Anaes · Applied cardiovascular & respiratory physiology
Renal: GFR & tubular function
Also known as Glomerular filtration rate · Filtration fraction · Clearance · Tubuloglomerular feedback · Proximal tubule · NHE3
The kidney filters plasma at the glomerulus and then selectively reabsorbs and secretes along the nephron, and the glomerular filtration rate (about 125 mL per minute) is the single best measure of kidney function. The framework rests on five exam-critical ideas: GFR is normally about 125 mL per minute and the filtration fraction (GFR over renal plasma flow) is about 20 percent, set by the balance of Starling forces across the glomerular capillary and the relative tone of the afferent and efferent arterioles; GFR is held constant across a range of blood pressures by autoregulation (myogenic and tubuloglomerular feedback from the macula densa); the clearance of a freely filtered, neither-reabsorbed-nor-secreted solute (inulin) equals GFR, and creatinine clearance approximates it clinically; the nephron segments each specialise — the proximal tubule reabsorbs about 65 percent of the bulk filtrate (including all glucose and amino acids and most bicarbonate and sodium, via the NHE3 sodium-hydrogen exchanger), the loop of Henle is the countercurrent multiplier that concentrates the medulla, and the distal nephron and collecting duct fine-tune sodium (aldosterone) and water (ADH); and the kidney is uniquely vulnerable to anaesthesia and nephrotoxins because it receives a high blood flow and depends on glomerular pressure and tubular energy. Built on the GFR-physiology review (Ayub 2026), the macula densa tubuloglomerular-feedback study (Li 2026), the renal NHE3 study (Nogueira Coelho 2026), the proximal-tubule-dysfunction study (Ikeme 2026), the SGLT2-inhibition study (Gao 2026), and the chloride-and-RAAS study (Adin 2026).
Practise this topic
On this page
Study tools
Your progress
Saved on this device.
Target exams
Red flags
- GFR is about 125 mL per minute and filtration fraction about 20 percent; a fall in GFR is the hallmark of kidney injury, and a small rise in serum creatinine reflects a large fall in GFR because of the curved creatinine-GFR relationship.
- NSAIDs (constrict the afferent arteriole), ACE inhibitors and angiotensin receptor blockers (dilate the efferent arteriole) each lower glomerular capillary pressure and GFR — the mechanism of functional, reversible acute kidney injury, and the basis of the 'double whammy' when combined with hypovolaemia.
- Tubuloglomerular feedback (the macula densa sensing tubular NaCl and adjusting the afferent arteriole) links tubular reabsorption to filtration, so a damaged tubule (less reabsorption) signals the glomerulus to constrict, lowering GFR — a feature of acute tubular necrosis.
- The proximal tubule reabsorbs about 65 percent of filtered sodium and water and essentially all glucose and amino acids; SGLT2 inhibitors block proximal glucose reabsorption, and loss of proximal NHE3 disrupts sodium, bicarbonate and potassium handling.
- Autoregulation holds GFR constant from a mean arterial pressure of about 80 to 180 mmHg, but it is abolished by hypovolaemia and overridden by sympathetic vasoconstriction (shock, stress response), which is why the perioperative kidney is vulnerable.
Meet the patient
A 74-year-old hypertensive diabetic presents for bowel surgery. He takes ramipril, furosemide and, for his back, ibuprofen. He has been fasting and bowel-prepped overnight. At induction his pressure drops, and by morning his urine output is 10 mL per hour and his creatinine has risen. The kidney that filtered fine yesterday now does not.[1]
The question this topic answers is the one his kidney is failing on: what holds glomerular filtration pressure up when the patient is dry? The answer is afferent prostaglandin dilation and efferent angiotensin-II constriction — exactly the two defences his three drugs and his fast have dismantled. That is the triple whammy, and it is the most examinable idea in renal physiology.[1]
References6ShowHide
- [1]Ayub F, et al. The Physiological Basis of Acute GFR Decline With Renoprotective Therapies Mayo Clin Proc, 2026.PMID 42336099
- [2]Li M, et al. Macula densa-specific NOS1 knockout determines susceptibility to ischemic acute kidney injury Clin Sci (Lond), 2026.PMID 41837645
- [3]Nogueira Coelho J, et al. Renal NHE3 is required to limit hypokalemia and metabolic acidosis during dietary potassium deficiency Pflugers Arch, 2026.PMID 42260191
- [4]Ikeme JC, et al. Proximal tubule reabsorptive dysfunction and risk of cardiovascular death among community-living adults: the HUNT-3 cohort Eur Heart J Open, 2026.PMID 42291457
- [5]Gao Y, et al. Repurposing SGLT2 Inhibitors for Cirrhotic Ascites: From Mechanistic Research to Clinical Exploration J Clin Transl Hepatol, 2026.PMID 41810110
- [6]Adin D, et al. Influence of serum chloride concentrations on the renin-angiotensin-aldosterone system in dogs with congestive heart failure Am J Physiol Renal Physiol, 2026.PMID 42324236