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{{Milk-alkali syndrome}}
{{Milk-alkali syndrome}}
{{CMG}}
{{CMG}} {{AE}} {{SHA}}
==Overview==
==Overview==
==Pathophysiology==
The exact [[pathogenesis]] of milk-alkali syndrome is unknown. Hypercalcemia in milk-alkali syndrome involves several mechanisms including: [[Intestine|intestinal]] absorption of [[calcium]] is increased, [[bone]] buffering of [[calcium]] becomes saturated, and [[Kidney|renal]] excretion of [[calcium]] is decreased. Several factors that increase [[bicarbonate]] [[reabsorption]] and contribute to the [[alkalosis]] in milk-alkali syndrome include: [[Hypovolemia|volume depletion]] due to increased [[sodium]] and free water [[excretion]] caused by increased [[calcium]] intake, suppression of [[Parathyroid hormone|PTH]], direct [[Nephron|tubular]] effects of [[calcium]] and other factors that cause [[Hypovolemia|volume depletion]] or [[alkalosis]] such as [[Nausea and vomiting|vomiting]] or [[thiazide]] use.
The name "milk-alkali syndrome" derives from when patients would take in excessive amounts of milk and antacids to control their dyspepsia, leading to overingestion of two key ingredients that lead to the disorder, excess calcium and excess base.  Ingesting over two grams of elemental [[calcium]] per day produces this disorder in susceptible individuals. [[Gastrointestinal tract|Gastrointestinal]] absorption of such a large amount of calcium leads to [[hypercalcemia]].  This inhibits [[parathyroid hormone]] secretion by the [[parathyroid gland]] and may also lead to [[diabetes insipidus]].  The body's attempt to rid itself of the excess base in the urine may cause bicarbonaturia and subsequent hypovolemia due to transport of sodium ions to accompany the bicarbonate.


Hypovolemia may increase the reabsorption of calcium and [[bicarbonate]] in the [[proximal convoluted tubule]]s of the kidney. Elevated bicarbonate levels in the blood raises the [[pH]], producing an alkalemia. In this state, excess bicarbonate eventually begins to reach the [[distal convoluted tubule]], leading to sodium retention in the lumen, an effect similar to the action of [[thiazide]] diuretics, hence increasing lumen positivity and driving calcium through the passive calcium channels to bind intracellular [[calbindin]]. Finally, because of the decreased intracellular sodium, there is an increased driving force for the basolateral Na+/Ca++ antiporter, thus facilitating calcium reabsorption.  Basically, hypovolemia is the culprit that prevents correction of the hypercalcemia.
== Pathophysiology ==


The understanding of this mechanism led to the development of a simple yet elegant treatment for hypercalcemia. The first and most important step is [[Route of administration#Parenteral by injection or infusion|intravenous infusion]] of [[Saline (medicine)|normal saline]] to restore the intravascular volume, which reverses the calcium and bicarbonate retention in the PCT. Then a [[loop diuretic]] is used, but only after the volume replacement is complete, otherwise volume contraction would result, which would further exacerbate the hypercalcemia. The loop diuretics inhibit the [[Na-K-2Cl symporter]] and hence eliminate passive diffusion of potassium into the lumen via the [[ROMK]] channel. This effectively removes the net positive charge from the lumen, one of the main driving forces for calcium reabsorption via the paracellular pathway. In addition, loop diuretics increase the flow of luminal contents, which helps flush the calcium to the distal nephron.
* The exact [[pathogenesis]] of milk-alkali syndrome is unknown.
* Consumption of excessive amounts of [[calcium]] and absorbable alkali causes milk-alkali syndrome.<ref name="pmid19252114">{{cite journal| author=Medarov BI| title=Milk-alkali syndrome. | journal=Mayo Clin Proc | year= 2009 | volume= 84 | issue= 3 | pages= 261-7 | pmid=19252114 | doi=10.1016/S0025-6196(11)61144-0 | pmc=2664604 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19252114  }} </ref>


==Overview==
=== Pathogenesis ===
The exact pathogenesis of [disease name] is not fully understood.
The [[pathogenesis]] of milk-alkali syndrome involves the [[Kidney|kidneys]], [[Bone|bones]], and [[Intestine|intestines]].<ref name="pmid23543983">{{cite journal| author=Arroyo M, Fenves AZ, Emmett M| title=The calcium-alkali syndrome. | journal=Proc (Bayl Univ Med Cent) | year= 2013 | volume= 26 | issue= 2 | pages= 179-81 | pmid=23543983 | doi=10.1080/08998280.2013.11928954 | pmc=3603742 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23543983  }} </ref>
 
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
===== '''Hypercalcemia''' =====


The progression to [disease name] usually involves the [molecular pathway].
* Hypercalcemia involves the following:<ref name="pmid17699269">{{cite journal| author=Felsenfeld AJ, Levine BS| title=Milk alkali syndrome and the dynamics of calcium homeostasis. | journal=Clin J Am Soc Nephrol | year= 2006 | volume= 1 | issue= 4 | pages= 641-54 | pmid=17699269 | doi=10.2215/CJN.01451005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17699269  }} </ref>
**[[Intestine|Intestinal]] absorption of [[calcium]] is increased.
**[[Bone]] buffering of [[calcium]] becomes saturated.
**[[Kidney|Renal]] excretion of [[calcium]] is decreased.


OR
*[[Intestine|Intestines]] absorb the high quantities of consumed [[calcium]] and cause [[hypercalcemia]].
*[[Bone (disambiguation)|Bones]] have a limited capacity of [[calcium]] buffering and the variations in this capacity may contribute to hypercalcemia.
*[[Hypercalcemia]] causes [[vasoconstriction]] in the [[Kidney|kidneys]], which decreases [[Glomerular filtration rate|glomerular filtration rate (GFR)]] and [[calcium]] excretion in the [[Kidney|kidneys]].<ref name="pmid17699269">{{cite journal| author=Felsenfeld AJ, Levine BS| title=Milk alkali syndrome and the dynamics of calcium homeostasis. | journal=Clin J Am Soc Nephrol | year= 2006 | volume= 1 | issue= 4 | pages= 641-54 | pmid=17699269 | doi=10.2215/CJN.01451005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17699269  }} </ref>
*[[Hypercalcemia]] activates [[calcium]]-sensing receptors (CaSRs) in different areas and the following effects happen:<ref name="pmid19923405">{{cite journal| author=Riccardi D, Brown EM| title=Physiology and pathophysiology of the calcium-sensing receptor in the kidney. | journal=Am J Physiol Renal Physiol | year= 2010 | volume= 298 | issue= 3 | pages= F485-99 | pmid=19923405 | doi=10.1152/ajprenal.00608.2009 | pmc=2838589 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19923405  }} </ref>
**[[Nephron|Renal tubules]]
*** Thick ascending [[loop of Henle]]:
****[[Reabsorption]] of [[sodium chloride]] is blocked, which leads to [[diuresis]] and an increase in [[calcium]] excretion in the [[Kidney|kidneys]]. These, in turn, result in [[Hypovolemia|volume depletion]] and [[metabolic alkalosis]].
***[[Distal convoluted tubule|Distal convoluted tubules]] (luminal membrane) :
****[[Calcium]] [[reabsorption]] through [[TRPV5|transient receptor potential vanilloid member 5 (TRPV5)]] channels is increased.
***[[Collecting duct system|Collecting duct]] (luminal membranes):
**** Expression of [[Aquaporin 2|aquaporin 2 water channels]] is decreased, and that decreases water [[reabsorption]] and dilutes the [[urine]].
* 25-hydroxylation of [[vitamin D]] in the [[Kidney|kidneys]] is reduced by excessive [[calcium]] consumption, which decreases [[calcium]] absorption in the [[intestine]].<ref name="pmid19252114">{{cite journal| author=Medarov BI| title=Milk-alkali syndrome. | journal=Mayo Clin Proc | year= 2009 | volume= 84 | issue= 3 | pages= 261-7 | pmid=19252114 | doi=10.1016/S0025-6196(11)61144-0 | pmc=2664604 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19252114  }} </ref>
*[[Hypercalcemia]] inhibits [[Parathyroid hormone|parathyroid hormone (PTH)]] which decreases [[bone turnover]] and the capacity of the [[bone]] for [[calcium]] buffering and increases the [[excretion]] of [[calcium]] in the [[Kidney|kidneys]].<ref name="pmid17699269">{{cite journal| author=Felsenfeld AJ, Levine BS| title=Milk alkali syndrome and the dynamics of calcium homeostasis. | journal=Clin J Am Soc Nephrol | year= 2006 | volume= 1 | issue= 4 | pages= 641-54 | pmid=17699269 | doi=10.2215/CJN.01451005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17699269  }} </ref>
*[[Hypercalcemia]] causes [[nausea and vomiting]], which in turn deteriorate [[Hypovolemia|volume depletion]] and [[metabolic alkalosis]].<ref name="pmid17699269">{{cite journal| author=Felsenfeld AJ, Levine BS| title=Milk alkali syndrome and the dynamics of calcium homeostasis. | journal=Clin J Am Soc Nephrol | year= 2006 | volume= 1 | issue= 4 | pages= 641-54 | pmid=17699269 | doi=10.2215/CJN.01451005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17699269  }} </ref>


The pathophysiology of [disease/malignancy] depends on the histological subtype.
===== '''Metabolic Alkalosis''' =====


==Pathophysiology==
* Increases the affinity of the CaSRs to [[calcium]], which increases natriuresis.  
===Physiology===
* Stimulates [[TRPV5]] which increases [[calcium]] [[reabsorption]] and worsens [[hypercalcemia]].<ref name="pmid16268810">{{cite journal| author=Picolos MK, Lavis VR, Orlander PR| title=Milk-alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients. | journal=Clin Endocrinol (Oxf) | year= 2005 | volume= 63 | issue= 5 | pages= 566-76 | pmid=16268810 | doi=10.1111/j.1365-2265.2005.02383.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16268810  }} </ref><ref name="pmid19923405">{{cite journal| author=Riccardi D, Brown EM| title=Physiology and pathophysiology of the calcium-sensing receptor in the kidney. | journal=Am J Physiol Renal Physiol | year= 2010 | volume= 298 | issue= 3 | pages= F485-99 | pmid=19923405 | doi=10.1152/ajprenal.00608.2009 | pmc=2838589 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19923405  }} </ref>
The normal physiology of [name of process] can be understood as follows:
* Several factors that increase [[bicarbonate]] [[reabsorption]] and contribute to the [[alkalosis]] in milk-alkali syndrome include:<ref name="pmid9436295">{{cite journal| author=Fiorino AS| title=Hypercalcemia and alkalosis due to the milk-alkali syndrome: a case report and review. | journal=Yale J Biol Med | year= 1996 | volume= 69 | issue= 6 | pages= 517-23 | pmid=9436295 | doi= | pmc=2589043 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9436295  }} </ref>
**[[Hypovolemia|Volume depletion]] due to increased [[sodium]] and free water [[excretion]] caused by increased [[calcium]] intake
** Suppression of [[Parathyroid hormone|PTH]] 
** Direct [[Nephron|tubular]] effects of [[calcium]]  
** Other factors that cause [[Hypovolemia|volume depletion]] or [[alkalosis]] such as [[Nausea and vomiting|vomiting]] or [[thiazide]] use


===Pathogenesis===
== Histopathology ==
*The exact pathogenesis of [disease name] is not completely understood.
OR
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Genetics==
* There is limited evidence on the renal [[Histopathology|histopathological]] findings of milk-alkali syndrome.<ref name="pmid19252114" />
[Disease name] is transmitted in [mode of genetic transmission] pattern.
* The following findings on [[Autopsy|autopsies]] have been reported:<ref name="pmid18126919">{{cite journal| author=BURNETT CH, COMMONS RR| title=Hypercalcemia without hypercalcuria or hypophosphatemia, calcinosis and renal insufficiency; a syndrome following prolonged intake of milk and alkali. | journal=N Engl J Med | year= 1949 | volume= 240 | issue= 20 | pages= 787-94 | pmid=18126919 | doi=10.1056/NEJM194905192402001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18126919  }} </ref><ref name="pmid13016590">{{cite journal| author=WERMER P, KUSCHNER M, RILEY EA| title=Case reports; reversible metastatic calcification associated with excessive milk and alkali intake. | journal=Am J Med | year= 1953 | volume= 14 | issue= 1 | pages= 108-15 | pmid=13016590 | doi=10.1016/0002-9343(53)90362-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13016590  }} </ref><ref name="pmid14375805">{{cite journal| author=HOLTEN C, LUNDBAEK K| title=Renal insufficiency and severe calcinosis due to excessive alkali-intake. | journal=Acta Med Scand | year= 1955 | volume= 151 | issue= 3 | pages= 177-83 | pmid=14375805 | doi=10.1111/j.0954-6820.1955.tb10281.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14375805  }} </ref><ref name="pmid13124355">{{cite journal| author=DUFAULT FX, TOBIAS GJ| title=Potentially reversible renal failure following excessive calcium and alkali intake in peptic ulcer therapy. | journal=Am J Med | year= 1954 | volume= 16 | issue= 2 | pages= 231-6 | pmid=13124355 | doi=10.1016/0002-9343(54)90339-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13124355  }} </ref>
** [[Nephrocalcinosis]]
** [[Glomerulus]] hyalinization (partial to complete)
** Thickened [[Bowman's capsule]]
** [[Atrophy]] of the [[Tubule|tubules]]
** [[Vascular]] changes
** Diffuse [[Lymphocyte|lymphocytic]] infiltration


OR
* The following findings on [[Biopsy|biopsies]] have been reported:<ref name="pmid14349424">{{cite journal| author=SCHOLZ DA, KEATING FR| title=Milk-alkali syndrome; review of eight cases. | journal=AMA Arch Intern Med | year= 1955 | volume= 95 | issue= 3 | pages= 460-8 | pmid=14349424 | doi=10.1001/archinte.1955.00250090098012 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14349424  }} </ref><ref name="pmid13739449">{{cite journal| author=RANDALL RE, STRAUSS MB, McNEELY WF| title=The milk-alkali synfcmme. | journal=Arch Intern Med | year= 1961 | volume= 107 | issue=  | pages= 163-81 | pmid=13739449 | doi=10.1001/archinte.1961.03620020013003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13739449  }} </ref><ref name="pmid1010876">{{cite journal| author=Junor BJ, Catto GR| title=Renal biopsy in the milk-alkali syndrome. | journal=J Clin Pathol | year= 1976 | volume= 29 | issue= 12 | pages= 1074-6 | pmid=1010876 | doi=10.1136/jcp.29.12.1074 | pmc=476303 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1010876  }} </ref>
** Focal [[calcification]] in the [[Nephron|renal tubules]]
** [[Degeneration]] of the [[Nephron|tubular]] [[epithelium]]
** Granular material (presumably [[calcium]] laden) in and around the [[Connecting tubule|collecting tubules]]
** Hyalinization of some [[Glomerulus|glomeruli]]
** Thickened basement membrane


Genes involved in the pathogenesis of [disease name] include:
* It has been suggested that the [[prognosis]] of milk-alkali syndrome is associated with the severity of the [[Histology|histologic]] changes on the [[Biopsy|biopsies]] and that renal [[calcium]] deposition are usually not detectable on [[X-rays|x-ray]].<ref name="pmid1010876">{{cite journal| author=Junor BJ, Catto GR| title=Renal biopsy in the milk-alkali syndrome. | journal=J Clin Pathol | year= 1976 | volume= 29 | issue= 12 | pages= 1074-6 | pmid=1010876 | doi=10.1136/jcp.29.12.1074 | pmc=476303 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1010876  }} </ref>
*[Gene1]
*[Gene2]
*[Gene3]
 
OR
 
The development of [disease name] is the result of multiple genetic mutations such as:
 
*[Mutation 1]
*[Mutation 2]
*[Mutation 3]
 
==Associated Conditions==
Conditions associated with [disease name] include:
 
*[Condition 1]
*[Condition 2]
*[Condition 3]
 
==Gross Pathology==
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
==Microscopic Pathology==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].


==References==
==References==
{{reflist|2}}
{{reflist|2}}
{{WH}}
{{WS}}
[[Category:Needs content]]
[[Category:Needs content]]
[[Category:Electrolyte disturbances]]
[[Category:Electrolyte disturbances]]

Latest revision as of 13:03, 16 July 2020

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

Overview

The exact pathogenesis of milk-alkali syndrome is unknown. Hypercalcemia in milk-alkali syndrome involves several mechanisms including: intestinal absorption of calcium is increased, bone buffering of calcium becomes saturated, and renal excretion of calcium is decreased. Several factors that increase bicarbonate reabsorption and contribute to the alkalosis in milk-alkali syndrome include: volume depletion due to increased sodium and free water excretion caused by increased calcium intake, suppression of PTH, direct tubular effects of calcium and other factors that cause volume depletion or alkalosis such as vomiting or thiazide use.

Pathophysiology

  • The exact pathogenesis of milk-alkali syndrome is unknown.
  • Consumption of excessive amounts of calcium and absorbable alkali causes milk-alkali syndrome.[1]

Pathogenesis

The pathogenesis of milk-alkali syndrome involves the kidneys, bones, and intestines.[2]

Hypercalcemia
Metabolic Alkalosis

Histopathology

References

  1. ↑ 1.0 1.1 1.2 Medarov BI (2009). "Milk-alkali syndrome". Mayo Clin Proc. 84 (3): 261–7. doi:10.1016/S0025-6196(11)61144-0. PMC 2664604. PMID 19252114.
  2. ↑ Arroyo M, Fenves AZ, Emmett M (2013). "The calcium-alkali syndrome". Proc (Bayl Univ Med Cent). 26 (2): 179–81. doi:10.1080/08998280.2013.11928954. PMC 3603742. PMID 23543983.
  3. ↑ 3.0 3.1 3.2 3.3 Felsenfeld AJ, Levine BS (2006). "Milk alkali syndrome and the dynamics of calcium homeostasis". Clin J Am Soc Nephrol. 1 (4): 641–54. doi:10.2215/CJN.01451005. PMID 17699269.
  4. ↑ 4.0 4.1 Riccardi D, Brown EM (2010). "Physiology and pathophysiology of the calcium-sensing receptor in the kidney". Am J Physiol Renal Physiol. 298 (3): F485–99. doi:10.1152/ajprenal.00608.2009. PMC 2838589. PMID 19923405.
  5. ↑ Picolos MK, Lavis VR, Orlander PR (2005). "Milk-alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients". Clin Endocrinol (Oxf). 63 (5): 566–76. doi:10.1111/j.1365-2265.2005.02383.x. PMID 16268810.
  6. ↑ Fiorino AS (1996). "Hypercalcemia and alkalosis due to the milk-alkali syndrome: a case report and review". Yale J Biol Med. 69 (6): 517–23. PMC 2589043. PMID 9436295.
  7. ↑ BURNETT CH, COMMONS RR (1949). "Hypercalcemia without hypercalcuria or hypophosphatemia, calcinosis and renal insufficiency; a syndrome following prolonged intake of milk and alkali". N Engl J Med. 240 (20): 787–94. doi:10.1056/NEJM194905192402001. PMID 18126919.
  8. ↑ WERMER P, KUSCHNER M, RILEY EA (1953). "Case reports; reversible metastatic calcification associated with excessive milk and alkali intake". Am J Med. 14 (1): 108–15. doi:10.1016/0002-9343(53)90362-3. PMID 13016590.
  9. ↑ HOLTEN C, LUNDBAEK K (1955). "Renal insufficiency and severe calcinosis due to excessive alkali-intake". Acta Med Scand. 151 (3): 177–83. doi:10.1111/j.0954-6820.1955.tb10281.x. PMID 14375805.
  10. ↑ DUFAULT FX, TOBIAS GJ (1954). "Potentially reversible renal failure following excessive calcium and alkali intake in peptic ulcer therapy". Am J Med. 16 (2): 231–6. doi:10.1016/0002-9343(54)90339-3. PMID 13124355.
  11. ↑ SCHOLZ DA, KEATING FR (1955). "Milk-alkali syndrome; review of eight cases". AMA Arch Intern Med. 95 (3): 460–8. doi:10.1001/archinte.1955.00250090098012. PMID 14349424.
  12. ↑ RANDALL RE, STRAUSS MB, McNEELY WF (1961). "The milk-alkali synfcmme". Arch Intern Med. 107: 163–81. doi:10.1001/archinte.1961.03620020013003. PMID 13739449.
  13. ↑ 13.0 13.1 Junor BJ, Catto GR (1976). "Renal biopsy in the milk-alkali syndrome". J Clin Pathol. 29 (12): 1074–6. doi:10.1136/jcp.29.12.1074. PMC 476303. PMID 1010876.
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