Urine concentration: the countercurrent mechanism and ADH action
How the loop of Henle, urea recycling and the vasa recta build the medullary gradient, how ADH acts through V2 receptors and aquaporin-2, how solute intake sets urine volume, and how this explains AVP deficiency, AVP resistance and drug effects on water handling.
Tier 1Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- The kidney can vary urine osmolality from about 50 to 1,200 mOsm/kg. Two things are needed to concentrate urine: a hypertonic medullary interstitium and ADH (arginine vasopressin) making the collecting duct permeable to water.
- The thick ascending limb pumps NaCl into the medulla without water. The countercurrent arrangement multiplies this into a gradient from 290 mOsm/kg at the corticomedullary junction to about 1,200 at the papilla. Urea recycling supplies about half the inner medullary solute.
- ADH acts on V2 receptors to insert aquaporin-2. Without ADH the collecting duct is water-tight and the dilute fluid from the distal tubule is excreted.
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Sources
- Brenner and Rector's The Kidney, 11th editionElsevier, 2020
- Guyton and Hall Textbook of Medical Physiology, 14th editionElsevier, 2021
- Refardt J, Atila C, Chifu I et al. Arginine or hypertonic saline-stimulated copeptin to diagnose AVP deficiency. N Engl J Med 2023;389:1877-87New England Journal of Medicine, 2023
- Arima H, Cheetham T, Christ-Crain M et al. Changing the name of diabetes insipidus: a position statement of the Working Group for Renaming Diabetes Insipidus. J Clin Endocrinol Metab 2023;108:1-3Endocrine Society, 2023
- Australian Medicines HandbookAU/NZAustralian Medicines Handbook Pty Ltd, 2026
- Last updated
- 14 November 2026
What changed
- 14 November 2026 Personal emails, About story and Australian-style copy