) lets oncotic pressure climb and filtration stalls.
- Pathologic determinants: Kf falls in glomerulonephritis (immune injury, foot-process fusion) and chronic diabetes; Bowman's pressure rises with ureteric obstruction; plasma oncotic pressure rises with dehydration or multiple myeloma proteins.
- Measurement: inulin clearance is the gold standard (freely filtered, neither reabsorbed nor secreted); creatinine clearance slightly overestimates GFR due to tubular secretion; clinical practice reports estimated GFR (Cockcroft-Gault, CKD-EPI) with serum creatinine.
How to work through a falling GFR
Trace a patient with prostatic obstruction: back-pressure raises Bowman's capsule hydrostatic pressure, the net filtration pressure falls towards zero, and GFR drops — relieving the obstruction restores it, which is why post-obstructive diuresis follows once the tubules recover their handling of the 180 L they suddenly see again. Now trace hypovolaemia: sympathetic tone constricts the afferent arteriole, capillary hydrostatic pressure falls, and the renin-angiotensin system simultaneously constricts the efferent arteriole, partially defending GFR — the very mechanism an ACE inhibitor removes, explaining the small creatinine rise (up to about 30% is tolerated) when such a patient starts the drug, and the acute kidney injury when both prostaglandin-mediated afferent dilation (NSAIDs) and angiotensin II efferent constriction (ACE inhibitors) are removed in a volume-depleted patient. The triple-whammy of NSAID plus ACE inhibitor plus diuretic in an elderly dehydrated patient is applied Starling physiology at its purest.
Finally, interpret the creatinine curve with respect for the tubular secretory component: a serum creatinine doubling from 0.8 to 1.6 mg/dL does not mean GFR has merely halved — it represents a loss of well over half of GFR, because secretion masks early decline; this non-linear relationship is why eGFR equations, not raw creatinine, stage chronic kidney disease.
Where students slip
Two errors recur. First, students treat oncotic pressure as a fixed 32 mmHg; it is the average, rising steeply along the glomerular capillary as protein-free fluid leaves, and this dynamic is exactly why filtration fraction (normally 0.2, the ratio of GFR 125 to RPF 625 mL/min) cannot rise indefinitely. Second, the efferent effect is memorised backwards: mild angiotensin II retains filtration by holding capillary pressure up when the afferent side is threatened — a defence, not a threat — until the dose is high enough to strangle flow. In viva, expect the follow-up on why inulin and not glucose or PAH: glucose is reabsorbed (clearance near zero), PAH is secreted (clearance measures RPF, about 625 mL/min), and only inulin satisfies all three criteria of free filtration with no transport.
Frequently asked questions
What is the normal GFR and how much filtrate forms daily?
About 125 mL/min, roughly 180 L per day, of which over 99% is reabsorbed leaving 1-1.5 L of urine — a favourite arithmetic in physiology examinations.
Which Starling force is unique to the glomerulus compared with systemic capillaries?
There is no meaningful interstitial oncotic term, but the key difference is the low Bowman's capsule hydrostatic pressure (about 18 mmHg) and filtration occurring along the whole capillary with a rising plasma oncotic pressure.
How does afferent differ from efferent constriction in effect?
Afferent constriction lowers both GFR and renal plasma flow; efferent constriction raises GFR at mild degrees (higher capillary pressure) while lowering plasma flow, so filtration fraction rises.
Why does creatinine clearance overestimate GFR?
Creatinine is not only filtered but also secreted by the proximal tubule, adding perhaps 10-20% to the collected amount, whereas inulin is filtered with no transport either way.
Why can ACE inhibitors trigger acute kidney injury in renal artery stenosis?
The stenotic kidney depends on efferent arteriolar angiotensin II to maintain glomerular capillary pressure; blocking it drops the net filtration pressure and GFR abruptly — bilateral stenosis or a single functioning kidney makes this clinically overt.