o GFR ≈ 120 mL/min; represents the volume of plasma filtered per minute by both kidneys.
o Controlled by afferent/efferent arteriolar tone and glomerular capillary pressure.
o ↓ GFR seen in hypoperfusion, renal artery stenosis, or intrinsic renal disease.
o Estimation via serum creatinine (affected by muscle mass) and equations (e.g. MDRD, CKD-EPI).
o Triggered by low renal perfusion, low sodium, or sympathetic stimulation.
o Renin from JG cells converts angiotensinogen → angiotensin I → (ACE) angiotensin II.
o Angiotensin II: systemic vasoconstriction, efferent arteriole constriction, stimulates aldosterone.
o Aldosterone: from adrenal cortex; ↑ Na⁺ reabsorption and K⁺ secretion in DCT/CD.
o Proximal Convoluted Tubule (PCT):
Reabsorbs ~65% of filtered Na⁺ and water, all glucose and amino acids, most HCO₃⁻.
Target for carbonic anhydrase inhibitors (e.g. acetazolamide).
o Loop of Henle (LoH):
Descending limb: water permeable, passive reabsorption, concentrates filtrate.
Thick ascending limb: impermeable to water; active reabsorption of Na⁺, K⁺, Cl⁻ via NKCC2.
Site of action of loop diuretics (e.g. furosemide).
o Distal Convoluted Tubule (DCT):
Further Na⁺ and Cl⁻ reabsorption; site of thiazide action.
Calcium reabsorption under PTH control.
o Collecting Duct (CD):
Aldosterone increases Na⁺ reabsorption, K⁺ and H⁺ secretion.
ADH (vasopressin) promotes water reabsorption by inserting aquaporins.
o Synthesised in hypothalamus, stored/released from posterior pituitary.
o Released in response to ↑ plasma osmolality or ↓ volume (e.g. haemorrhage).
o Acts on V2 receptors in collecting duct → aquaporin insertion → concentrated urine.
o Inhibited in diabetes insipidus (cranial or nephrogenic).
o Urea: produced from protein metabolism; reabsorbed passively in PCT.
Rises in hypovolaemia or upper GI bleeding.
o Creatinine: from muscle metabolism; filtered by glomerulus, not reabsorbed.
↑ with renal dysfunction, but influenced by age, sex, and muscle mass.
Used to calculate eGFR; eGFR less accurate in AKI or extremes of body habitus.
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Author & Educational Disclaimer
Author:
Dr Phillip Cockrell BM FRCP DipClinEd
Dr Phillip Cockrell is a UK Consultant Physician in Internal Medicine, currently working at Queen Alexandra Hospital, Portsmouth University Hospitals NHS Trust. He has previously worked as a registrar across Intensive Care Medicine, Gastroenterology, Cardiology, Stroke Medicine, Acute Medicine, and Respiratory Medicine.
He has held senior leadership roles including Associate Clinical Director of the Acute Medical Unit, Clinical Director of Internal Medicine, and Chief of Medicine. Dr Cockrell has over 15 years’ experience in postgraduate medical education, having lectured extensively across the MRCP syllabus and contributed to MRCP revision teaching and course development.
Dr Cockrell holds a Bachelor of Medicine (BM), Fellowship of the Royal College of Physicians (FRCP), and a Diploma in Clinical Education (DipClinEd). His teaching approach is based on structured consolidation of complex medical topics to support efficient and effective revision for postgraduate examinations.
Purpose of this content:
The material on this page is intended solely for educational purposes to support revision for the MRCP (UK) Part 1 examination. It reflects examination-relevant principles of internal medicine and is designed to aid learning and pattern recognition.
Medical disclaimer:
This content is designed for postgraduate medical examination revision and does not constitute medical advice, diagnosis, or treatment guidance and must not be used as a substitute for professional clinical judgement, local guidelines, or specialist consultation. Clinical decisions should always be made in the context of individual patient circumstances and current national guidance.
