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Bartter syndrome historical perspective
Introduction
Main article: Bartter syndrome
Overview
Overview
Bartter syndrome was first discovered by Bartter et al.and introduced in a seminal paper in the December issue of the American Journal of Medicine in 1962. Authors in the paper reported two pediatric patients with growth and developmental delay associated with hypokalemic alkalosis and normal blood pressure despite high aldosterone production. The syndrome named after Bartter. This disease was observed in children as well as in adults, females as well as males.Authors described in the paper that this disease is characterized by hypokalemia, metabolic alkalosis, hyperreninemia, secondary hyperaldosteronism, and normal blood pressure.
Historical Perspective
Historical Perspective
- Bartter syndrome was first discovered by Bartter et al.and introduced in a seminal paper in the December issue of the American Journal of Medicine in 1962.
- Authors in the paper reported two pediatric patients with growth and developmental delay associated with hypokalemic alkalosis and normal blood pressure despite high aldosterone production.
- The syndrome named after Bartter. This disease was observed in children as well as in adults, females as well as males.[1]
- Authors described in the paper that this disease is characterized by hypokalemia, metabolic alkalosis, hyperreninemia, secondary hyperaldosteronism, and normal blood pressure.
- Hyperrinemia on histopathological examination is characterized by hyperplasia of juxtaglomerular complex.[2]
- Fichman [3] , Verberckmoes [4], and Gill [5] in 1976 explained that the production of prostaglandin E2 increases in urine in patients with Bartter syndrome. Later, only the urinary metabolite 6 keto, PGF1, has been measured. Further investigation disclosed that the potent vasodilator PGI2 increases in the blood vessels in Bartter syndrome.[6]
- Earlier, physicians misdiagnosed cystic fibrosis as having Bartter syndrome. In cystic fibrosis, patients lose excessive quantities of sodium, potassium, and chloride in sweat. Excessive loss of electrolytes occurs in urine in a similar pattern in Bartter syndrome.[7]
References
References
- ↑ Proesmans W (2006). “Threading through the mizmaze of Bartter syndrome”. Pediatr Nephrol. 21 (7): 896–902. doi:10.1007/s00467-006-0113-7. PMID 16773399.
- ↑ 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.
- ↑ Fichman MP, Telfer N, Zia P, Speckart P, Golub M, Rude R (1976). “Role of prostaglandins in the pathogenesis of Bartter’s syndrome”. Am J Med. 60 (6): 785–97. doi:10.1016/0002-9343(76)90892-5. PMID 798488.
- ↑ “www.kidney-international.org”.
- ↑ Gill JR, Frölich JC, Bowden RE, Taylor AA, Keiser HR, Seyberth HW; et al. (1976). “Bartter’s syndrome: a disorder characterized by high urinary prostaglandins and a dependence of hyperreninemia on prostaglandin synthesis”. Am J Med. 61 (1): 43–51. doi:10.1016/0002-9343(76)90029-2. PMID 820194.
- ↑ Güllner HG, Cerletti C, Bartter FC, Smith JB, Gill JR (1979). “Prostacyclin overproduction in Bartter’s syndrome”. Lancet. 2 (8146): 767–9. doi:10.1016/s0140-6736(79)92116-0. PMID 90861.
- ↑ Davison AG, Snodgrass GJ (1983). “Cystic fibrosis mimicking Bartter’s syndrome”. Acta Paediatr Scand. 72 (5): 781–3. doi:10.1111/j.1651-2227.1983.tb09814.x. PMID 6356778.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Tayyaba Ali, M.D.[2]