Electrolyte disturbance: Difference between revisions

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'''For patient information, click [[Electrolyte disturbance (patient information)|here]]'''
{{Electrolyte disturbance}}
{{Electrolyte disturbance}}
{{CMG}}{{AE}}{{SMP}}
{{CMG}}; {{AE}}{{SMP}}{{MMJ}}


{{SK}} abnormal electrolytes, abnormal lytes, lytes
{{SK}} abnormal electrolytes, abnormal lytes, lytes


==Overview==
==Overview==
Electrolytes are electrically charged solutes necessary to maintain body [[homeostasis]]. The main electrolytes include [[Sodium]] (Na), [[Potassium]] (K), [[Chloride]] (Cl), [[Calcium]] (Ca), [[Phosphorus]] (P), and [[Magnesium]] (Mg). These electrolytes are involved in multiple [[Physiology|physiologic]] and neurohormonal reactions necessary to maintain [[neuromuscular]], [[neuronal]], [[Myocardium|myocardial]], and [[Acid-base homeostasis|acid-base balance]]. Their balance are mainly regulated by [[Kidney|renal]] and [[endocrine]] systems, any changes in their balance may be life threatening. Electrolytes are in balance to achieve neutral electrical charges. Electrolytes could be classified based on their electrical charge to anions and cations. Anions include bicarbonate, chloride, and phosphorus. Cations are calcium, magnesium, potassium, and sodium. Sodium and chloride are the major extracellular ions that has the greatest impact on serum osmolality (solute concentration in 1 liter of water). Calcium and bicarbonate are the other major extracellular electrolytes. Main intracellular electrolytes are potassium, phosphorus, and magnesium.   
Electrolytes are electrically charged solutes necessary to maintain body [[homeostasis]]. The main electrolytes include [[Sodium]] (Na), [[Potassium]] (K), [[Chloride]] (Cl), [[Calcium]] (Ca), [[Phosphorus]] (P), and [[Magnesium]] (Mg). These electrolytes are involved in multiple [[Physiology|physiologic]] and neurohormonal reactions necessary to maintain [[neuromuscular]], [[neuronal]], [[Myocardium|myocardial]], and [[Acid-base homeostasis|acid-base balance]]. Their balance are mainly regulated by [[Kidney|renal]] and [[endocrine]] systems, any changes in their balance may be life threatening. Electrolytes are in balance to achieve neutral electrical charges. Electrolytes could be classified based on their electrical charge to [[anions]] and [[cations]]. Anions include [[bicarbonate]], [[chloride]], and [[phosphorus]]. Cations are [[calcium]], [[magnesium]], [[potassium]], and [[sodium]]. Sodium and chloride are the major extracellular ions that has the greatest impact on serum [[osmolality]] (solute concentration in 1 liter of water). [[Calcium]] and bicarbonate are the other major extracellular electrolytes. Main intracellular electrolytes are potassium, phosphorus, and magnesium.   


==Causes==
==Causes==
{| class="wikitable"
The following table summarize the common causes for electrolytes imbalance.<br>
!Electrolyte
<br>
!Ionic formula
 
!Normal limits (mg/dl)
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
!Disturbance
! align="center" style="background:#4479BA; color: #FFFFFF;" |Electrolyte
! colspan="2" |Common causes
! align="center" style="background:#4479BA; color: #FFFFFF;" |Ionic formula
!
! align="center" style="background:#4479BA; color: #FFFFFF;" |Normal limits (meq/l)
!
! align="center" style="background:#4479BA; color: #FFFFFF;" |Disturbance
! align="center" style="background:#4479BA; color: #FFFFFF;" |Lab value
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |Common causes
|-
|-
| rowspan="4" |[[Sodium]]
| rowspan="5" align="center" style="background:#DCDCDC;" |[[Sodium|'''Sodium''']]
| rowspan="4" |Na<sup>+</sup>
| rowspan="5" style="padding: 5px 5px; background: #F5F5F5;" align="center" |Na<sup>+</sup>
| rowspan="4" |135-145
| rowspan="5" style="padding: 5px 5px; background: #F5F5F5;" align="center" |135-145
| rowspan="3" |[[hyponatremia]]
| rowspan="3" style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyponatremia]]
|Hypovolemic
| rowspan="3" style="padding: 5px 5px; background: #F5F5F5;" align="center" |<135 meq/L
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Hypovolemic<ref name="pmid10440307">{{cite journal |vauthors=Alam NH, Majumder RN, Fuchs GJ |title=Efficacy and safety of oral rehydration solution with reduced osmolarity in adults with cholera: a randomised double-blind clinical trial. CHOICE study group |journal=Lancet |volume=354 |issue=9175 |pages=296–9 |date=July 1999 |pmid=10440307 |doi= |url=}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Renal loss ([[Diuretic|diuretics]])
* Renal loss ([[Diuretic|diuretics]])
* Extrarenal loss ([[Bleeding|hemorrhage]], [[diarrhea]], [[Perspiration|sweating]])
* Extrarenal loss ([[Bleeding|hemorrhage]], [[diarrhea]], [[Perspiration|sweating]])
|
|
|-
|-
|Euvolemic
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Euvolemic<ref name="pmid16632011">{{cite journal |vauthors=Pham PC, Pham PM, Pham PT |title=Vasopressin excess and hyponatremia |journal=Am. J. Kidney Dis. |volume=47 |issue=5 |pages=727–37 |date=May 2006 |pmid=16632011 |doi=10.1053/j.ajkd.2006.01.020 |url=}}</ref><ref name="pmid17507705">{{cite journal |vauthors=Ellison DH, Berl T |title=Clinical practice. The syndrome of inappropriate antidiuresis |journal=N. Engl. J. Med. |volume=356 |issue=20 |pages=2064–72 |date=May 2007 |pmid=17507705 |doi=10.1056/NEJMcp066837 |url=}}</ref><ref name="pmid2548097">{{cite journal |vauthors=Oelkers W |title=Hyponatremia and inappropriate secretion of vasopressin (antidiuretic hormone) in patients with hypopituitarism |journal=N. Engl. J. Med. |volume=321 |issue=8 |pages=492–6 |date=August 1989 |pmid=2548097 |doi=10.1056/NEJM198908243210802 |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Syndrome of inappropriate antidiuretic hormone|SIADH]], [[Glucocorticoid deficiency 1|glucocorticoid deficiency]], [[psychogenic polydipsia]]
* [[Syndrome of inappropriate antidiuretic hormone|SIADH]]
|-
* [[Glucocorticoid deficiency 1|Glucocorticoid deficiency]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Hypervolemic<ref name="pmid8074021">{{cite journal |vauthors=Leier CV, Dei Cas L, Metra M |title=Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: hyponatremia, hypokalemia, and hypomagnesemia |journal=Am. Heart J. |volume=128 |issue=3 |pages=564–74 |date=September 1994 |pmid=8074021 |doi= |url=}}</ref><ref name="pmid2146429">{{cite journal |vauthors=Rodríguez-Iturbe B, Colic D, Parra G, Gutkowska J |title=Atrial natriuretic factor in the acute nephritic and nephrotic syndromes |journal=Kidney Int. |volume=38 |issue=3 |pages=512–7 |date=September 1990 |pmid=2146429 |doi= |url=}}</ref><ref name="pmid18671303">{{cite journal |vauthors=Ginès P, Guevara M |title=Hyponatremia in cirrhosis: pathogenesis, clinical significance, and management |journal=Hepatology |volume=48 |issue=3 |pages=1002–10 |date=September 2008 |pmid=18671303 |doi=10.1002/hep.22418 |url=}}</ref>
* [[Psychogenic polydipsia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Congestive heart failure|CHF]], [[cirrhosis]], [[nephrotic syndrome]], [[Renal insufficiency|renal failure]]
|
|-
|
| rowspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hypernatremia]]
| rowspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="center" |>145 meq/L
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Extrarenal loss<ref name="pmid3799631">{{cite journal |vauthors=Rose BD |title=New approach to disturbances in the plasma sodium concentration |journal=Am. J. Med. |volume=81 |issue=6 |pages=1033–40 |date=December 1986 |pmid=3799631 |doi= |url=}}</ref><ref name="pmid15765239">{{cite journal |vauthors=Shamsuddin AK, Yanagimoto S, Kuwahara T, Zhang Y, Nomura C, Kondo N |title=Changes in the index of sweat ion concentration with increasing sweat during passive heat stress in humans |journal=Eur. J. Appl. Physiol. |volume=94 |issue=3 |pages=292–7 |date=June 2005 |pmid=15765239 |doi=10.1007/s00421-005-1314-7 |url=}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Vomiting]], [[diarrhea]], [[Insensible water loss|insensible loss]]
|-
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Renal loss<ref name="pmid3449889">{{cite journal |vauthors=Thompson CJ, Baylis PH |title=Thirst in diabetes insipidus: clinical relevance of quantitative assessment |journal=Q. J. Med. |volume=65 |issue=246 |pages=853–62 |date=October 1987 |pmid=3449889 |doi= |url=}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Diuretic|Diuretics]], [[diabetes insipidus]] (central and nephrogenic)
|-
|-
|Hypervolemic
| rowspan="4" align="center" style="background:#DCDCDC;" |[[Potassium|'''Potassium''']]
|
| rowspan="4" style="padding: 5px 5px; background: #F5F5F5;" align="center" |K<sup>+</sup>
* [[Congestive heart failure|CHF]]
| rowspan="4" style="padding: 5px 5px; background: #F5F5F5;" align="center" |3.5-5
* [[Cirrhosis]]
| rowspan="3" style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hypokalemia]]
* [[Nephrotic syndrome]]
| rowspan="3" style="padding: 5px 5px; background: #F5F5F5;" align="center" |<3.5 meq/L
* [[Renal insufficiency|Renal failure]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Transcellular shifts<ref name="pmid3084904">{{cite journal |vauthors=Adrogué HJ, Lederer ED, Suki WN, Eknoyan G |title=Determinants of plasma potassium levels in diabetic ketoacidosis |journal=Medicine (Baltimore) |volume=65 |issue=3 |pages=163–72 |date=May 1986 |pmid=3084904 |doi= |url=}}</ref><ref name="pmid7025622">{{cite journal |vauthors=Adrogué HJ, Madias NE |title=Changes in plasma potassium concentration during acute acid-base disturbances |journal=Am. J. Med. |volume=71 |issue=3 |pages=456–67 |date=September 1981 |pmid=7025622 |doi= |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Insulin]] therapy, [[alkalosis]]
|
|-
|-
|[[hypernatremia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |GI loss<ref name="pmid20124467">{{cite journal |vauthors=Ho JM, Juurlink DN, Cavalcanti RB |title=Hypokalemia following polyethylene glycol-based bowel preparation for colonoscopy in older hospitalized patients with significant comorbidities |journal=Ann Pharmacother |volume=44 |issue=3 |pages=466–70 |date=March 2010 |pmid=20124467 |doi=10.1345/aph.1M341 |url=}}</ref><ref name="pmid12695271">{{cite journal |vauthors=Beloosesky Y, Grinblat J, Weiss A, Grosman B, Gafter U, Chagnac A |title=Electrolyte disorders following oral sodium phosphate administration for bowel cleansing in elderly patients |journal=Arch. Intern. Med. |volume=163 |issue=7 |pages=803–8 |date=April 2003 |pmid=12695271 |doi=10.1001/archinte.163.7.803 |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Diarrhea]], [[laxative abuse]], [[vomiting]]
|
|
|
|-
|-
| rowspan="2" |[[Potassium]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Renal loss<ref name="pmid18839206">{{cite journal |vauthors=Wang WH, Giebisch G |title=Regulation of potassium (K) handling in the renal collecting duct |journal=Pflugers Arch. |volume=458 |issue=1 |pages=157–68 |date=May 2009 |pmid=18839206 |pmc=2730119 |doi=10.1007/s00424-008-0593-3 |url=}}</ref><ref name="pmid19570885">{{cite journal |vauthors=Vallon V, Schroth J, Lang F, Kuhl D, Uchida S |title=Expression and phosphorylation of the Na+-Cl- cotransporter NCC in vivo is regulated by dietary salt, potassium, and SGK1 |journal=Am. J. Physiol. Renal Physiol. |volume=297 |issue=3 |pages=F704–12 |date=September 2009 |pmid=19570885 |pmc=2739704 |doi=10.1152/ajprenal.00030.2009 |url=}}</ref><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><ref name="pmid9681697">{{cite journal |vauthors=Monnens L, Bindels R, Grünfeld JP |title=Gitelman syndrome comes of age |journal=Nephrol. Dial. Transplant. |volume=13 |issue=7 |pages=1617–9 |date=July 1998 |pmid=9681697 |doi= |url=}}</ref>
| rowspan="2" |K<sup>+</sup>
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
| rowspan="2" |3.5-5
* Acidosis: [[Diabetic ketoacidosis|DKA]], [[Renal tubular acidosis|RTA]] (I and II)
|[[hypokalemia]]
* Alkalosis: [[Bartter syndrome|Bartter's syndrome]], [[Gitelman syndrome|Gitelman's syndrome]]
|
|
|
|
|-
|-
|[[hyperkalemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]]<ref name="pmid17395950">{{cite journal |vauthors=Smellie WS |title=Spurious hyperkalaemia |journal=BMJ |volume=334 |issue=7595 |pages=693–5 |date=March 2007 |pmid=17395950 |pmc=1839224 |doi=10.1136/bmj.39119.607986.47 |url=}}</ref><ref name="pmid5092154">{{cite journal |vauthors=Gonick HC, Kleeman CR, Rubini ME, Maxwell MH |title=Functional impairment in chronic renal disease. 3. Studies of potassium excretion |journal=Am. J. Med. Sci. |volume=261 |issue=5 |pages=281–90 |date=May 1971 |pmid=5092154 |doi= |url=}}</ref><ref name="pmid2376088">{{cite journal |vauthors=Arthur S, Greenberg A |title=Hyperkalemia associated with intravenous labetalol therapy for acute hypertension in renal transplant recipients |journal=Clin. Nephrol. |volume=33 |issue=6 |pages=269–71 |date=June 1990 |pmid=2376088 |doi= |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |>5 meq/L
|
| colspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[ACE inhibitors]], [[acidosis]], [[Addison's disease|addisonian crisis]], [[beta blockers]], [[blood transfusion]], [[cirrhosis]], [[diabetic nephropathy]], high potassium diet, [[malnutrition]], [[renal tubular acidosis]] type IV, [[Renal insufficiency|renal failure]]
|
|
|-
|-
| rowspan="2" |[[Calcium]]
| rowspan="2" align="center" style="background:#DCDCDC;" |[[Calcium|'''Calcium''']]
| rowspan="2" |Ca<sup>2+</sup>
| rowspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="center" |Ca<sup>2+</sup>
| rowspan="2" |8.9-10.1
| rowspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="center" |8.5-10.2
|[[hypocalcemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hypocalcemia]]<ref name="pmid19923405">{{cite journal |vauthors=Riccardi D, Brown EM |title=Physiology and pathophysiology of the calcium-sensing receptor in the kidney |journal=Am. J. Physiol. Renal Physiol. |volume=298 |issue=3 |pages=F485–99 |date=March 2010 |pmid=19923405 |pmc=2838589 |doi=10.1152/ajprenal.00608.2009 |url=}}</ref><ref name="pmid7024719">{{cite journal |vauthors=Neufeld M, Maclaren NK, Blizzard RM |title=Two types of autoimmune Addison's disease associated with different polyglandular autoimmune (PGA) syndromes |journal=Medicine (Baltimore) |volume=60 |issue=5 |pages=355–62 |date=September 1981 |pmid=7024719 |doi= |url=}}</ref><ref name="pmid6709029">{{cite journal |vauthors=Cholst IN, Steinberg SF, Tropper PJ, Fox HE, Segre GV, Bilezikian JP |title=The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects |journal=N. Engl. J. Med. |volume=310 |issue=19 |pages=1221–5 |date=May 1984 |pmid=6709029 |doi=10.1056/NEJM198405103101904 |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<8.5 meq/L
|
| colspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Hypoparathyroidism]], [[pseudohypoparathyroidism]], [[hypomagnesemia]], [[Vitamin D deficiency|hypovitaminosis D]],
|
 
|
[[Chronic renal failure|chronic kidney disease]], [[hypoalbuminemia]]
|-
|-
|[[hypercalcemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hypercalcemia]]<ref name="pmid2239937">{{cite journal |vauthors=Meric F, Yap P, Bia MJ |title=Etiology of hypercalcemia in hemodialysis patients on calcium carbonate therapy |journal=Am. J. Kidney Dis. |volume=16 |issue=5 |pages=459–64 |date=November 1990 |pmid=2239937 |doi= |url=}}</ref><ref name="pmid9612524">{{cite journal |vauthors=Glendenning P, Gutteridge DH, Retallack RW, Stuckey BG, Kermode DG, Kent GN |title=High prevalence of normal total calcium and intact PTH in 60 patients with proven primary hyperparathyroidism: a challenge to current diagnostic criteria |journal=Aust N Z J Med |volume=28 |issue=2 |pages=173–8 |date=April 1998 |pmid=9612524 |doi= |url=}}</ref><ref name="pmid8865795">{{cite journal |vauthors=Alikhan Z, Singh A |title=Hyperthyroidism manifested as hypercalcemia |journal=South. Med. J. |volume=89 |issue=10 |pages=997–8 |date=October 1996 |pmid=8865795 |doi= |url=}}</ref><ref name="pmid2679445">{{cite journal |vauthors=Distler W |title=[The climacteric--physiology or pathology?] |language=German |journal=Arch. Gynecol. Obstet. |volume=245 |issue=1-4 |pages=947–52 |date=1989 |pmid=2679445 |doi= |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |>10.2 meq/L
|
| colspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Hyperparathyroidism]], [[familial hypocalciuric hypercalcemia]], [[Cancer|malignancy]], [[Milk-alkali syndrome]],
|
 
|
[[vitamin D]] toxicity, [[sarcoidosis]], [[Diuretic|diuretics]], [[lithium]]
|-
|-
| rowspan="2" |[[Phosphate]]
| rowspan="2" align="center" style="background:#DCDCDC;" |[[Phosphate|'''Phosphate''']]
| rowspan="2" |PO<sub>4</sub><sup>3-</sup>
| rowspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="center" |PO<sub>4</sub><sup>3-</sup>
| rowspan="2" |2.5-4.5
| rowspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="center" |2.5-4.5
|[[hypophosphatemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hypophosphatemia]]<ref name="pmid15888903">{{cite journal |vauthors=Marinella MA |title=Refeeding syndrome and hypophosphatemia |journal=J Intensive Care Med |volume=20 |issue=3 |pages=155–9 |date=2005 |pmid=15888903 |doi=10.1177/0885066605275326 |url=}}</ref><ref name="pmid14105225">{{cite journal |vauthors=MOSTELLAR ME, TUTTLE EP |title=EFFECTS OF ALKALOSIS ON PLASMA CONCENTRATION AND URINARY EXCRETION OF INORGANIC PHOSPHATE IN MAN |journal=J. Clin. Invest. |volume=43 |issue= |pages=138–49 |date=January 1964 |pmid=14105225 |pmc=289504 |doi=10.1172/JCI104888 |url=}}</ref><ref name="pmid8743494">{{cite journal |vauthors=Murer H, Lötscher M, Kaissling B, Levi M, Kempson SA, Biber J |title=Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation |journal=Kidney Int. |volume=49 |issue=6 |pages=1769–73 |date=June 1996 |pmid=8743494 |doi= |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<2.5 meq/L
|
| colspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Refeeding syndrome]], [[respiratory alkalosis]], [[Alcoholism|alcohol abuse]], [[malabsorption]]
|
|
|-
|-
|[[hyperphosphatemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperphosphatemia]]<ref name="pmid6894477">{{cite journal |vauthors=Tsokos GC, Balow JE, Spiegel RJ, Magrath IT |title=Renal and metabolic complications of undifferentiated and lymphoblastic lymphomas |journal=Medicine (Baltimore) |volume=60 |issue=3 |pages=218–29 |date=May 1981 |pmid=6894477 |doi= |url=}}</ref><ref name="pmid4423658">{{cite journal |vauthors=Grossman RA, Hamilton RW, Morse BM, Penn AS, Goldberg M |title=Nontraumatic rhabdomyolysis and acute renal failure |journal=N. Engl. J. Med. |volume=291 |issue=16 |pages=807–11 |date=October 1974 |pmid=4423658 |doi=10.1056/NEJM197410172911601 |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |>4.5 meq/L
|
| colspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="left" |Transcellular shift, [[tumor lysis syndrome]] , [[rhabdomyolysis]], [[hypoparathyroidism]], [[pseudohypoparathyroidism]], [[acute kidney injury]], [[Chronic renal failure|chronic kidney disease]]
|
|
|-
|-
| rowspan="2" |[[Magnesium]]
| rowspan="2" align="center" style="background:#DCDCDC;" |[[Magnesium|'''Magnesium''']]
| rowspan="2" |Mg<sup>2+</sup>
| rowspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="center" |Mg<sup>2+</sup>
| rowspan="2" |1.5-2.5
| rowspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="center" |1.5-2.5
|[[hypomagnesemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hypomagnesemia]]<ref name="pmid1722865">{{cite journal |vauthors=Shah GM, Kirschenbaum MA |title=Renal magnesium wasting associated with therapeutic agents |journal=Miner Electrolyte Metab |volume=17 |issue=1 |pages=58–64 |date=1991 |pmid=1722865 |doi= |url=}}</ref><ref name="pmid8808192">{{cite journal |vauthors=Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC |title=Pathogenetic mechanisms of hypomagnesemia in alcoholic patients |journal=J Trace Elem Med Biol |volume=9 |issue=4 |pages=210–4 |date=December 1995 |pmid=8808192 |doi=10.1016/S0946-672X(11)80026-X |url=}}</ref><ref name="pmid8639008">{{cite journal |vauthors=Tosiello L |title=Hypomagnesemia and diabetes mellitus. A review of clinical implications |journal=Arch. Intern. Med. |volume=156 |issue=11 |pages=1143–8 |date=June 1996 |pmid=8639008 |doi= |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |<1.5 meq/L
|
| colspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Alcohol]] use, uncontrolled [[diabetes mellitus]], [[hypercalcemia]], [[Gitelman syndrome]], [[Loop diuretic|loop]] and [[Thiazide|thiazide diuretics]]
|
|
|-
|-
|[[hypermagnesemia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hypermagnesemia]]<ref name="pmid14178364">{{cite journal |vauthors=RANDALL RE, COHEN MD, SPRAY CC, ROSSMEISL EC |title=HYPERMAGNESEMIA IN RENAL FAILURE. ETIOLOGY AND TOXIC MANIFESTATIONS |journal=Ann. Intern. Med. |volume=61 |issue= |pages=73–88 |date=July 1964 |pmid=14178364 |doi= |url=}}</ref><ref name="pmid1489003">{{cite journal |vauthors=Clark BA, Brown RS |title=Unsuspected morbid hypermagnesemia in elderly patients |journal=Am. J. Nephrol. |volume=12 |issue=5 |pages=336–43 |date=1992 |pmid=1489003 |doi=10.1159/000168469 |url=}}</ref>
|
| style="padding: 5px 5px; background: #F5F5F5;" align="center" |>2.5 meq/L
|
| colspan="2" style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Renal insufficiency|Renal failure]], massive oral ingestion
|
|
|}
|}


*Drug side effect: [[Hydrochlorothiazide]], [[Pergolide]]
== Diagnosis ==
Diagnosis of electrolyte disturbances is suspected by clinical presentation and will be confirmed by laboratory values. Clinical manifestations depend on the severity of disturbances and their chronicity however, the presentation may vary according to underlying condition. The following table summarizes common symptoms and signs of electrolytes disturbances and important ECG findings.


==Table of common electrolyte disturbances==
<br>
==Electrolyte Abnormalities and ECG Changes==
{| align="center"
The most notable feature of [[hyperkalemia]] is the "tent shaped" or "peaked" [[T wave]]. Delayed ventricular [[depolarization]] leads to a widened [[QRS complex]] and the [[P wave]] becomes wider and flatter. When [[hyperkalemia]] becomes severe, the [[ECG]] resembles a sine wave as the [[P wave]] disappears from view. In contrast, [[hypokalemia]] is associated with flattenting of the [[T wave]] and the appearance of a [[U wave]].  When untreated, [[hypokalemia]] may lead to severe [[arrhythmias]].  
|-
 
|
The fast ventricular depolarization and [[repolarization]] associated with [[hypercalcemia]] lead to a characteristic shortening of the [[QT interval]]. [[Hypocalcemia]] has the opposite effect, lengthening the [[QT interval]].
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
 
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |Disturbance
==Differentiating electrolyte disturbances from other diseases==
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |Chronicity/ Level (meq/L)
 
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |Common clinical manifestations
Electrolyte disturbance must be differentiated from other causes of headache, altered mental status and seizures such as brain tumors and delirium trmemns.
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |ECG findings
|-
! align="center" style="background:#4479BA; color: #FFFFFF;" |Symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" |Signs
|-
| rowspan="2" align="center" style="background:#DCDCDC;" |[[Hyponatremia|'''Hyponatremia''']]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Early/125-130
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Nausea]], [[malaise]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Cramp|Muscle cramps]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |N/A
|-
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Late/115-120
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Headache]], [[lethargy]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Respiratory distress, [[coma]], [[seizure]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Non specific ST-T changes
|-
| align="center" style="background:#DCDCDC;" |[[Hypernatremia|'''Hypernatremia''']]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |>145
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Malaise
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Lethargy]], [[confusion]], [[coma]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Non specific ST-T changes
|-
| align="center" style="background:#DCDCDC;" |'''[[Hypokalemia]]<ref name="pmid5032523">{{cite journal |vauthors=Knochel JP, Schlein EM |title=On the mechanism of rhabdomyolysis in potassium depletion |journal=J. Clin. Invest. |volume=51 |issue=7 |pages=1750–8 |date=July 1972 |pmid=5032523 |pmc=292322 |doi=10.1172/JCI106976 |url=}}</ref>'''
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |<2.5-3
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Nausea]], [[anorexia]], [[vomiting]], [[muscle weakness]], [[muscle cramps]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Rhabdomyolysis]], [[respiratory failure]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ECG changes: [[ST depression]], decrease in [[T wave]] amplitude, [[The U Wave|U wave]], [[QT prolongation]]
* Arrhythmia: [[PAC]], [[Premature ventricular contraction|PVC]], [[sinus bradycardia]], paroxysmal atrial or [[junctional tachycardia]], [[atrioventricular block]], and [[ventricular tachycardia]] or [[fibrillation]]
|-
| align="center" style="background:#DCDCDC;" |'''[[Hyperkalemia]]<ref name="pmid11043630">{{cite journal |vauthors=Mattu A, Brady WJ, Robinson DA |title=Electrocardiographic manifestations of hyperkalemia |journal=Am J Emerg Med |volume=18 |issue=6 |pages=721–9 |date=October 2000 |pmid=11043630 |doi=10.1053/ajem.2000.7344 |url=}}</ref><ref name="pmid1119378">{{cite journal |vauthors=Bashour T, Hsu I, Gorfinkel HJ, Wickramesekaran R, Rios JC |title=Atrioventricular and intraventricular conduction in hyperkalemia |journal=Am. J. Cardiol. |volume=35 |issue=2 |pages=199–203 |date=February 1975 |pmid=1119378 |doi= |url=}}</ref>'''
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |>7.5
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Muscle weakness]], [[polyuria]], [[polydipsia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Paralysis]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ECG changes (in order of severity): [[Peaked T waves|Tall peaked T]], shortened QT interval, prolongation of [[PR interval]] and [[QRS complex|QRS duration]], P wave disappearance, QRS widening, [[Sine wave pattern|sine wave]]
* Arrhythmia:  [[Sinus bradycardia]], [[Sinoatrial arrest|sinus arrest]], slow [[Idioventricular rhythm|idioventricular rhythms]], [[ventricular tachycardia]], [[Bundle branch block|bundle branch blocks]], [[ventricular fibrillation]], and [[asystole]]
|-
| align="center" style="background:#DCDCDC;" |'''[[Hypocalcemia]]<ref name="pmid16079644">{{cite journal |vauthors=Benoit SR, Mendelsohn AB, Nourjah P, Staffa JA, Graham DJ |title=Risk factors for prolonged QTc among US adults: Third National Health and Nutrition Examination Survey |journal=Eur J Cardiovasc Prev Rehabil |volume=12 |issue=4 |pages=363–8 |date=August 2005 |pmid=16079644 |doi= |url=}}</ref><ref name="pmid17289071">{{cite journal |vauthors=Meyer T, Ruppert V, Karatolios K, Maisch B |title=Hereditary long QT syndrome due to autoimmune hypoparathyroidism in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome |journal=J Electrocardiol |volume=40 |issue=6 |pages=504–9 |date=2007 |pmid=17289071 |doi=10.1016/j.jelectrocard.2006.12.013 |url=}}</ref>'''
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |<7-7.5
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Paresthesia|Paresthesias]], [[muscle spasm]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Trousseau's sign]], [[Chvostek's sign]], [[Seizure|seizures]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ECG changes: [[QT prolongation|QT interval prolongation]], QRS shortening
* Arrhythmia: [[Sinus bradycardia]], [[Atrioventricular block|AV block]]
|-
| align="center" style="background:#DCDCDC;" |'''[[Hypercalcemia]]<ref name="pmid1424189">{{cite journal |vauthors=Rosenqvist M, Nordenström J, Andersson M, Edhag OK |title=Cardiac conduction in patients with hypercalcaemia due to primary hyperparathyroidism |journal=Clin. Endocrinol. (Oxf) |volume=37 |issue=1 |pages=29–33 |date=July 1992 |pmid=1424189 |doi= |url=}}</ref>'''
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |>12
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Fatigue]], [[depression]], [[insomnia]], [[Nausea and vomiting|nausea, vomiting]], [[constipation]], [[polyuria]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Hyperreflexia]], [[confusion]], coma
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* ECG changes: [[QT interval shortening]]
* Arrhythmia: [[Supraventricular arrhythmia|Supraventricular]] or ventricular arrhythmias
|-
| align="center" style="background:#DCDCDC;" |'''[[Hypophosphatemia]]<ref name="pmid6773412">{{cite journal |vauthors=Silvis SE, DiBartolomeo AG, Aaker HM |title=Hypophosphatemia and neurological changes secondary to oral caloric intake: a variant of hyperalimentation syndrome |journal=Am. J. Gastroenterol. |volume=73 |issue=3 |pages=215–22 |date=March 1980 |pmid=6773412 |doi= |url=}}</ref><ref name="pmid9717944">{{cite journal |vauthors=Weisinger JR, Bellorín-Font E |title=Magnesium and phosphorus |journal=Lancet |volume=352 |issue=9125 |pages=391–6 |date=August 1998 |pmid=9717944 |doi=10.1016/S0140-6736(97)10535-9 |url=}}</ref><ref name="pmid7506845">{{cite journal |vauthors=Ognibene A, Ciniglio R, Greifenstein A, Jarjoura D, Cugino A, Blend D, Whittier F |title=Ventricular tachycardia in acute myocardial infarction: the role of hypophosphatemia |journal=South. Med. J. |volume=87 |issue=1 |pages=65–9 |date=January 1994 |pmid=7506845 |doi= |url=}}</ref>'''
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |<1
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Irritability]], [[Paresthesia|paresthesias]], [[dysphagia]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Delirium]], [[seizure]], [[coma]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Ventricular arrhythmias]]
|-
| align="center" style="background:#DCDCDC;" |'''[[Hyperphosphatemia]]<ref name="pmid28646995">{{cite journal |vauthors=Ketteler M, Block GA, Evenepoel P, Fukagawa M, Herzog CA, McCann L, Moe SM, Shroff R, Tonelli MA, Toussaint ND, Vervloet MG, Leonard MB |title=Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters |journal=Kidney Int. |volume=92 |issue=1 |pages=26–36 |date=July 2017 |pmid=28646995 |doi=10.1016/j.kint.2017.04.006 |url=}}</ref>'''
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |>4.5
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Muscle cramps]], [[Paresthesia|paresthesias]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Tetanus]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[QT prolongation|QT interval prolongation]] (mainly due to associated hypocalcemia)
|-
| align="center" style="background:#DCDCDC;" |'''[[Hypomagnesemia]]<ref name="pmid13840893">{{cite journal |vauthors=VALLEE BL, WACKER WE, ULMER DD |title=The magnesium-deficiency tetany syndrome in man |journal=N. Engl. J. Med. |volume=262 |issue= |pages=155–61 |date=January 1960 |pmid=13840893 |doi=10.1056/NEJM196001282620401 |url=}}</ref>'''
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |<1
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Tremor]], [[tetanus]], [[Muscle weakness|weakness]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Apathy]], [[delirium]], [[coma]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*[[ECG]] changes: [[QRS complex|QRS widening]], [[peaked T waves]], increased [[PR interval]]
*Arrhythmia: [[Atrial]] and [[ventricular arrhythmias]]
|-
| align="center" style="background:#DCDCDC;" |'''[[Hypermagnesemia]]<ref name="pmid2161126">{{cite journal |vauthors=Krendel DA |title=Hypermagnesemia and neuromuscular transmission |journal=Semin Neurol |volume=10 |issue=1 |pages=42–5 |date=March 1990 |pmid=2161126 |doi=10.1055/s-2008-1041252 |url=}}</ref>'''
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |>4
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |Nausea, [[flushing]], [[headache]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |[[Somnolence]], [[hypotension]], absent [[Deep tendon reflex|DTR]]
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
*ECG changes: [[PR interval]] prolongation, increased [[QRS complex|QRS]] duration, [[QT prolongation|Q-T interval prolongation]]
*Arrhythmia: [[Third degree AV block|Complete heart block]]
|}


==References==
==References==

Latest revision as of 01:41, 18 September 2019


Electrolyte Disturbance Main Page

Patient Information

Overview

Classification

Hyponatremia
Hypernatremia
Hypokalemia
Hyperkalemia
Hypocalcemia
Hypercalcemia
Hypophosphatemia
Hyperphosphatemia
Hypomagnesemia
Hypermagnesemia

Causes

Diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]Mohamadmostafa Jahansouz M.D.[3]

Synonyms and keywords: abnormal electrolytes, abnormal lytes, lytes

Overview

Electrolytes are electrically charged solutes necessary to maintain body homeostasis. The main electrolytes include Sodium (Na), Potassium (K), Chloride (Cl), Calcium (Ca), Phosphorus (P), and Magnesium (Mg). These electrolytes are involved in multiple physiologic and neurohormonal reactions necessary to maintain neuromuscular, neuronal, myocardial, and acid-base balance. Their balance are mainly regulated by renal and endocrine systems, any changes in their balance may be life threatening. Electrolytes are in balance to achieve neutral electrical charges. Electrolytes could be classified based on their electrical charge to anions and cations. Anions include bicarbonate, chloride, and phosphorus. Cations are calcium, magnesium, potassium, and sodium. Sodium and chloride are the major extracellular ions that has the greatest impact on serum osmolality (solute concentration in 1 liter of water). Calcium and bicarbonate are the other major extracellular electrolytes. Main intracellular electrolytes are potassium, phosphorus, and magnesium.

Causes

The following table summarize the common causes for electrolytes imbalance.

Electrolyte Ionic formula Normal limits (meq/l) Disturbance Lab value Common causes
Sodium Na+ 135-145 Hyponatremia <135 meq/L Hypovolemic[1]
Euvolemic[2][3][4] SIADH, glucocorticoid deficiency, psychogenic polydipsia
Hypervolemic[5][6][7] CHF, cirrhosis, nephrotic syndrome, renal failure
Hypernatremia >145 meq/L Extrarenal loss[8][9] Vomiting, diarrhea, insensible loss
Renal loss[10] Diuretics, diabetes insipidus (central and nephrogenic)
Potassium K+ 3.5-5 Hypokalemia <3.5 meq/L Transcellular shifts[11][12] Insulin therapy, alkalosis
GI loss[13][14] Diarrhea, laxative abuse, vomiting
Renal loss[15][16][17][18]
Hyperkalemia[19][20][21] >5 meq/L ACE inhibitors, acidosis, addisonian crisis, beta blockers, blood transfusion, cirrhosis, diabetic nephropathy, high potassium diet, malnutrition, renal tubular acidosis type IV, renal failure
Calcium Ca2+ 8.5-10.2 Hypocalcemia[22][23][24] <8.5 meq/L Hypoparathyroidism, pseudohypoparathyroidism, hypomagnesemia, hypovitaminosis D,

chronic kidney disease, hypoalbuminemia

Hypercalcemia[25][26][27][28] >10.2 meq/L Hyperparathyroidism, familial hypocalciuric hypercalcemia, malignancy, Milk-alkali syndrome,

vitamin D toxicity, sarcoidosis, diuretics, lithium

Phosphate PO43- 2.5-4.5 Hypophosphatemia[29][30][31] <2.5 meq/L Refeeding syndrome, respiratory alkalosis, alcohol abuse, malabsorption
Hyperphosphatemia[32][33] >4.5 meq/L Transcellular shift, tumor lysis syndrome , rhabdomyolysis, hypoparathyroidism, pseudohypoparathyroidism, acute kidney injury, chronic kidney disease
Magnesium Mg2+ 1.5-2.5 Hypomagnesemia[34][35][36] <1.5 meq/L Alcohol use, uncontrolled diabetes mellitus, hypercalcemia, Gitelman syndrome, loop and thiazide diuretics
Hypermagnesemia[37][38] >2.5 meq/L Renal failure, massive oral ingestion

Diagnosis

Diagnosis of electrolyte disturbances is suspected by clinical presentation and will be confirmed by laboratory values. Clinical manifestations depend on the severity of disturbances and their chronicity however, the presentation may vary according to underlying condition. The following table summarizes common symptoms and signs of electrolytes disturbances and important ECG findings.


Disturbance Chronicity/ Level (meq/L) Common clinical manifestations ECG findings
Symptoms Signs
Hyponatremia Early/125-130 Nausea, malaise Muscle cramps N/A
Late/115-120 Headache, lethargy Respiratory distress, coma, seizure Non specific ST-T changes
Hypernatremia >145 Malaise Lethargy, confusion, coma Non specific ST-T changes
Hypokalemia[39] <2.5-3 Nausea, anorexia, vomiting, muscle weakness, muscle cramps Rhabdomyolysis, respiratory failure
Hyperkalemia[40][41] >7.5 Muscle weakness, polyuria, polydipsia Paralysis
Hypocalcemia[42][43] <7-7.5 Paresthesias, muscle spasm Trousseau's sign, Chvostek's sign, seizures
Hypercalcemia[44] >12 Fatigue, depression, insomnia, nausea, vomiting, constipation, polyuria Hyperreflexia, confusion, coma
Hypophosphatemia[45][46][47] <1 Irritability, paresthesias, dysphagia Delirium, seizure, coma Ventricular arrhythmias
Hyperphosphatemia[48] >4.5 Muscle cramps, paresthesias Tetanus QT interval prolongation (mainly due to associated hypocalcemia)
Hypomagnesemia[49] <1 Tremor, tetanus, weakness Apathy, delirium, coma
Hypermagnesemia[50] >4 Nausea, flushing, headache Somnolence, hypotension, absent DTR

References

  1. ↑ Alam NH, Majumder RN, Fuchs GJ (July 1999). "Efficacy and safety of oral rehydration solution with reduced osmolarity in adults with cholera: a randomised double-blind clinical trial. CHOICE study group". Lancet. 354 (9175): 296–9. PMID 10440307.
  2. ↑ Pham PC, Pham PM, Pham PT (May 2006). "Vasopressin excess and hyponatremia". Am. J. Kidney Dis. 47 (5): 727–37. doi:10.1053/j.ajkd.2006.01.020. PMID 16632011.
  3. ↑ Ellison DH, Berl T (May 2007). "Clinical practice. The syndrome of inappropriate antidiuresis". N. Engl. J. Med. 356 (20): 2064–72. doi:10.1056/NEJMcp066837. PMID 17507705.
  4. ↑ Oelkers W (August 1989). "Hyponatremia and inappropriate secretion of vasopressin (antidiuretic hormone) in patients with hypopituitarism". N. Engl. J. Med. 321 (8): 492–6. doi:10.1056/NEJM198908243210802. PMID 2548097.
  5. ↑ Leier CV, Dei Cas L, Metra M (September 1994). "Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: hyponatremia, hypokalemia, and hypomagnesemia". Am. Heart J. 128 (3): 564–74. PMID 8074021.
  6. ↑ Rodríguez-Iturbe B, Colic D, Parra G, Gutkowska J (September 1990). "Atrial natriuretic factor in the acute nephritic and nephrotic syndromes". Kidney Int. 38 (3): 512–7. PMID 2146429.
  7. ↑ Ginès P, Guevara M (September 2008). "Hyponatremia in cirrhosis: pathogenesis, clinical significance, and management". Hepatology. 48 (3): 1002–10. doi:10.1002/hep.22418. PMID 18671303.
  8. ↑ Rose BD (December 1986). "New approach to disturbances in the plasma sodium concentration". Am. J. Med. 81 (6): 1033–40. PMID 3799631.
  9. ↑ Shamsuddin AK, Yanagimoto S, Kuwahara T, Zhang Y, Nomura C, Kondo N (June 2005). "Changes in the index of sweat ion concentration with increasing sweat during passive heat stress in humans". Eur. J. Appl. Physiol. 94 (3): 292–7. doi:10.1007/s00421-005-1314-7. PMID 15765239.
  10. ↑ Thompson CJ, Baylis PH (October 1987). "Thirst in diabetes insipidus: clinical relevance of quantitative assessment". Q. J. Med. 65 (246): 853–62. PMID 3449889.
  11. ↑ Adrogué HJ, Lederer ED, Suki WN, Eknoyan G (May 1986). "Determinants of plasma potassium levels in diabetic ketoacidosis". Medicine (Baltimore). 65 (3): 163–72. PMID 3084904.
  12. ↑ Adrogué HJ, Madias NE (September 1981). "Changes in plasma potassium concentration during acute acid-base disturbances". Am. J. Med. 71 (3): 456–67. PMID 7025622.
  13. ↑ Ho JM, Juurlink DN, Cavalcanti RB (March 2010). "Hypokalemia following polyethylene glycol-based bowel preparation for colonoscopy in older hospitalized patients with significant comorbidities". Ann Pharmacother. 44 (3): 466–70. doi:10.1345/aph.1M341. PMID 20124467.
  14. ↑ Beloosesky Y, Grinblat J, Weiss A, Grosman B, Gafter U, Chagnac A (April 2003). "Electrolyte disorders following oral sodium phosphate administration for bowel cleansing in elderly patients". Arch. Intern. Med. 163 (7): 803–8. doi:10.1001/archinte.163.7.803. PMID 12695271.
  15. ↑ Wang WH, Giebisch G (May 2009). "Regulation of potassium (K) handling in the renal collecting duct". Pflugers Arch. 458 (1): 157–68. doi:10.1007/s00424-008-0593-3. PMC 2730119. PMID 18839206.
  16. ↑ Vallon V, Schroth J, Lang F, Kuhl D, Uchida S (September 2009). "Expression and phosphorylation of the Na+-Cl- cotransporter NCC in vivo is regulated by dietary salt, potassium, and SGK1". Am. J. Physiol. Renal Physiol. 297 (3): F704–12. doi:10.1152/ajprenal.00030.2009. PMC 2739704. PMID 19570885.
  17. ↑ 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.
  18. ↑ Monnens L, Bindels R, Grünfeld JP (July 1998). "Gitelman syndrome comes of age". Nephrol. Dial. Transplant. 13 (7): 1617–9. PMID 9681697.
  19. ↑ Smellie WS (March 2007). "Spurious hyperkalaemia". BMJ. 334 (7595): 693–5. doi:10.1136/bmj.39119.607986.47. PMC 1839224. PMID 17395950.
  20. ↑ Gonick HC, Kleeman CR, Rubini ME, Maxwell MH (May 1971). "Functional impairment in chronic renal disease. 3. Studies of potassium excretion". Am. J. Med. Sci. 261 (5): 281–90. PMID 5092154.
  21. ↑ Arthur S, Greenberg A (June 1990). "Hyperkalemia associated with intravenous labetalol therapy for acute hypertension in renal transplant recipients". Clin. Nephrol. 33 (6): 269–71. PMID 2376088.
  22. ↑ Riccardi D, Brown EM (March 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.
  23. ↑ Neufeld M, Maclaren NK, Blizzard RM (September 1981). "Two types of autoimmune Addison's disease associated with different polyglandular autoimmune (PGA) syndromes". Medicine (Baltimore). 60 (5): 355–62. PMID 7024719.
  24. ↑ Cholst IN, Steinberg SF, Tropper PJ, Fox HE, Segre GV, Bilezikian JP (May 1984). "The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects". N. Engl. J. Med. 310 (19): 1221–5. doi:10.1056/NEJM198405103101904. PMID 6709029.
  25. ↑ Meric F, Yap P, Bia MJ (November 1990). "Etiology of hypercalcemia in hemodialysis patients on calcium carbonate therapy". Am. J. Kidney Dis. 16 (5): 459–64. PMID 2239937.
  26. ↑ Glendenning P, Gutteridge DH, Retallack RW, Stuckey BG, Kermode DG, Kent GN (April 1998). "High prevalence of normal total calcium and intact PTH in 60 patients with proven primary hyperparathyroidism: a challenge to current diagnostic criteria". Aust N Z J Med. 28 (2): 173–8. PMID 9612524.
  27. ↑ Alikhan Z, Singh A (October 1996). "Hyperthyroidism manifested as hypercalcemia". South. Med. J. 89 (10): 997–8. PMID 8865795.
  28. ↑ Distler W (1989). "[The climacteric--physiology or pathology?]". Arch. Gynecol. Obstet. (in German). 245 (1–4): 947–52. PMID 2679445.
  29. ↑ Marinella MA (2005). "Refeeding syndrome and hypophosphatemia". J Intensive Care Med. 20 (3): 155–9. doi:10.1177/0885066605275326. PMID 15888903.
  30. ↑ MOSTELLAR ME, TUTTLE EP (January 1964). "EFFECTS OF ALKALOSIS ON PLASMA CONCENTRATION AND URINARY EXCRETION OF INORGANIC PHOSPHATE IN MAN". J. Clin. Invest. 43: 138–49. doi:10.1172/JCI104888. PMC 289504. PMID 14105225.
  31. ↑ Murer H, Lötscher M, Kaissling B, Levi M, Kempson SA, Biber J (June 1996). "Renal brush border membrane Na/Pi-cotransport: molecular aspects in PTH-dependent and dietary regulation". Kidney Int. 49 (6): 1769–73. PMID 8743494.
  32. ↑ Tsokos GC, Balow JE, Spiegel RJ, Magrath IT (May 1981). "Renal and metabolic complications of undifferentiated and lymphoblastic lymphomas". Medicine (Baltimore). 60 (3): 218–29. PMID 6894477.
  33. ↑ Grossman RA, Hamilton RW, Morse BM, Penn AS, Goldberg M (October 1974). "Nontraumatic rhabdomyolysis and acute renal failure". N. Engl. J. Med. 291 (16): 807–11. doi:10.1056/NEJM197410172911601. PMID 4423658.
  34. ↑ Shah GM, Kirschenbaum MA (1991). "Renal magnesium wasting associated with therapeutic agents". Miner Electrolyte Metab. 17 (1): 58–64. PMID 1722865.
  35. ↑ Elisaf M, Merkouropoulos M, Tsianos EV, Siamopoulos KC (December 1995). "Pathogenetic mechanisms of hypomagnesemia in alcoholic patients". J Trace Elem Med Biol. 9 (4): 210–4. doi:10.1016/S0946-672X(11)80026-X. PMID 8808192.
  36. ↑ Tosiello L (June 1996). "Hypomagnesemia and diabetes mellitus. A review of clinical implications". Arch. Intern. Med. 156 (11): 1143–8. PMID 8639008.
  37. ↑ RANDALL RE, COHEN MD, SPRAY CC, ROSSMEISL EC (July 1964). "HYPERMAGNESEMIA IN RENAL FAILURE. ETIOLOGY AND TOXIC MANIFESTATIONS". Ann. Intern. Med. 61: 73–88. PMID 14178364.
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  49. ↑ VALLEE BL, WACKER WE, ULMER DD (January 1960). "The magnesium-deficiency tetany syndrome in man". N. Engl. J. Med. 262: 155–61. doi:10.1056/NEJM196001282620401. PMID 13840893.
  50. ↑ Krendel DA (March 1990). "Hypermagnesemia and neuromuscular transmission". Semin Neurol. 10 (1): 42–5. doi:10.1055/s-2008-1041252. PMID 2161126.

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