Describe how the kidney handles sodium. (50 marks) What factors influence urinary sodium excretion (50 marks)
Candidates were essentially expected to describe the fate of sodium as t passes through the
kidney from filtration at the glomerulus to ending up in the urine. Essentially, most Na+ is
reabsorbed at the proximal tubule (65%), reabsorption being down an electrochemical
gradient (inside cell negative and low Na+ concentration) which is maintained by active
Na+/K+ ATPase activity at the basolateral membrane. Then Loop of Henle reabsorbs a
further 15% of filtered Na+. At descending limb – no Na+ reabsorption. At ascending limb,
thick segment – active process as per proximal tubule, but mostly coupled to K+ and Cl- and
paracellular diffusion through tight junctions. Finally the distal convoluted tubule and
collecting ducts, a further almost 20% reabsorbed – leaving < 1%
Factors influencing loss are
- aldosterone = stimulates Na+ reabsorption at the collecting tubules
- intra renal factors such as interstitial pressure which is lowered during
hypovolaemia and reduced renal perfusion, thus promoting Na+ reabsorption
gradient
- sympathetic nervous system – influences interstitial pressure and increases renin
production
- angiotensin II – stimulates reabsorption at proximal tubule
- Atrial Naturetic Peptide/Factor – inhibits Na+ reabsorption
- Others – dopamine, cortisol, insulin => increase Na+ reabsorption, but minor
factors
Reference – Textbook of medical Physiology, Guyton, Chp 28
Weinstein, A. M. "Sodium and chloride transport: proximal nephron." Seldin and Giebisch's The Kidney. Elsevier Inc., 2008. 849-887.1081-1142
Reeves, W. Brian, and Thomas E. Andreoli. "Sodium chloride transport in the loop of Henle, distal convoluted tubule, and collecting duct." Seldin and Giebisch's The Kidney. Elsevier Inc., 2018 1143-1180
Matsubara, Mitsunobu. "Renal sodium handling for body fluid maintenance and blood pressure regulation." Yakugaku Zasshi 124.6 (2004): 301-309.