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{{Metabolic alkalosis}}
{{Metabolic alkalosis}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{MMT}}
==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
The normal [[physiological]] pH of [[blood]] is 7.35 to 7.45. An increase above this range is known to be [[Alkalosis]]. [[Metabolic Alkalosis]] is defined as a [[disease]] state where [[blood pH]] is more than 7.45 due to secondary metabolic processes. The primary [[PH buffer|pH]] buffers in maintaining [[chemical equilibrium]] of physiological [[Blood pH]] are [[alkaline]] [[Bicarbonate|Bicarbonate ions(HCO3]]) and [[acidic]] [[Carbon dioxide|carbon dioxide(CO2)]]. When there is increase amount of [[Bicarbonate|Bicarbonate(HCO3)]] in body or decrease amount of [[carbon dioxide]] or loss of [[hydrogen ions]] it causes [[alkalosis]].  [[Metabolic alkalosis]] occurs due to trapping of [[Bicarbonate|Bicarbonate ions]] (HCO3) or loss of [[hydrogen ions]] in body due to some [[metabolic]] causes for example- [[Gastrointestinal|gastrointestinal loss]] of [[hydrogen ions]], [[Intracellular|intracellular shifting]] of [[hydrogen ions]], [[renal]] [[hydrogen]] loss, increased [[Bicarbonate|bicarbonate ions]] in [[extracellular]] [[Compartments|compartment]], [[Diuretic|diuretic i]]<nowiki/>nduced [[alkalosis]] or [[contraction alkalosis]]. Patient with normal [[renal physiology]] will compensate this increase amount of [[bicarbonate]] through excretion. But impaired [[renal function]] [[secondary]] to [[Chloride|chloride depletion]], [[hypokalemia]], [[hyperaldosteronism]], reduced [[Glomerular filtration rate|glomerular function rate]], reduced [[Effective circulating volume|effective arterial blood volume]] ([[EABV|EABV)]]) in [[heart failure]] or [[cirrhosis]] will lead to [[metabolic alkalosis]]. When the [[physiologic]] [[blood pH]] is above 7.45, it triggers [[Respiratory centre of the medulla|respiratory center]] to cause [[hypoventilation]], thus decreased [[Carbon dioxide|PCO2]] leading to [[Compensatory responses for acid-base disorders|compensatory]] [[respiratory acidosis]]. The [[Carbon dioxide|PCO2]] elavates from 0.5 to 0.7 mmHg per 1.0 millimole elevation in [[Bicarbonate|plasma bicarbonate concentration]]. In severe [[Metabolic alkalosis]] [[Carbon dioxide|PCO2]] can reach 60 mmHg. The [[mortality rate]] with [[metabolic alkalosis]] is 45% with [[Arterial blood ph|arterial blood pH]] 7.55 to 80% with arterial blood pH of 7.65. [[Supportive]] [[Treatment]] is usually given according to cause of the [[Disease|disease.]]
 
OR
 
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
 
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Pathophysiology==
==Pathophysiology==


===Loss of hydrogen ions===
===[[H+]] loss===
====GI loss====
====Gastrointestinal loss====
* [[Vomiting]] (excretion of hydrogen ions and the retention of bicarbonate)
**[[Emesis] (most commonly seen in [[pyloric stenosis]]), [[Nasogastric tube|NG suction]] , [[Zollinger-Ellison syndrome|Zollinger-ellison]] syndrome, [[Bulimia nervosa|Bulimia]].<ref name="pmid1928424">{{cite journal |vauthors=Galla JH, Gifford JD, Luke RG, Rome L |title=Adaptations to chloride-depletion alkalosis |journal=Am J Physiol |volume=261 |issue=4 Pt 2 |pages=R771–81 |date=October 1991 |pmid=1928424 |doi=10.1152/ajpregu.1991.261.4.R771 |url=}}</ref>
* [[Nasogastric tube]] suction
**[[Diuretic|Diuretics]]: [[Loop diuretic|Loop]] and [[thiazide diuretics]].
**[[Diarrhea]]: [[Villous adenoma]]<ref name="pmid5927076">{{cite journal |vauthors=Babior BM |title=Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances |journal=Am J Med |volume=41 |issue=4 |pages=615–21 |date=October 1966 |pmid=5927076 |doi=10.1016/0002-9343(66)90223-3 |url=}}</ref>, [[congenital chloride diarrhea]]<ref name="pmid8896562">{{cite journal |vauthors=Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J |title=Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea |journal=Nat Genet |volume=14 |issue=3 |pages=316–9 |date=November 1996 |pmid=8896562 |doi=10.1038/ng1196-316 |url=}}</ref>
**[[Cystic fibrosis]].<ref name="pmid7618650">{{cite journal |vauthors=Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG |title=Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis |journal=Am J Nephrol |volume=15 |issue=3 |pages=245–50 |date=1995 |pmid=7618650 |doi=10.1159/000168839 |url=}}</ref>
**[[Chloride]] deficient [[Infant formula|infant formula.]]
**Gastrocystoplasty <ref name="pmid7609133">{{cite journal |vauthors=Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI |title=Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty |journal=J Urol |volume=154 |issue=2 Pt 1 |pages=546–9 |date=August 1995 |pmid=7609133 |doi=10.1097/00005392-199508000-00066 |url=}}</ref>
**Post hypercapneic [[metabolic alkalosis]].
====Renal====
====Renal====
* Over-[[diuresis]]
**Dietary [[potassium]] depletion.<ref name="pmid8648937">{{cite journal |vauthors=Sabatini S |title=The cellular basis of metabolic alkalosis |journal=Kidney Int |volume=49 |issue=3 |pages=906–17 |date=March 1996 |pmid=8648937 |doi=10.1038/ki.1996.125 |url=}}</ref>
* [[Hyperaldosteronism]] causing retention of sodium followed with compensatory excretion of hydrogen
**[[Primary Hyperaldosteronism|Primary hyperaldosteronism]]: [[Conn syndrome]] or [[adenoma]], [[hyperplasia]], [[carcinoma]], [[renin]] or [[glucocorticoid]] responsive.
* Administration of non-resorbable anions such as, [[penicillin]], [[carbenicillin]], which complexs with positively-charged hydrogen ions in the [[renal tubules]].
**[[Secondary hyperaldosteronism]]: [[Renovascular hypertension|Reno vascular hypertension]], [[edema]] ([[cirrhosis]], [[heart failure]], [[Nephrotic syndrome|nephrotic syndrome)]], [[Juxtaglomerular apparatus|juxtaglomerular cell]]([[Renin-secreting tumors|renin producing) tumor]], [[renal cell carcinoma]], [[hemangiopericytoma]], [[nephroblastoma]]
**[[Mineralocorticoid]] excess due to primary decorticosterone excess ([[11β-hydroxylase deficiency|11 beta]], [[17 alpha-hydroxylase deficiency|17 alpha hydroxylase deficienc]]<nowiki/>y), [[licorice]]([[glycyrrhetinic acid]]), [[Liddle's syndrome|liddle syndrome]].<ref name="pmid1731223">{{cite journal |vauthors=Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM |title=A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension |journal=Nature |volume=355 |issue=6357 |pages=262–5 |date=January 1992 |pmid=1731223 |doi=10.1038/355262a0 |url=}}</ref> <ref name="pmid9452995">{{cite journal |vauthors=Warnock DG |title=Liddle syndrome: an autosomal dominant form of human hypertension |journal=Kidney Int |volume=53 |issue=1 |pages=18–24 |date=January 1998 |pmid=9452995 |doi=10.1046/j.1523-1755.1998.00728.x |url=}}</ref>
**[[Bartter syndrome|Bartter]] and [[Gitelman syndrome]]. <ref name="pmid9767561">{{cite journal |vauthors=Kurtz I |title=Molecular pathogenesis of Bartter's and Gitelman's syndromes |journal=Kidney Int |volume=54 |issue=4 |pages=1396–410 |date=October 1998 |pmid=9767561 |doi=10.1046/j.1523-1755.1998.00124.x |url=}}</ref>


===Increase in the serum bicarbonate===
===Elevated HCO3- level in serum===
* Ingestion of [[sodium bicarbonate]], baking soda, citrate, lactate, or acetate.
* Intake of [[NaCO3]], citrate, baking powder, lactate and acetate.
===Shift of hydrogen ions into intracellular space===
===Transport of H+ to IC space===
* Seen in [[hypokalemia]].  Due to a low extracellular potassium concentration, potassium shifts out of the cells, and in order to maintain electrical neutrality, hydrogen shifts into the cells, leaving behind bicarbonate.
* Occurs in [[hypokalemia]].  Decreased extracellular K+, potassium transports from the cells, and to keep electrical potential in a balanced state, Transport of H+ to IC space.
===Contraction alkalosis===
===Contraction Alkalosis===
* This results from a loss of water in the extracellular space which is poor in bicarbonate, typically from diuretic use. Since water is lost while bicarbonate is retained, the concentration of bicarbonate increases.
* Loss of low concerntation of HCO3 mixed H2O in EC space by diuretics. HCO3 is elevated in serum..


===Compensation for Metabolic Alkalosis===
===Compensatory mechanism of Metabolic Alkalosis===
* The body attempts to compensate for the increase in pH by retaining [[carbon dioxide]] (CO<sub>2</sub>) through [[hypoventilation]] ([[respiratory compensation]]). CO<sub>2</sub> combines with elements in the bloodstream to form carbonic acid, thus decreasing pH.
* [[hypoventilation]] ([[respiratory compensation]]) elevates pH by restoring [[carbon dioxide]] (CO<sub>2</sub>) through . Carbonic acid is generated by CO<sub>2</sub>. The acidic medium is created for compensation.
* The pCO2 rises 0.5 - 1 for every 1 unit increase in serum HCO3 from a baseline of 24.   
* The pCO2 elevates from  0.5 to 1 per 1 u serum HCO3 elevation.   
* The maximum pCO2 in compensation is 55-60.
* Body can compensate up tp 55-60 mmHg of partial pressure of CO2.
* [[Renal compensation]] for metabolic alkalosis consists of increased excretion of HCO<sub>3</sub><sup>-</sup> (bicarbonate), because the filtered load of HCO<sub>3</sub><sup>-</sup> exceeds the ability of the renal tubule to reabsorb it.
* Increased secretion of HCO<sub>3</sub><sup>-</sup> (bicarbonate) by kidney is done.


==Genetics==
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
 
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
*Genes involved in the pathogenesis of Metabolic Alkalosis include CFTR, SCNN1A/SCNN1B/SCNN1G<ref name="pmid29534496">{{cite journal |vauthors=Tetti M, Monticone S, Burrello J, Matarazzo P, Veglio F, Pasini B, Jeunemaitre X, Mulatero P |title=Liddle Syndrome: Review of the Literature and Description of a New Case |journal=Int J Mol Sci |volume=19 |issue=3 |pages= |date=March 2018 |pmid=29534496 |pmc=5877673 |doi=10.3390/ijms19030812 |url=}}</ref>, NKCC2<ref name="pmid8841184">{{cite journal |vauthors=Simon DB, Karet FE, Rodriguez-Soriano J, Hamdan JH, DiPietro A, Trachtman H, Sanjad SA, Lifton RP |title=Genetic heterogeneity of Bartter's syndrome revealed by mutations in the K+ channel, ROMK |journal=Nat Genet |volume=14 |issue=2 |pages=152–6 |date=October 1996 |pmid=8841184 |doi=10.1038/ng1096-152 |url=}}</ref> SLC12A3/CLCNKB<ref name="pmid21415153">{{cite journal |vauthors=Vargas-Poussou R, Dahan K, Kahila D, Venisse A, Riveira-Munoz E, Debaix H, Grisart B, Bridoux F, Unwin R, Moulin B, Haymann JP, Vantyghem MC, Rigothier C, Dussol B, Godin M, Nivet H, Dubourg L, Tack I, Gimenez-Roqueplo AP, Houillier P, Blanchard A, Devuyst O, Jeunemaitre X |title=Spectrum of mutations in Gitelman syndrome |journal=J Am Soc Nephrol |volume=22 |issue=4 |pages=693–703 |date=April 2011 |pmid=21415153 |pmc=3065225 |doi=10.1681/ASN.2010090907 |url=}}</ref> and SLC26A3 <ref name="pmid31145360">{{cite journal |vauthors=Kamal NM, Khan HY, El-Shabrawi MHF, Sherief LM |title=Congenital chloride losing diarrhea: A single center experience in a highly consanguineous population |journal=Medicine (Baltimore) |volume=98 |issue=22 |pages=e15928 |date=May 2019 |pmid=31145360 |pmc=6709049 |doi=10.1097/MD.0000000000015928 |url=}}</ref> causing Cystic Fibrosis, Liddle Syndrome, Bartter syndrome, Gitelman syndrome and Congenital Chloride Diarrhhea respectively.
*The development of [disease name] is the result of multiple genetic mutations.


==Associated Conditions==
==Associated Conditions==
Conditions associated with metabolic alkalosis :
**[[Vomiting]] (most commonly seen in [[pyloric stenosis]]
**[[Nasogastric tube|NG suction]]
**[[Zollinger-Ellison syndrome|Zollinger-ellison]] syndrome
**[[Bulimia nervosa|Bulimia]].<ref name="pmid1928424">{{cite journal |vauthors=Galla JH, Gifford JD, Luke RG, Rome L |title=Adaptations to chloride-depletion alkalosis |journal=Am J Physiol |volume=261 |issue=4 Pt 2 |pages=R771–81 |date=October 1991 |pmid=1928424 |doi=10.1152/ajpregu.1991.261.4.R771 |url=}}</ref>
**[[Diuretic|Diuretics]]: [[Loop diuretic|Loop]] and [[thiazide diuretics]].
**[[Villous adenoma]]<ref name="pmid5927076">{{cite journal |vauthors=Babior BM |title=Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances |journal=Am J Med |volume=41 |issue=4 |pages=615–21 |date=October 1966 |pmid=5927076 |doi=10.1016/0002-9343(66)90223-3 |url=}}</ref>
**[[congenital chloride diarrhea]]<ref name="pmid8896562">{{cite journal |vauthors=Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J |title=Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea |journal=Nat Genet |volume=14 |issue=3 |pages=316–9 |date=November 1996 |pmid=8896562 |doi=10.1038/ng1196-316 |url=}}</ref>
**[[Cystic fibrosis]]<ref name="pmid7618650">{{cite journal |vauthors=Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG |title=Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis |journal=Am J Nephrol |volume=15 |issue=3 |pages=245–50 |date=1995 |pmid=7618650 |doi=10.1159/000168839 |url=}}</ref>
**[[Chloride]] deficient [[Infant formula|infant formula.]]
**Gastrocystoplasty <ref name="pmid7609133">{{cite journal |vauthors=Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI |title=Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty |journal=J Urol |volume=154 |issue=2 Pt 1 |pages=546–9 |date=August 1995 |pmid=7609133 |doi=10.1097/00005392-199508000-00066 |url=}}</ref>
**Post hypercapneic [[metabolic alkalosis]].
**Dietary [[potassium]] depletion.<ref name="pmid8648937">{{cite journal |vauthors=Sabatini S |title=The cellular basis of metabolic alkalosis |journal=Kidney Int |volume=49 |issue=3 |pages=906–17 |date=March 1996 |pmid=8648937 |doi=10.1038/ki.1996.125 |url=}}</ref>
**[[Primary Hyperaldosteronism|Primary hyperaldosteronism]]: [[Conn syndrome]] or [[adenoma]], [[hyperplasia]], [[carcinoma]], [[renin]] or [[glucocorticoid]] responsive.
**[[Secondary hyperaldosteronism]]: [[Renovascular hypertension|Reno vascular hypertension]], [[edema]] ([[cirrhosis]], [[heart failure]], [[Nephrotic syndrome|nephrotic syndrome)]], [[Juxtaglomerular apparatus|juxtaglomerular cell]]([[Renin-secreting tumors|renin producing) tumor]], [[renal cell carcinoma]], [[hemangiopericytoma]], [[nephroblastoma]]
**[[Mineralocorticoid]] excess due to primary decorticosterone excess ([[11β-hydroxylase deficiency|11 beta]], [[17 alpha-hydroxylase deficiency|17 alpha hydroxylase deficienc]]<nowiki/>y), [[licorice]]([[glycyrrhetinic acid]]), [[Liddle's syndrome|liddle syndrome]].<ref name="pmid1731223">{{cite journal |vauthors=Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM |title=A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension |journal=Nature |volume=355 |issue=6357 |pages=262–5 |date=January 1992 |pmid=1731223 |doi=10.1038/355262a0 |url=}}</ref> <ref name="pmid9452995">{{cite journal |vauthors=Warnock DG |title=Liddle syndrome: an autosomal dominant form of human hypertension |journal=Kidney Int |volume=53 |issue=1 |pages=18–24 |date=January 1998 |pmid=9452995 |doi=10.1046/j.1523-1755.1998.00728.x |url=}}</ref>
**[[Bartter syndrome|Bartter]] and [[Gitelman syndrome]]. <ref name="pmid9767561">{{cite journal |vauthors=Kurtz I |title=Molecular pathogenesis of Bartter's and Gitelman's syndromes |journal=Kidney Int |volume=54 |issue=4 |pages=1396–410 |date=October 1998 |pmid=9767561 |doi=10.1046/j.1523-1755.1998.00124.x |url=}}</ref>
**[[Laxative]]
**[[Chronic kidney disease]]
**[[Hypovolemia]] or [[Diuresis|massive diuresis]] with [[loop diuretics]].
**[[Milk-alkali syndrome]] or [[bone metastasis]].
**Massive [[blood transfusion]].
**[[Acetate]] containing [[Colloid|colloid sollution]].
**[[Exogenous]] [[alkali]] admintration.
**Combined [[antacid]] and cation exchange resin administration.
**Sodium [[Penicillin|penicillins]].


==Gross Pathology==
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
**There is no specific gross pathological finding related to metabolic alkalosis. Gross characteristics are dependent on specific cause of metabolic alkalosis.


==Microscopic Pathology==
==Microscopic Pathology==
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
**There is no specific microscopic pathological finding related to metabolic alkalosis. Gross characteristics are dependent on specific cause of metabolic alkalosis.
 


==References==
==References==

Latest revision as of 04:57, 25 February 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]

Overview

The normal physiological pH of blood is 7.35 to 7.45. An increase above this range is known to be Alkalosis. Metabolic Alkalosis is defined as a disease state where blood pH is more than 7.45 due to secondary metabolic processes. The primary pH buffers in maintaining chemical equilibrium of physiological Blood pH are alkaline Bicarbonate ions(HCO3) and acidic carbon dioxide(CO2). When there is increase amount of Bicarbonate(HCO3) in body or decrease amount of carbon dioxide or loss of hydrogen ions it causes alkalosis. Metabolic alkalosis occurs due to trapping of Bicarbonate ions (HCO3) or loss of hydrogen ions in body due to some metabolic causes for example- gastrointestinal loss of hydrogen ions, intracellular shifting of hydrogen ions, renal hydrogen loss, increased bicarbonate ions in extracellular compartment, diuretic induced alkalosis or contraction alkalosis. Patient with normal renal physiology will compensate this increase amount of bicarbonate through excretion. But impaired renal function secondary to chloride depletion, hypokalemia, hyperaldosteronism, reduced glomerular function rate, reduced effective arterial blood volume (EABV)) in heart failure or cirrhosis will lead to metabolic alkalosis. When the physiologic blood pH is above 7.45, it triggers respiratory center to cause hypoventilation, thus decreased PCO2 leading to compensatory respiratory acidosis. The PCO2 elavates from 0.5 to 0.7 mmHg per 1.0 millimole elevation in plasma bicarbonate concentration. In severe Metabolic alkalosis PCO2 can reach 60 mmHg. The mortality rate with metabolic alkalosis is 45% with arterial blood pH 7.55 to 80% with arterial blood pH of 7.65. Supportive Treatment is usually given according to cause of the disease.

Pathophysiology

H+ loss

Gastrointestinal loss

Renal

Elevated HCO3- level in serum

  • Intake of NaCO3, citrate, baking powder, lactate and acetate.

Transport of H+ to IC space

  • Occurs in hypokalemia. Decreased extracellular K+, potassium transports from the cells, and to keep electrical potential in a balanced state, Transport of H+ to IC space.

Contraction Alkalosis

  • Loss of low concerntation of HCO3 mixed H2O in EC space by diuretics. HCO3 is elevated in serum..

Compensatory mechanism of Metabolic Alkalosis

  • hypoventilation (respiratory compensation) elevates pH by restoring carbon dioxide (CO2) through . Carbonic acid is generated by CO2. The acidic medium is created for compensation.
  • The pCO2 elevates from 0.5 to 1 per 1 u serum HCO3 elevation.
  • Body can compensate up tp 55-60 mmHg of partial pressure of CO2.
  • Increased secretion of HCO3- (bicarbonate) by kidney is done.

Genetics

  • Genes involved in the pathogenesis of Metabolic Alkalosis include CFTR, SCNN1A/SCNN1B/SCNN1G[10], NKCC2[11] SLC12A3/CLCNKB[12] and SLC26A3 [13] causing Cystic Fibrosis, Liddle Syndrome, Bartter syndrome, Gitelman syndrome and Congenital Chloride Diarrhhea respectively.

Associated Conditions

Conditions associated with metabolic alkalosis :

Gross Pathology

    • There is no specific gross pathological finding related to metabolic alkalosis. Gross characteristics are dependent on specific cause of metabolic alkalosis.

Microscopic Pathology

    • There is no specific microscopic pathological finding related to metabolic alkalosis. Gross characteristics are dependent on specific cause of metabolic alkalosis.


References

  1. ↑ 1.0 1.1 Galla JH, Gifford JD, Luke RG, Rome L (October 1991). "Adaptations to chloride-depletion alkalosis". Am J Physiol. 261 (4 Pt 2): R771–81. doi:10.1152/ajpregu.1991.261.4.R771. PMID 1928424.
  2. ↑ 2.0 2.1 Babior BM (October 1966). "Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances". Am J Med. 41 (4): 615–21. doi:10.1016/0002-9343(66)90223-3. PMID 5927076.
  3. ↑ 3.0 3.1 Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J (November 1996). "Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea". Nat Genet. 14 (3): 316–9. doi:10.1038/ng1196-316. PMID 8896562.
  4. ↑ 4.0 4.1 Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG (1995). "Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis". Am J Nephrol. 15 (3): 245–50. doi:10.1159/000168839. PMID 7618650.
  5. ↑ 5.0 5.1 Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI (August 1995). "Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty". J Urol. 154 (2 Pt 1): 546–9. doi:10.1097/00005392-199508000-00066. PMID 7609133.
  6. ↑ 6.0 6.1 Sabatini S (March 1996). "The cellular basis of metabolic alkalosis". Kidney Int. 49 (3): 906–17. doi:10.1038/ki.1996.125. PMID 8648937.
  7. ↑ 7.0 7.1 Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM (January 1992). "A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension". Nature. 355 (6357): 262–5. doi:10.1038/355262a0. PMID 1731223.
  8. ↑ 8.0 8.1 Warnock DG (January 1998). "Liddle syndrome: an autosomal dominant form of human hypertension". Kidney Int. 53 (1): 18–24. doi:10.1046/j.1523-1755.1998.00728.x. PMID 9452995.
  9. ↑ 9.0 9.1 Kurtz I (October 1998). "Molecular pathogenesis of Bartter's and Gitelman's syndromes". Kidney Int. 54 (4): 1396–410. doi:10.1046/j.1523-1755.1998.00124.x. PMID 9767561.
  10. ↑ Tetti M, Monticone S, Burrello J, Matarazzo P, Veglio F, Pasini B, Jeunemaitre X, Mulatero P (March 2018). "Liddle Syndrome: Review of the Literature and Description of a New Case". Int J Mol Sci. 19 (3). doi:10.3390/ijms19030812. PMC 5877673. PMID 29534496.
  11. ↑ Simon DB, Karet FE, Rodriguez-Soriano J, Hamdan JH, DiPietro A, Trachtman H, Sanjad SA, Lifton RP (October 1996). "Genetic heterogeneity of Bartter's syndrome revealed by mutations in the K+ channel, ROMK". Nat Genet. 14 (2): 152–6. doi:10.1038/ng1096-152. PMID 8841184.
  12. ↑ Vargas-Poussou R, Dahan K, Kahila D, Venisse A, Riveira-Munoz E, Debaix H, Grisart B, Bridoux F, Unwin R, Moulin B, Haymann JP, Vantyghem MC, Rigothier C, Dussol B, Godin M, Nivet H, Dubourg L, Tack I, Gimenez-Roqueplo AP, Houillier P, Blanchard A, Devuyst O, Jeunemaitre X (April 2011). "Spectrum of mutations in Gitelman syndrome". J Am Soc Nephrol. 22 (4): 693–703. doi:10.1681/ASN.2010090907. PMC 3065225. PMID 21415153.
  13. ↑ Kamal NM, Khan HY, El-Shabrawi M, Sherief LM (May 2019). "Congenital chloride losing diarrhea: A single center experience in a highly consanguineous population". Medicine (Baltimore). 98 (22): e15928. doi:10.1097/MD.0000000000015928. PMC 6709049 Check |pmc= value (help). PMID 31145360. Vancouver style error: initials (help)

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