Bartter syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
- Bartter syndrome is a renal tubular salt-wasting disorder in which the kidneys cannot reabsorb sodium and chloride in the thick ascending limb of the loop of Henle.
- Impairment of sodium and chloride reabsorption is the primary defect in the Bartter syndrome that initiates the cascade.
- This leads to increased delivery of salt to the distal tubules and excessive salt and water loss from the body. The resultant volume depletion causes activation of the renin-angiotensin-aldosterone system (RAAS) and subsequent secondary hyperaldosteronism. Long-term stimulation causes hyperplasia of the juxtaglomerular apparatus and elevates renin levels.[1][2]
References
- ↑ Deschênes G, Fila M (2011). "Primary molecular disorders and secondary biological adaptations in bartter syndrome". Int J Nephrol. 2011: 396209. doi:10.4061/2011/396209. PMC 3177086. PMID 21941653.
- ↑ BARTTER FC, PRONOVE P, GILL JR, MACCARDLE RC (1962). "Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome". Am J Med. 33: 811–28. doi:10.1016/0002-9343(62)90214-0. PMID 13969763.