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Latest revision as of 19:52, 5 August 2020

Main article: Bartter syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Tayyaba Ali, M.D.[2]

Overview

Bartter syndrome diagnosis should be differentiated from other diseases manifesting with hypokalemia and hypochloremic metabolic alkalosis such as Gitelman syndrome, EAST syndrome also is known as SeSAME syndrome, Diuretic abuse, cyclical vomiting, Hyperprostaglandin E syndrome(HPS), Familial hypomagnesemia, cystic fibrosis, Gullner syndrome, Mineralocorticoid excess, Activating mutation of the calcium-sensing receptor (CaSR) gene, Hypomagnesemia is often associated with hypokalemia, hypocalcemia, and metabolic alkalosis, Congenital chloride diarrhea, Hypochloremic alkalosis and Hypokalemia. Prolonged hypokalemia can lead to impaired ability of kidneys to concentrate urine, increased bicarbonate reabsorption.

Differentiating Bartter syndrome from other Diseases

Bartter syndrome diagnosis should be differentiated from other diseases manifesting with hypokalemia and hypochloremic metabolic alkalosis.^[1]


Disease	Findings
Gitelman syndrome	Hypocalciuria (low urinary calcium) is a distinct feature and interstitial nephritis may develop because of the persistent hypokalemia. Adults can present with chondrocalcinosis with swollen and warm joints with overlying tenderness. Sudden cardiac arrest has been reported occasionally.^[2] Growth retardation is absent in Gitelman syndrome.^[3]
EAST syndrome	EAST syndrome also is known as SeSAME syndrome is a rare inherited disorder that presents in infancy. It results from homozygous mutations in the KCNJ10 gene, which encodes for a potassium channel that is expressed in the basolateral membrane of distal tubules, as well as in the brain. It is characterized by Epilepsy, severe Ataxia, moderate Sensorineural deafness, and Tubulopathy leading to renal salt wasting, hypokalemia, metabolic alkalosis, and normal blood pressure.^[4]^[5]
Diuretic abuse	Diuretic abuse should be considered in all patients with unexplained hypokalemia and metabolic alkalosis.^[6]^[7]^[8] Sometimes parents or caregivers administer diuretics in infants. It is hard to differentiate diuretic abuse from Bartter syndrome by blood and urinary electrolyte measurements. A diuretic screen is warranted.^[9]
Cyclical vomiting	In the case of cyclical vomiting for a variety of reasons, urine chloride concentration differs from that of Bartter syndrome. This is usually less than 25 mEq/L in patients with chronic vomiting as a result of hypovolemia and hypochloremia. In Bartter syndrome the urine chloride concentration is typically much higher (usually greater than 40 mEq/L).^[10]
Hyperprostaglandin E syndrome	Hyperprostaglandin E syndrome(HPS) occurs during pregnancy before a birth. It is an antenatal variant of Bartter syndrome characterized by polyhydramnios and preterm delivery. In the postnatal period, it is characterized by salt-wasting, hypercalciuria, and nephrocalcinosis.^[11]
Familial hypomagnesemia with hypercalciuria/nephrocalcinosis	Familial hypomagnesemia with hypercalciuria/nephrocalcinosis is an autosomal recessive disorder associated with hypercalciuria. The disease presents in childhood or adolescence with hypocalcemic symptoms. Renal insufficiency occurs as a result of nephrolithiasis and nephrocalcinosis. Familial hypomagnesemia with hypercalciuria/nephrocalcinosis is a result of a mutation in the claudin-16 gene (also known as paracellin-1). Claudin-16 is a tight junction protein that facilitates the passive, paracellular reabsorption of both magnesium and calcium in the thick ascending limb of the loop of Henle.^[12]^[13]^[14]^[15]^[16]
Cystic fibrosis	Patients with cystic fibrosis lose salt-rich sweat. Patients with moderate cystic fibrosis manifest with unexplained hypokalemia and metabolic alkalosis.^[17]^[18]^[19] In contrast to Bartter syndrome, spot urine chloride concentration is low in cystic fibrosis indicating chloride conservation in response to volume contraction.^[20]^[21]
Gullner syndrome - Familial hypokalemic alkalosis with proximal tubulopathy	Gullner syndrome presents with hypokalemic alkalosis, hyperreninemia, hyperaldosteronism, high urinary prostaglandin E2 excretion and normal blood pressure. Histologic examination of tissue obtained by biopsy from the kidneys showed intense staining of the proximal tubular cells, as well as extreme hypertrophy of the proximal tubular basement membranes. In contrast to Bartter syndrome, the juxtaglomerular apparatus were of normal appearance.^[22]
Mineralocorticoid excess	Mineralocorticoid excess is presented with low birth weight, failure to thrive, hypercalciuria and nephrocalcinosis from an unknown mechanism, and renal failure. In contrast to Bartter syndrome, severe hypertension in early childhood with extensive target organ damage occurs in mineralocorticoid excess.^[23] In contrast to Bartter syndrome, mineralocorticoid excess is characterized by low plasma renin and aldosterone.^[24]^[25]
Activating mutations of the CaSR calcium-sensing receptor	Patients with activating mutation of the calcium-sensing receptor (CaSR) gene presents with potassium wasting, hypokalemia, and metabolic alkalosis, similar to Bartter syndrome.^[26]^[27] An activating (or gain-of-function) mutation of the calcium-sensing receptor (CaSR) gene impairs the calcium balance in the body and cause hypocalcemia. Activating mutation in the receptor increases the threshold for the receptor to detect the low calcium level. This causes the parathyroid hormone (PTH) to not release at serum calcium level that normally signals PTH release.^[28]^[29]^[30]
Hypomagnesemia	There are two major mechanisms by which hypomagnesemia can be induced such as gastrointestinal loss and renal loss. Hypomagnesemia is often associated with hypokalemia, hypocalcemia, and metabolic alkalosis.^[31] In contrast to Bartter syndrome, Hypomagnesemia is a common condition that occurs in up to 12 percent of hospitalized patients.^[32]
Congenital chloride diarrhea	Early diagnosis is a prerequisite for congenital chloride diarrhea in a newborn. It is a medical emergency that leads to severe dehydration and infant death.^[33] This disorder is due to a mutation in a gene that encodes an exchange protein, expressed in the ileum and colon, which works as a channel to absorbs chloride from the intestinal lumen and secretes bicarbonate. Mutation impairs the function of the chloride-bicarbonate channel and results in very high stool chloride concentrations (>100 mEq/L). In contrast to Bartter syndrome, the urinary chloride measurement is less than 20 mEq/L.^[34]
Hypochloremic alkalosis	Hypochloremic alkalosis is caused by an extreme lack or loss of chloride, such as from prolonged vomiting.^[35] In contrast to Bartter syndrome, the measurement of a spot urine chloride concentration is less than 25 mEq/l in hypochloremic alkalosis.^[10]
Hypokalemia	Hypokalemia can be induced by a gastrointestinal loss such as diarrhea and vomiting and urinary loss such as diuretic therapy. It can be induced transiently by entering into cells.^[36] Prolonged hypokalemia can lead to impaired ability of kidneys to concentrate urine, increased bicarbonate reabsorption. In contrast to Bartter syndrome, blood pressure is elevated in hypokalemia.^[37]

References

↑ Gitelman HJ, Graham JB, Welt LG (1966). "A new familial disorder characterized by hypokalemia and hypomagnesemia". Trans Assoc Am Physicians. 79: 221–35. PMID 5929460.
↑ Scognamiglio R, Negut C, Calò LA (2007). "Aborted sudden cardiac death in two patients with Bartter's/Gitelman's syndromes". Clin Nephrol. 67 (3): 193–7. doi:10.5414/cnp67193. PMID 17390745.
↑ Urbanová M, Reiterová J, Stěkrová J, Lněnička P, Ryšavá R (2011). "DNA analysis of renal electrolyte transporter genes among patients suffering from Bartter and Gitelman syndromes: summary of mutation screening". Folia Biol (Praha). 57 (2): 65–73. PMID 21631963.
↑ Bockenhauer D, Feather S, Stanescu HC, Bandulik S, Zdebik AA, Reichold M; et al. (2009). "Epilepsy, ataxia, sensorineural deafness, tubulopathy, and KCNJ10 mutations". N Engl J Med. 360 (19): 1960–70. doi:10.1056/NEJMoa0810276. PMC 3398803. PMID 19420365.
↑ Scholl UI, Choi M, Liu T, Ramaekers VT, Häusler MG, Grimmer J; et al. (2009). "Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME syndrome) caused by mutations in KCNJ10". Proc Natl Acad Sci U S A. 106 (14): 5842–7. doi:10.1073/pnas.0901749106. PMC 2656559. PMID 19289823.
↑ Jamison RL, Ross JC, Kempson RL, Sufit CR, Parker TE (1982). "Surreptitious diuretic ingestion and pseudo-Bartter's syndrome". Am J Med. 73 (1): 142–7. doi:10.1016/0002-9343(82)90941-x. PMID 7091169.
↑ Colussi G, Rombolà G, Airaghi C, De Ferrari ME, Minetti L (1992). "Pseudo-Bartter's syndrome from surreptitious diuretic intake: differential diagnosis with true Bartter's syndrome". Nephrol Dial Transplant. 7 (9): 896–901. doi:10.1093/ndt/7.9.896. PMID 1328936.
↑ Sasaki H, Kawasaki T, Yamamoto T, Ninomiya H, Ono J, Yamamoto T; et al. (1986). "[Pseudo-Bartter's syndrome induced by surreptitious ingestion of furosemide to lose weight: a case report and possible pathophysiology]". Nihon Naibunpi Gakkai Zasshi. 62 (8): 867–81. doi:10.1507/endocrine1927.62.8_867. PMID 3023152.
↑ D'Avanzo M, Santinelli R, Tolone C, Bettinelli A, Bianchetti MG (1995). "Concealed administration of frusemide simulating Bartter syndrome in a 4.5-year-old boy". Pediatr Nephrol. 9 (6): 749–50. doi:10.1007/BF00868731. PMID 8747119.
↑ ^10.0 ^10.1 Veldhuis JD, Bardin CW, Demers LM (1979). "Metabolic mimicry of Bartter's syndrome by covert vomiting: utility of urinary chloride determinations". Am J Med. 66 (2): 361–3. doi:10.1016/0002-9343(79)90566-7. PMID 425977.
↑ Cetinkaya M, Köksal N, Ozkan H, Dönmez O, Sağlam H, Kiriştioğlu I (2008). "Hyperprostaglandin E syndrome: use of indomethacin and steroid, and death due to necrotizing enterocolitis and sepsis". Turk J Pediatr. 50 (4): 386–90. PMID 19014056.
↑ Praga M, Vara J, González-Parra E, Andrés A, Alamo C, Araque A; et al. (1995). "Familial hypomagnesemia with hypercalciuria and nephrocalcinosis". Kidney Int. 47 (5): 1419–25. doi:10.1038/ki.1995.199. PMID 7637271.
↑ Nicholson JC, Jones CL, Powell HR, Walker RG, McCredie DA (1995). "Familial hypomagnesaemia--hypercalciuria leading to end-stage renal failure". Pediatr Nephrol. 9 (1): 74–6. doi:10.1007/BF00858976. PMID 7742227.
↑ Benigno V, Canonica CS, Bettinelli A, von Vigier RO, Truttmann AC, Bianchetti MG (2000). "Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review". Nephrol Dial Transplant. 15 (5): 605–10. doi:10.1093/ndt/15.5.605. PMID 10809799.
↑ Müller D, Kausalya PJ, Bockenhauer D, Thumfart J, Meij IC, Dillon MJ; et al. (2006). "Unusual clinical presentation and possible rescue of a novel claudin-16 mutation". J Clin Endocrinol Metab. 91 (8): 3076–9. doi:10.1210/jc.2006-0200. PMID 16705067.
↑ Konrad M, Hou J, Weber S, Dötsch J, Kari JA, Seeman T; et al. (2008). "CLDN16 genotype predicts renal decline in familial hypomagnesemia with hypercalciuria and nephrocalcinosis". J Am Soc Nephrol. 19 (1): 171–81. doi:10.1681/ASN.2007060709. PMC 2391030. PMID 18003771.
↑ Kose M, Pekcan S, Ozcelik U, Cobanoglu N, Yalcin E, Dogru D; et al. (2008). "An epidemic of pseudo-Bartter syndrome in cystic fibrosis patients". Eur J Pediatr. 167 (1): 115–6. doi:10.1007/s00431-007-0413-3. PMID 17323076.
↑ Kennedy JD, Dinwiddie R, Daman-Willems C, Dillon MJ, Matthew DJ (1990). "Pseudo-Bartter's syndrome in cystic fibrosis". Arch Dis Child. 65 (7): 786–7. doi:10.1136/adc.65.7.786. PMC 1792454. PMID 2386386.
↑ Bates CM, Baum M, Quigley R (1997). "Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent". J Am Soc Nephrol. 8 (2): 352–5. PMID 9048354.
↑ Davé S, Honney S, Raymond J, Flume PA (2005). "An unusual presentation of cystic fibrosis in an adult". Am J Kidney Dis. 45 (3): e41–4. doi:10.1053/j.ajkd.2004.11.009. PMID 15754262.
↑ Leoni GB, Pitzalis S, Podda R, Zanda M, Silvetti M, Caocci L; et al. (1995). "A specific cystic fibrosis mutation (T3381) associated with the phenotype of isolated hypotonic dehydration". J Pediatr. 127 (2): 281–3. doi:10.1016/s0022-3476(95)70310-1. PMID 7543567.
↑ Güllner HG, Bartter FC, Gill JR, Dickman PS, Wilson CB, Tiwari JL (1983). "A sibship with hypokalemic alkalosis and renal proximal tubulopathy". Arch Intern Med. 143 (8): 1534–40. doi:10.1001/archinte.1983.00350080040011. PMID 6347111.
↑ Morineau G, Sulmont V, Salomon R, Fiquet-Kempf B, Jeunemaître X, Nicod J; et al. (2006). "Apparent mineralocorticoid excess: report of six new cases and extensive personal experience". J Am Soc Nephrol. 17 (11): 3176–84. doi:10.1681/ASN.2006060570. PMID 17035606.
↑ Dave-Sharma S, Wilson RC, Harbison MD, Newfield R, Azar MR, Krozowski ZS; et al. (1998). "Examination of genotype and phenotype relationships in 14 patients with apparent mineralocorticoid excess". J Clin Endocrinol Metab. 83 (7): 2244–54. doi:10.1210/jcem.83.7.4986. PMID 9661590.
↑ Bockenhauer D, van't Hoff W, Dattani M, Lehnhardt A, Subtirelu M, Hildebrandt F; et al. (2010). "Secondary nephrogenic diabetes insipidus as a complication of inherited renal diseases". Nephron Physiol. 116 (4): p23–9. doi:10.1159/000320117. PMC 3896046. PMID 20733335.
↑ Watanabe S, Fukumoto S, Chang H, Takeuchi Y, Hasegawa Y, Okazaki R; et al. (2002). "Association between activating mutations of calcium-sensing receptor and Bartter's syndrome". Lancet. 360 (9334): 692–4. doi:10.1016/S0140-6736(02)09842-2. PMID 12241879.
↑ Konrad M, Weber S (2003). "Recent advances in molecular genetics of hereditary magnesium-losing disorders". J Am Soc Nephrol. 14 (1): 249–60. doi:10.1097/01.asn.0000049161.60740.ce. PMID 12506158.
↑ Brown EM (2007). "Clinical lessons from the calcium-sensing receptor". Nat Clin Pract Endocrinol Metab. 3 (2): 122–33. doi:10.1038/ncpendmet0388. PMID 17237839.
↑ Pollak MR, Brown EM, Estep HL, McLaine PN, Kifor O, Park J; et al. (1994). "Autosomal dominant hypocalcaemia caused by a Ca(2+)-sensing receptor gene mutation". Nat Genet. 8 (3): 303–7. doi:10.1038/ng1194-303. PMID 7874174.
↑ D'Souza-Li L, Yang B, Canaff L, Bai M, Hanley DA, Bastepe M; et al. (2002). "Identification and functional characterization of novel calcium-sensing receptor mutations in familial hypocalciuric hypercalcemia and autosomal dominant hypocalcemia". J Clin Endocrinol Metab. 87 (3): 1309–18. doi:10.1210/jcem.87.3.8280. PMID 11889203.
↑ Tong GM, Rude RK (2005). "Magnesium deficiency in critical illness". J Intensive Care Med. 20 (1): 3–17. doi:10.1177/0885066604271539. PMID 15665255.
↑ Wong ET, Rude RK, Singer FR, Shaw ST (1983). "A high prevalence of [[hypomagnesemia]] and [[hypermagnesemia]] in hospitalized patients". Am J Clin Pathol. 79 (3): 348–52. doi:10.1093/ajcp/79.3.348. PMID 6829504. URL–wikilink conflict (help)
↑ Wedenoja S, Höglund P, Holmberg C (2010). "Review article: the clinical management of congenital chloride diarrhoea". Aliment Pharmacol Ther. 31 (4): 477–85. doi:10.1111/j.1365-2036.2009.04197.x. PMID 19912155.
↑ EVANSON JM, STANBURY SW (1965). "CONGENITAL CHLORIDORRHOEA OR SO-CALLED CONGENITAL ALKALOSIS WITH DIARRHOEA". Gut. 6: 29–38. doi:10.1136/gut.6.1.29. PMC 1552247. PMID 14259421.
↑ "Alkalosis: MedlinePlus Medical Encyclopedia".
↑ Gennari FJ (1998). "Hypokalemia". N Engl J Med. 339 (7): 451–8. doi:10.1056/NEJM199808133390707. PMID 9700180.
↑ Kim GH, Han JS (2002). "Therapeutic approach to hypokalemia". Nephron. 92 Suppl 1: 28–32. doi:10.1159/000065374. PMID 12401935.

Template:WikiDoc Sources

[1] Gitelman HJ, Graham JB, Welt LG (1966). "A new familial disorder characterized by hypokalemia and hypomagnesemia". Trans Assoc Am Physicians. 79: 221–35. PMID 5929460.

[pmid17390745-2] Scognamiglio R, Negut C, Calò LA (2007). "Aborted sudden cardiac death in two patients with Bartter's/Gitelman's syndromes". Clin Nephrol. 67 (3): 193–7. doi:10.5414/cnp67193. PMID 17390745.

[pmid21631963-3] Urbanová M, Reiterová J, Stěkrová J, Lněnička P, Ryšavá R (2011). "DNA analysis of renal electrolyte transporter genes among patients suffering from Bartter and Gitelman syndromes: summary of mutation screening". Folia Biol (Praha). 57 (2): 65–73. PMID 21631963.

[pmid19420365-4] Bockenhauer D, Feather S, Stanescu HC, Bandulik S, Zdebik AA, Reichold M; et al. (2009). "Epilepsy, ataxia, sensorineural deafness, tubulopathy, and KCNJ10 mutations". N Engl J Med. 360 (19): 1960–70. doi:10.1056/NEJMoa0810276. PMC 3398803. PMID 19420365.

[pmid19289823-5] Scholl UI, Choi M, Liu T, Ramaekers VT, Häusler MG, Grimmer J; et al. (2009). "Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME syndrome) caused by mutations in KCNJ10". Proc Natl Acad Sci U S A. 106 (14): 5842–7. doi:10.1073/pnas.0901749106. PMC 2656559. PMID 19289823.

[pmid7091169-6] Jamison RL, Ross JC, Kempson RL, Sufit CR, Parker TE (1982). "Surreptitious diuretic ingestion and pseudo-Bartter's syndrome". Am J Med. 73 (1): 142–7. doi:10.1016/0002-9343(82)90941-x. PMID 7091169.

[pmid1328936-7] Colussi G, Rombolà G, Airaghi C, De Ferrari ME, Minetti L (1992). "Pseudo-Bartter's syndrome from surreptitious diuretic intake: differential diagnosis with true Bartter's syndrome". Nephrol Dial Transplant. 7 (9): 896–901. doi:10.1093/ndt/7.9.896. PMID 1328936.

[pmid3023152-8] Sasaki H, Kawasaki T, Yamamoto T, Ninomiya H, Ono J, Yamamoto T; et al. (1986). "[Pseudo-Bartter's syndrome induced by surreptitious ingestion of furosemide to lose weight: a case report and possible pathophysiology]". Nihon Naibunpi Gakkai Zasshi. 62 (8): 867–81. doi:10.1507/endocrine1927.62.8_867. PMID 3023152.

[pmid8747119-9] D'Avanzo M, Santinelli R, Tolone C, Bettinelli A, Bianchetti MG (1995). "Concealed administration of frusemide simulating Bartter syndrome in a 4.5-year-old boy". Pediatr Nephrol. 9 (6): 749–50. doi:10.1007/BF00868731. PMID 8747119.

[pmid425977-10] 10.0 ^10.1 Veldhuis JD, Bardin CW, Demers LM (1979). "Metabolic mimicry of Bartter's syndrome by covert vomiting: utility of urinary chloride determinations". Am J Med. 66 (2): 361–3. doi:10.1016/0002-9343(79)90566-7. PMID 425977.

[pmid19014056-11] Cetinkaya M, Köksal N, Ozkan H, Dönmez O, Sağlam H, Kiriştioğlu I (2008). "Hyperprostaglandin E syndrome: use of indomethacin and steroid, and death due to necrotizing enterocolitis and sepsis". Turk J Pediatr. 50 (4): 386–90. PMID 19014056.

[pmid7637271-12] Praga M, Vara J, González-Parra E, Andrés A, Alamo C, Araque A; et al. (1995). "Familial hypomagnesemia with hypercalciuria and nephrocalcinosis". Kidney Int. 47 (5): 1419–25. doi:10.1038/ki.1995.199. PMID 7637271.

[pmid7742227-13] Nicholson JC, Jones CL, Powell HR, Walker RG, McCredie DA (1995). "Familial hypomagnesaemia--hypercalciuria leading to end-stage renal failure". Pediatr Nephrol. 9 (1): 74–6. doi:10.1007/BF00858976. PMID 7742227.

[pmid10809799-14] Benigno V, Canonica CS, Bettinelli A, von Vigier RO, Truttmann AC, Bianchetti MG (2000). "Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review". Nephrol Dial Transplant. 15 (5): 605–10. doi:10.1093/ndt/15.5.605. PMID 10809799.

[pmid16705067-15] Müller D, Kausalya PJ, Bockenhauer D, Thumfart J, Meij IC, Dillon MJ; et al. (2006). "Unusual clinical presentation and possible rescue of a novel claudin-16 mutation". J Clin Endocrinol Metab. 91 (8): 3076–9. doi:10.1210/jc.2006-0200. PMID 16705067.

[pmid18003771-16] Konrad M, Hou J, Weber S, Dötsch J, Kari JA, Seeman T; et al. (2008). "CLDN16 genotype predicts renal decline in familial hypomagnesemia with hypercalciuria and nephrocalcinosis". J Am Soc Nephrol. 19 (1): 171–81. doi:10.1681/ASN.2007060709. PMC 2391030. PMID 18003771.

[pmid17323076-17] Kose M, Pekcan S, Ozcelik U, Cobanoglu N, Yalcin E, Dogru D; et al. (2008). "An epidemic of pseudo-Bartter syndrome in cystic fibrosis patients". Eur J Pediatr. 167 (1): 115–6. doi:10.1007/s00431-007-0413-3. PMID 17323076.

[pmid2386386-18] Kennedy JD, Dinwiddie R, Daman-Willems C, Dillon MJ, Matthew DJ (1990). "Pseudo-Bartter's syndrome in cystic fibrosis". Arch Dis Child. 65 (7): 786–7. doi:10.1136/adc.65.7.786. PMC 1792454. PMID 2386386.

[pmid9048354-19] Bates CM, Baum M, Quigley R (1997). "Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent". J Am Soc Nephrol. 8 (2): 352–5. PMID 9048354.

[pmid15754262-20] Davé S, Honney S, Raymond J, Flume PA (2005). "An unusual presentation of cystic fibrosis in an adult". Am J Kidney Dis. 45 (3): e41–4. doi:10.1053/j.ajkd.2004.11.009. PMID 15754262.

[pmid7543567-21] Leoni GB, Pitzalis S, Podda R, Zanda M, Silvetti M, Caocci L; et al. (1995). "A specific cystic fibrosis mutation (T3381) associated with the phenotype of isolated hypotonic dehydration". J Pediatr. 127 (2): 281–3. doi:10.1016/s0022-3476(95)70310-1. PMID 7543567.

[pmid6347111-22] Güllner HG, Bartter FC, Gill JR, Dickman PS, Wilson CB, Tiwari JL (1983). "A sibship with hypokalemic alkalosis and renal proximal tubulopathy". Arch Intern Med. 143 (8): 1534–40. doi:10.1001/archinte.1983.00350080040011. PMID 6347111.

[pmid17035606-23] Morineau G, Sulmont V, Salomon R, Fiquet-Kempf B, Jeunemaître X, Nicod J; et al. (2006). "Apparent mineralocorticoid excess: report of six new cases and extensive personal experience". J Am Soc Nephrol. 17 (11): 3176–84. doi:10.1681/ASN.2006060570. PMID 17035606.

[pmid9661590-24] Dave-Sharma S, Wilson RC, Harbison MD, Newfield R, Azar MR, Krozowski ZS; et al. (1998). "Examination of genotype and phenotype relationships in 14 patients with apparent mineralocorticoid excess". J Clin Endocrinol Metab. 83 (7): 2244–54. doi:10.1210/jcem.83.7.4986. PMID 9661590.

[pmid20733335-25] Bockenhauer D, van't Hoff W, Dattani M, Lehnhardt A, Subtirelu M, Hildebrandt F; et al. (2010). "Secondary nephrogenic diabetes insipidus as a complication of inherited renal diseases". Nephron Physiol. 116 (4): p23–9. doi:10.1159/000320117. PMC 3896046. PMID 20733335.

[pmid12241879-26] Watanabe S, Fukumoto S, Chang H, Takeuchi Y, Hasegawa Y, Okazaki R; et al. (2002). "Association between activating mutations of calcium-sensing receptor and Bartter's syndrome". Lancet. 360 (9334): 692–4. doi:10.1016/S0140-6736(02)09842-2. PMID 12241879.

[pmid12506158-27] Konrad M, Weber S (2003). "Recent advances in molecular genetics of hereditary magnesium-losing disorders". J Am Soc Nephrol. 14 (1): 249–60. doi:10.1097/01.asn.0000049161.60740.ce. PMID 12506158.

[pmid17237839-28] Brown EM (2007). "Clinical lessons from the calcium-sensing receptor". Nat Clin Pract Endocrinol Metab. 3 (2): 122–33. doi:10.1038/ncpendmet0388. PMID 17237839.

[pmid7874174-29] Pollak MR, Brown EM, Estep HL, McLaine PN, Kifor O, Park J; et al. (1994). "Autosomal dominant hypocalcaemia caused by a Ca(2+)-sensing receptor gene mutation". Nat Genet. 8 (3): 303–7. doi:10.1038/ng1194-303. PMID 7874174.

[pmid11889203-30] D'Souza-Li L, Yang B, Canaff L, Bai M, Hanley DA, Bastepe M; et al. (2002). "Identification and functional characterization of novel calcium-sensing receptor mutations in familial hypocalciuric hypercalcemia and autosomal dominant hypocalcemia". J Clin Endocrinol Metab. 87 (3): 1309–18. doi:10.1210/jcem.87.3.8280. PMID 11889203.

[pmid15665255-31] Tong GM, Rude RK (2005). "Magnesium deficiency in critical illness". J Intensive Care Med. 20 (1): 3–17. doi:10.1177/0885066604271539. PMID 15665255.

[pmid6829504-32] Wong ET, Rude RK, Singer FR, Shaw ST (1983). "A high prevalence of [[hypomagnesemia]] and [[hypermagnesemia]] in hospitalized patients". Am J Clin Pathol. 79 (3): 348–52. doi:10.1093/ajcp/79.3.348. PMID 6829504. URL–wikilink conflict (help)

[pmid19912155-33] Wedenoja S, Höglund P, Holmberg C (2010). "Review article: the clinical management of congenital chloride diarrhoea". Aliment Pharmacol Ther. 31 (4): 477–85. doi:10.1111/j.1365-2036.2009.04197.x. PMID 19912155.

[pmid14259421-34] EVANSON JM, STANBURY SW (1965). "CONGENITAL CHLORIDORRHOEA OR SO-CALLED CONGENITAL ALKALOSIS WITH DIARRHOEA". Gut. 6: 29–38. doi:10.1136/gut.6.1.29. PMC 1552247. PMID 14259421.

[urlAlkalosis:_MedlinePlus_Medical_Encyclopedia-35] "Alkalosis: MedlinePlus Medical Encyclopedia".

[pmid9700180-36] Gennari FJ (1998). "Hypokalemia". N Engl J Med. 339 (7): 451–8. doi:10.1056/NEJM199808133390707. PMID 9700180.

[pmid12401935-37] Kim GH, Han JS (2002). "Therapeutic approach to hypokalemia". Nephron. 92 Suppl 1: 28–32. doi:10.1159/000065374. PMID 12401935.

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@@ Line 1: / Line 1: @@
 __NOTOC__
+Main article: [[Bartter syndrome|Bartter syndrome]]
 {{Bartter syndrome}}
 {{CMG}}{{AE}}{{TAM}}
 ==Overview==
+[[Bartter syndrome]] diagnosis should be differentiated from other diseases manifesting with [[hypokalemia]] and [[metabolic alkalosis|hypochloremic metabolic alkalosis]] such as Gitelman syndrome, EAST syndrome also is known as SeSAME syndrome, [[Diuretic|Diuretic abuse]], [[vomiting|cyclical vomiting]], Hyperprostaglandin E syndrome(HPS), Familial [[hypomagnesemia]], [[cystic fibrosis]], Gullner syndrome, [[Mineralocorticoid]] excess, [[mutation|Activating mutation]] of the calcium-sensing receptor (CaSR) gene, [[Hypomagnesemia]] is often associated with [[hypokalemia]], [[hypocalcemia]], and [[metabolic alkalosis]], Congenital chloride diarrhea, [[Hypochloremic alkalosis]] and [[Hypokalemia]]. Prolonged [[hypokalemia]] can lead to impaired ability of kidneys to concentrate urine, increased [[bicarbonate]] reabsorption.
 ==Differentiating Bartter syndrome from other Diseases==
-Bartter syndrome diagnosis should be differentiated from other diseases manifesting with hypokalemia and hypochloremic metabolic alkalosis.<ref>{{cite journal | author=Gitelman HJ, Graham JB, Welt LG | title=A new familial disorder characterized by hypokalemia and hypomagnesemia | journal=Trans Assoc Am Physicians | year=1966 | pages=221-35 | volume=79  | id=PMID 5929460}} </ref>
+[[Bartter syndrome]] diagnosis should be differentiated from other diseases manifesting with [[hypokalemia]] and [[metabolic alkalosis|hypochloremic metabolic alkalosis]].<ref>{{cite journal | author=Gitelman HJ, Graham JB, Welt LG | title=A new familial disorder characterized by hypokalemia and hypomagnesemia | journal=Trans Assoc Am Physicians | year=1966 | pages=221-35 | volume=79  | id=PMID 5929460}} </ref>
 {| style="border: 0px; font-size: 90%; margin: 3px;" align=center
 |+
@@ Line 15: / Line 18: @@
 *Adults can present with [[chondrocalcinosis]] with swollen and warm joints with overlying tenderness. Sudden cardiac arrest has been reported occasionally.<ref name="pmid17390745">{{cite journal| author=Scognamiglio R, Negut C, Calò LA| title=Aborted sudden cardiac death in two patients with Bartter's/Gitelman's syndromes. | journal=Clin Nephrol | year= 2007 | volume= 67 | issue= 3 | pages= 193-7 | pmid=17390745 | doi=10.5414/cnp67193 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17390745  }} </ref>
 *Growth retardation is absent in [[Gitelman syndrome]].<ref name="pmid21631963">{{cite journal| author=Urbanová M, Reiterová J, Stěkrová J, Lněnička P, Ryšavá R| title=DNA analysis of renal electrolyte transporter genes among patients suffering from Bartter and Gitelman syndromes: summary of mutation screening. | journal=Folia Biol (Praha) | year= 2011 | volume= 57 | issue= 2 | pages= 65-73 | pmid=21631963 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21631963  }} </ref>
+|-
+| style="padding: 5px 5px; background: #DCDCDC;" | '''EAST syndrome'''
+| style="padding: 5px 5px; background: #F5F5F5;" |
+*EAST syndrome also is known as SeSAME syndrome is a rare inherited disorder that presents in infancy.
+*It results from [[mutation|homozygous mutations]] in the KCNJ10 gene, which encodes for a [[potassium channel]] that is expressed in the [[basolateral membrane]] of [[distal tubules]], as well as in the brain.
+*It is characterized by [[Epilepsy]], [[Ataxia|severe Ataxia]], moderate [[Sensorineural deafness]], and Tubulopathy leading to renal salt wasting, [[hypokalemia]], [[metabolic alkalosis]], and normal blood pressure.<ref name="pmid19420365">{{cite journal| author=Bockenhauer D, Feather S, Stanescu HC, Bandulik S, Zdebik AA, Reichold M | display-authors=etal| title=Epilepsy, ataxia, sensorineural deafness, tubulopathy, and KCNJ10 mutations. | journal=N Engl J Med | year= 2009 | volume= 360 | issue= 19 | pages= 1960-70 | pmid=19420365 | doi=10.1056/NEJMoa0810276 | pmc=3398803 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19420365  }} </ref><ref name="pmid19289823">{{cite journal| author=Scholl UI, Choi M, Liu T, Ramaekers VT, Häusler MG, Grimmer J | display-authors=etal| title=Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME syndrome) caused by mutations in KCNJ10. | journal=Proc Natl Acad Sci U S A | year= 2009 | volume= 106 | issue= 14 | pages= 5842-7 | pmid=19289823 | doi=10.1073/pnas.0901749106 | pmc=2656559 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19289823  }} </ref>
 |-
 | style="padding: 5px 5px; background: #DCDCDC;" | '''[[Diuretic|Diuretic abuse]]'''
@@ Line 34: / Line 43: @@
 | style="padding: 5px 5px; background: #DCDCDC;" | '''Familial hypomagnesemia with hypercalciuria/nephrocalcinosis'''
 | style="padding: 5px 5px; background: #F5F5F5;" |
-*
+*Familial [[hypomagnesemia]] with [[hypercalciuria]]/[[nephrocalcinosis]] is an [[autosomal recessive]] disorder associated with [[hypercalciuria]]. The disease presents in childhood or adolescence with [[hypocalcemia|hypocalcemic]] symptoms.
-*
+*Renal insufficiency occurs as a result of nephrolithiasis and nephrocalcinosis.
+*Familial [[hypomagnesemia]] with [[hypercalciuria]]/[[nephrocalcinosis]] is a result of a [[mutation]] in the claudin-16 gene (also known as paracellin-1). Claudin-16 is a [[tight junction]] protein that facilitates the passive, paracellular reabsorption of both [[magnesium]] and [[calcium]] in the [[loop of Henle|thick ascending limb of the loop of Henle]].<ref name="pmid7637271">{{cite journal| author=Praga M, Vara J, González-Parra E, Andrés A, Alamo C, Araque A | display-authors=etal| title=Familial hypomagnesemia with hypercalciuria and nephrocalcinosis. | journal=Kidney Int | year= 1995 | volume= 47 | issue= 5 | pages= 1419-25 | pmid=7637271 | doi=10.1038/ki.1995.199 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7637271  }} </ref><ref name="pmid7742227">{{cite journal| author=Nicholson JC, Jones CL, Powell HR, Walker RG, McCredie DA| title=Familial hypomagnesaemia--hypercalciuria leading to end-stage renal failure. | journal=Pediatr Nephrol | year= 1995 | volume= 9 | issue= 1 | pages= 74-6 | pmid=7742227 | doi=10.1007/BF00858976 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7742227  }} </ref><ref name="pmid10809799">{{cite journal| author=Benigno V, Canonica CS, Bettinelli A, von Vigier RO, Truttmann AC, Bianchetti MG| title=Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review. | journal=Nephrol Dial Transplant | year= 2000 | volume= 15 | issue= 5 | pages= 605-10 | pmid=10809799 | doi=10.1093/ndt/15.5.605 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10809799  }} </ref><ref name="pmid16705067">{{cite journal| author=Müller D, Kausalya PJ, Bockenhauer D, Thumfart J, Meij IC, Dillon MJ | display-authors=etal| title=Unusual clinical presentation and possible rescue of a novel claudin-16 mutation. | journal=J Clin Endocrinol Metab | year= 2006 | volume= 91 | issue= 8 | pages= 3076-9 | pmid=16705067 | doi=10.1210/jc.2006-0200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16705067  }} </ref><ref name="pmid18003771">{{cite journal| author=Konrad M, Hou J, Weber S, Dötsch J, Kari JA, Seeman T | display-authors=etal| title=CLDN16 genotype predicts renal decline in familial hypomagnesemia with hypercalciuria and nephrocalcinosis. | journal=J Am Soc Nephrol | year= 2008 | volume= 19 | issue= 1 | pages= 171-81 | pmid=18003771 | doi=10.1681/ASN.2007060709 | pmc=2391030 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18003771  }} </ref>
 |-
 | style="padding: 5px 5px; background: #DCDCDC;" | '''[[Cystic fibrosis]]'''
@@ Line 45: / Line 55: @@
 | style="padding: 5px 5px; background: #DCDCDC;" | '''Gullner syndrome - Familial hypokalemic alkalosis with proximal tubulopathy'''
 | style="padding: 5px 5px; background: #F5F5F5;" |
-*
+*Gullner syndrome presents with [[metabolic alkalosis|hypokalemic alkalosis]], [[renin|hyperreninemia]], [[hyperaldosteronism]], high urinary [[prostaglandin|prostaglandin E2]] excretion and normal [[blood pressure]].
-*
+*Histologic examination of tissue obtained by biopsy from the kidneys showed intense staining of the [[tubular cells|proximal tubular cells]], as well as extreme hypertrophy of the [[basement membrane|proximal tubular basement membranes]].
+*In contrast to [[Bartter syndrome]], the [[juxtaglomerular apparatus]] were of normal appearance.<ref name="pmid6347111">{{cite journal| author=Güllner HG, Bartter FC, Gill JR, Dickman PS, Wilson CB, Tiwari JL| title=A sibship with hypokalemic alkalosis and renal proximal tubulopathy. | journal=Arch Intern Med | year= 1983 | volume= 143 | issue= 8 | pages= 1534-40 | pmid=6347111 | doi=10.1001/archinte.1983.00350080040011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6347111  }} </ref>
 |-
 | style="padding: 5px 5px; background: #DCDCDC;" | '''[[Mineralocorticoid excess]]'''
@@ Line 56: / Line 67: @@
 | style="padding: 5px 5px; background: #DCDCDC;" | '''Activating mutations of the CaSR calcium-sensing receptor'''
 | style="padding: 5px 5px; background: #F5F5F5;" |
-*
+*Patients with [[mutation|activating mutation]] of the calcium-sensing receptor (CaSR) gene presents with [[potassium]] wasting, [[hypokalemia]], and [[metabolic alkalosis]], similar to [[Bartter syndrome]].<ref name="pmid12241879">{{cite journal| author=Watanabe S, Fukumoto S, Chang H, Takeuchi Y, Hasegawa Y, Okazaki R | display-authors=etal| title=Association between activating mutations of calcium-sensing receptor and Bartter's syndrome. | journal=Lancet | year= 2002 | volume= 360 | issue= 9334 | pages= 692-4 | pmid=12241879 | doi=10.1016/S0140-6736(02)09842-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12241879  }} </ref><ref name="pmid12506158">{{cite journal| author=Konrad M, Weber S| title=Recent advances in molecular genetics of hereditary magnesium-losing disorders. | journal=J Am Soc Nephrol | year= 2003 | volume= 14 | issue= 1 | pages= 249-60 | pmid=12506158 | doi=10.1097/01.asn.0000049161.60740.ce | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12506158  }} </ref>
-*
+*An activating (or gain-of-function) mutation of the calcium-sensing receptor (CaSR) gene impairs the calcium balance in the body and cause hypocalcemia.
+*Activating mutation in the receptor increases the threshold for the receptor to detect the low calcium level. This causes the parathyroid hormone (PTH) to not release at serum calcium level that normally signals PTH release.<ref name="pmid17237839">{{cite journal| author=Brown EM| title=Clinical lessons from the calcium-sensing receptor. | journal=Nat Clin Pract Endocrinol Metab | year= 2007 | volume= 3 | issue= 2 | pages= 122-33 | pmid=17237839 | doi=10.1038/ncpendmet0388 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17237839  }} </ref><ref name="pmid7874174">{{cite journal| author=Pollak MR, Brown EM, Estep HL, McLaine PN, Kifor O, Park J | display-authors=etal| title=Autosomal dominant hypocalcaemia caused by a Ca(2+)-sensing receptor gene mutation. | journal=Nat Genet | year= 1994 | volume= 8 | issue= 3 | pages= 303-7 | pmid=7874174 | doi=10.1038/ng1194-303 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7874174  }} </ref><ref name="pmid11889203">{{cite journal| author=D'Souza-Li L, Yang B, Canaff L, Bai M, Hanley DA, Bastepe M | display-authors=etal| title=Identification and functional characterization of novel calcium-sensing receptor mutations in familial hypocalciuric hypercalcemia and autosomal dominant hypocalcemia. | journal=J Clin Endocrinol Metab | year= 2002 | volume= 87 | issue= 3 | pages= 1309-18 | pmid=11889203 | doi=10.1210/jcem.87.3.8280 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11889203  }} </ref>
 |-
 | style="padding: 5px 5px; background: #DCDCDC;" | '''[[Hypomagnesemia]]'''
@@ Line 73: / Line 85: @@
 | style="padding: 5px 5px; background: #DCDCDC;" | '''[[Hypochloremia|Hypochloremic alkalosis]]'''
 | style="padding: 5px 5px; background: #F5F5F5;" |
-*
+*[[Hypochloremic alkalosis]] is caused by an extreme lack or loss of [[chloride]], such as from prolonged vomiting.<ref name="urlAlkalosis: MedlinePlus Medical Encyclopedia">{{cite web |url=https://medlineplus.gov/ency/article/001183.htm |title=Alkalosis: MedlinePlus Medical Encyclopedia |format= |work= |accessdate=}}</ref>
-*
+*In contrast to [[Bartter syndrome]], the measurement of a spot urine [[chloride]] concentration is less than 25 mEq/l in [[hypochloremic alkalosis]].<ref name="pmid425977">{{cite journal| author=Veldhuis JD, Bardin CW, Demers LM| title=Metabolic mimicry of Bartter's syndrome by covert vomiting: utility of urinary chloride determinations. | journal=Am J Med | year= 1979 | volume= 66 | issue= 2 | pages= 361-3 | pmid=425977 | doi=10.1016/0002-9343(79)90566-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=425977  }} </ref>
 |-
 | style="padding: 5px 5px; background: #DCDCDC;" | '''[[Hypokalemia]]'''
 | style="padding: 5px 5px; background: #F5F5F5;" |
-*
+*[[Hypokalemia]] can be induced by a gastrointestinal loss such as [[diarrhea]] and [[vomiting]] and urinary loss such as [[diuretic]] therapy. It can be induced transiently by entering into cells.<ref name="pmid9700180">{{cite journal| author=Gennari FJ| title=Hypokalemia. | journal=N Engl J Med | year= 1998 | volume= 339 | issue= 7 | pages= 451-8 | pmid=9700180 | doi=10.1056/NEJM199808133390707 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9700180  }} </ref>
-*
+*Prolonged [[hypokalemia]] can lead to impaired ability of kidneys to concentrate urine, increased [[bicarbonate]] reabsorption.
+*In contrast to [[Bartter syndrome]], blood pressure is elevated in [[hypokalemia]].<ref name="pmid12401935">{{cite journal| author=Kim GH, Han JS| title=Therapeutic approach to hypokalemia. | journal=Nephron | year= 2002 | volume= 92 Suppl 1 | issue=  | pages= 28-32 | pmid=12401935 | doi=10.1159/000065374 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12401935  }} </ref>
 |}

Bartter syndrome differential diagnosis: Difference between revisions

Latest revision as of 19:52, 5 August 2020

Overview

Differentiating Bartter syndrome from other Diseases

References

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