Bartter syndrome pathophysiology: Difference between revisions
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*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. | *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. | *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 | *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.<ref name="pmid21941653">{{cite journal| author=Deschênes G, Fila M| title=Primary molecular disorders and secondary biological adaptations in bartter syndrome. | journal=Int J Nephrol | year= 2011 | volume= 2011 | issue= | pages= 396209 | pmid=21941653 | doi=10.4061/2011/396209 | pmc=3177086 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21941653 }} </ref><ref name="pmid13969763">{{cite journal| author=BARTTER FC, PRONOVE P, GILL JR, MACCARDLE RC| title=Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome. | journal=Am J Med | year= 1962 | volume= 33 | issue= | pages= 811-28 | pmid=13969763 | doi=10.1016/0002-9343(62)90214-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13969763 }} </ref> | ||
==References== | ==References== | ||
Revision as of 13:08, 30 July 2020
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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.