multiple electrolyte and metabolic emergencies in a...

Case ReportMultiple Electrolyte and MetabolicEmergencies in a Single Patient

Caprice Cadacio,1 Phuong-Thu Pham,2 Ruchika Bhasin,1

Anita Kamarzarian,1 and Phuong-Chi Pham1

1Olive View-UCLA Medical Center, 14445 Olive View Drive, 2B-182, Sylmar, CA 91342, USA2Ronald Reagan UCLA Medical Center, 200 Medical Plaza, Los Angeles, CA 90095, USA

Correspondence should be addressed to Phuong-Chi Pham; [email protected]

Received 12 December 2016; Accepted 12 January 2017; Published 31 January 2017

Academic Editor: Yoshihide Fujigaki

Copyright © 2017 Caprice Cadacio et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.

While some electrolyte disturbances are immediately life-threatening and must be emergently treated, others may be delayedwithout immediate adverse consequences. We discuss a patient with alcoholism and diabetes mellitus type 2 who presentedwith volume depletion and multiple life-threatening electrolyte and metabolic derangements including severe hyponatremia(serum sodium concentration [SNa] 107mEq/L), hypophosphatemia (“undetectable,” <1.0mg/dL), and hypokalemia (2.2mEq/L),moderate diabetic ketoacidosis ([DKA], pH 7.21, serum anion gap [SAG] 37) and hypocalcemia (ionized calcium 4.0mg/dL), mildhypomagnesemia (1.6mg/dL), and electrocardiogram with prolonged QTc. Following two liters of normal saline and associatedincrease in SNa by 4mEq/L and serum osmolality by 2.4mosm/Kg, renal service was consulted. We were challenged withminimizing the correction of SNa (or effective serum osmolality) to avoid the osmotic demyelinating syndrome while replacingvolume, potassium, phosphorus, calcium, and magnesium and concurrently treating DKA. Our management plan was furthercomplicated by an episode of significant aquaresis. A stepwise approach was strategized to prioritize and correct all disturbanceswith considerations that the treatment of one condition could affect or directly worsen another.The current case demonstrates thata thorough understanding of electrolyte physiology is required in managing complex electrolyte disturbances to avoid disastrousoutcomes.

1. Introduction

Managing various electrolyte and metabolic disturbances isgenerally a simple task for nephrologist. However, in complexcases, one must be vigilant of potentially life-threateninginteractions among multiple simultaneous treatment plansand cautiously formulate a comprehensive treatment algo-rithm to prevent disastrous outcomes.

2. Case Report

Clinical History. A 33-year old male with known alcoholabuse and diabetes mellitus type 2 presented with a two-day history of nausea, vomiting, watery diarrhea, and lightheadedness. Patient denied fevers and chills but endorsedmild midepigastric dull pain and poor oral intake.

Physical Exam. Temperature was 37.2∘C, blood pressure114/85mmHg, heart rate 109 beats per minute, respiratoryrate 22 per minute, and oxygen saturation 98%. Patient wasacutely ill-appearing, slow in verbal responses, alert andoriented, and free of stigmata of advanced liver disease. Oralmucosa was dry. Heart exam was notable for tachycardia.Lungs were clear bilaterally. Abdomen had hypoactive bowelsounds and mild midepigastric tenderness without guardingor rebound. Extremities were significant for a few ecchy-moses. Neurological exam was nonfocal.

Initial Laboratory Data. Serum chemistries at presentationand hospital course are presented in Table 1. Most notableabnormalities included serum sodium (SNa) 107mEq/L,potassium (SK) 2.8mEq/L, total CO

212mEq/L, glucose

331mg/dL, and anion gap (SAG) 37mEq/L. Others were

HindawiCase Reports in NephrologyVolume 2017, Article ID 4521319, 6 pageshttps://doi.org/10.1155/2017/4521319

https://doi.org/10.1155/2017/4521319

2 Case Reports in Nephrology

Table1:Clinicaldata.

Serum

chem

istry

Admission

Afte

r2Lno

rmal

salin

e(renalservice

was

consulted)

12to

14ho

urs

after

admission

8ho

ursa

fterinsulin

administratio

n(30to

32ho

ursa

ftera

dmission)

Disc

harge(12

days

after

admission)

Totalamou

ntreplaced

durin

gho

spita

lization

Electro

lyteconcentrations

offlu

idsa

dministered

Sodium

(mEq

/L)

107

111

113

117132

2literso

fnormalsalin

eatpresentatio

n154m

Eq/L

Potassium

(mEq

/L)

2.8

2.2

2.9to

3.2

2.7

4.5

480m

EqKC

l100m

Eq/L

TotalC

O2

(mEq

/L)

1211

614

25Corrected

with

insulin

Serum

aniongap

(mEq

/L)

3731

3019

10Corrected

with

insulin

—

Glucose

(mg/dL

)331

248

250

108

217

Corrected

with

insulin

—

Phosph

orus

(mg/dL

)Not

done

<1.0

<1.0

<1.0

5.5

240m

molKP

O4

15mmolmixed

in200m

Lno

rmalsalin

eorfreew

ater

asneeded

toachieve

sodium

correctio

ngoal

Totalcalcium

(mg/dL

)7.2

6.9

6.8

6.8

8.4

4gcalcium

glucon

ate

(9.3mmol)

10%solutio

nIonizedcalcium

(mg/dL

)[no

rmal

4.6–

5.4]

4.1

Not

done

4.0

Not

done

Not

done

Magnesiu

m(m

g/dL

)1.6

Not

done

3.1

Not

done

1.78g

4gmixed

in250m

Lno

rmalsalin

e

Case Reports in Nephrology 3

mild transaminitis, mildly elevated lipase, and hemoglobin12 g/dL.

Renal service was consulted following the increase inSNa from 107 to 111mEq/L over one hour (effective serumosmolality [Sosm] increase of 2.4mosm/Kg) with the admin-istration of two liters of normal saline.

Additional Investigations. Renal service requested STATserum phosphorus and magnesium which resulted as<1mg/dL and 1.6mg/dL, respectively. Other findings weremoderate serum ketones, lactic acid 1mmol/L, and Sosm255mosm/Kg (serum osmolality gap 6mosm/Kg).

Venous Blood Gas at Six Hours following Presentation toEmergency Department (ED). pH was 7.40, pCO

217mmHg,

and HCO310mEq/L (SAG 31mEq/L), and at thirteen hours,

pH was 7.21, pCO214mmHg, and HCO

36mEq/L (SAG

30mEq/L). Urine studies show osmolality 450mosm/Kg,sodium 25mEq/L, and potassium 25mEq/L.

Diagnoses. Diagnoses included volume depletion, diabeticketoacidosis (DKA) (with initial concurrent metabolic andrespiratory alkaloses), severe hyponatremia, hypokalemia,hypophosphatemia, mild to moderate hypocalcemia, andmild hypomagnesemia.

Clinical Follow-Up. Patient received emergent potassiumchloride (KCl) infusion via a central line (200mL/hr of100mEq/L KCl solution [total 480mEq KCl]) and potas-siumphosphate (KPO

4) (total 240mmol),magnesium sulfate

(total 8 g), and calcium gluconate (total 4 g) via peripherallines. Oral thiamine and folate were given daily. All netfluid and effective solutes (sodium and potassium) wereclosely monitored. Calculations were performed (based onCurbsideConsultant.com) every six hours to readjust all fluidrates as needed to ensure a goal sodium correction rate of4–6mEq/L/24 hours. Treatment of DKA was intentionallydelayed until SK reached 2.9mEq/L to avoid insulin-drivenintracellular potassium uptake, exacerbation of hypokalemia,and precipitation of life-threatening arrhythmias.Onhospitalday 3, patient developed significant aquaresis with approx-imated free water clearance of 230 to 300mL/hr (urineoutput of 3140mL over 8 hour; urine studies: osmolality186mosm/Kg, sodium 13mEq/L and potassium 16mEq/L;SNa 122mEq/L). Twomicrograms of desmopressin (DDAVP)and two liters of electrolyte-free water were given intra-venously to slow urine output and prevent rapid overcorrec-tion of SNa, respectively. Over the first four hospital days, SNacorrected at an average of 5mEq/L/day. Additionally, patientalso underwent upper gastroendoscopy for gastrointestinalbleed and nausea which revealed diffuse gastritis, presumedto be induced by his chronic alcohol consumption.His nausearesolved with proton pump inhibitor and supportive care.

3. Discussion

The current case was challenged by multiple concurrentproblems including the need for continuing volume sup-port and substantial administration of both KCl and KPO

4

without rapidly correcting hyponatremia, optimization of

all treatable osmotic demyelinating syndrome (ODS) risks,correction of DKA to prevent respiratory decompensationwithout worsening the life-threatening hypokalemia, andintermittent infusions of magnesium sulfate and calciumgluconate while anticipating and managing any significantaquaresis without derailing the planned SNa correction rate.The algorithm for the comprehensivemanagement of currentpatient is summarized in Figure 1.

Hypokalemia was the most life-threatening and one offirst abnormalities to be treated emergently. Etiologies likelyincluded poor dietary intake, renal wasting given recent vom-iting and poorly controlled diabetes, and diarrhea. Imme-diate life-saving interventions included KCl infusion via acentral line along with instructions to avoid alkalinizationor administration of insulin or glucose-containing fluids, thelatter because of endogenous insulin secretion, and to preventintracellular K+-shift and worsening hypokalemia.

While aggressive potassium administration was critical,SNa level had to be closely monitored because potassiumeffectively increases SNa. Serum sodium concentration hasbeen shown to be directly proportional to the sum of totalexchangeable Na+ and K+ content [1]. Mechanisms wherebyK+ administration can raise SNa include the following [2]:

(1) intracellular K+-uptake induces an equivalent extra-cellular Na+-movement and hence increased SNa,

(2) parallel K+-Cl- intracellular uptake leads to increasedintracellular osmolality which leads to intracellularfree water shift and lower extracellular free watervolume and hence increased SNa, or

(3) intracellular K+-uptake induces an equivalent extra-cellular H+-movement to maintain electrical neutral-ity. While H+ can bind to the extracellular buffersystem and not perturb extracellular osmolality, theintracellular K+-gained increases intracellular osmo-lality and hence intracellular free water shift. Thelower extracellular free water volume increases extra-cellular SNa.

Given the direct effect of K+ on SNa, both sources of potas-sium, KCl and KPO

4, were accounted for in all calculations

for expected changes in SNa. Further sodium administra-tion was withheld because potassium supplement alonewas determined to be sufficient to correct hyponatremia.Failure to recognize this fact and unwarranted infusion ofsodium-containing solutions could have easily led to rapidhyponatremia overcorrection.

Hypophosphatemiamay be a risk factor for ODS [3]. Ourroutine hyponatremia treatment protocol requested a STATlevel, which was likely life-saving. Patient’s severe hypophos-phatemia could arise from poor oral intake, renal wasting,hypomagnesemia-induced skeletal resistance to parathyroidhormone (PTH 161 pg/mL, 1,25 (OH)

2vitaminD 146 pg/mL),

and possibly some degree of intracellular uptake associatedwith primary respiratory alkalosis at presentation [4]. Thelatter could induce intracellular alkalemia and associatedincreased glycolysis and intracellular uptake of phosphorusfor ATP production [5]. Phosphorus replacement was given


Initial presentation

Renal consult andmanagement

SeverehypophosphatemiaReplace

potassium as

Immediatecentral lineplacement

Normal serum potassium, phosphorus, sodium, and magnesium levels

Determine rate of correction goal based on ODS risksCheck serummagnesium,phosphorus

Resolution of diabetic ketoacidosis

Mildhypomagnesemia

Replacemagnesium as

Moderate diabeticketoacidosis

Severehypokalemia hyponatremia hypovolemia

Normocalcemia

Immediate intervention

Indirect therapy; indirect outcome Direct therapy; direct outcome

Immediate life-threatening conditions Nonimmediate life-threatening, but serious conditions

Diabeticketoacidosis with

increasingrespiratory

distress

Other supportive measures

Outcome per both direct and indirect therapies

Hold insulin,alkalinization, andglucose-containing

fluidadministration

Monitor urineoutput, sodium,and potassium;administer freewater & DDAVPand adjust KCl infusion rate as

needed

Administer insulinand glucose

support cautiouslyonce hypokalemia

becomes lesssevere

Continue to replace potassium

needed; monitor for appropriaterise in serum sodium and

accordingly adjust infusion rates

Moderate hypokalemia

Mild to moderatehypocalcemia

Euvolemia

Replacecalcium as

calciumgluconate

Replacephosphorus as

Supplementthiamine as

clinicallyindicated

ED bolus 2liters of

normal saline

(KCl and KPO4)

KPO4

and phosphorus (KPO4) as

∗∗Marked∗Severe

MgSO4

Figure 1: Algorithm for the treatment ofmultiple concurrent life-threatening disturbances. ∗For hyponatremia, correction resulted frombothpotassium infusion (indirect therapy) and fine adjustment with intermittent free water infusion and single administration of desmopressin(direct therapy) to achieve rate of correction goal during an episode of aquaresis. ∗∗For volume depletion, patient received two liters ofnormal saline on presentation to the emergency department (direct therapy) and continuous KCl infusion at 200mL/hour (indirect therapy,i.e., themain purpose for KCl infusion, was potassium replacement, but patient benefited from the infusion asmaintenance intravenous fluid)over the following 2 to 3 days while his oral intake was poor. ODS: osmotic demyelination syndrome; ED: emergency department; DDAVP:desmopressin.

emergently to avoid respiratory and cardiac arrest amongother potential serious complications.

Volume depletion is typically managed with normal saline(NS), but not in current case. Patient received predomi-nantly K+-containing fluids (200mL/hour of 100mEq/L KClsolution and 25 to 50mL/hour of KPO

4solution [15mmol

KPO4mixed in 200mL of either normal saline or sterile

water as indicated by SNa]). Since K+ is an effective solute,either K+ or Na+-containing solutions that are relatively iso-tonic to patient’s effective osmolality will effectively expandintravascular volume. With the exception of two liters of NSgiven in the ED, patient's total body volume was repletedand maintained with the infusion of K+-containing fluidsintended for potassium and phosphorus repletion. Failure torecognize the volume expansion capacity of relatively isotonicKCl-containing fluid and unwarranted infusion of NS forthe sole purpose of volume support would have complicatedthe treatment of hyponatremia. Additionally, high volumeinfusions of multiple fluids would have led to excess urinaryloss of ketone bodies necessary for bicarbonate productionwith insulin administration [6].

Hypocalcemia was likely due to poor nutrition, mal-absorption, and hypomagnesemia-induced hypoparathy-roidism [7, 8]. Given prolonged QTc, patient received lowdose calcium gluconate intravenously following the initiationof KPO

4administration to avoid any potential calcium-

induced worsening of severe hypophosphatemia via calciumphosphate precipitation.

Diabetic ketoacidosis was potentially life-threatening, butnot the most serious derangement. Insulin administrationwas intentionally delayed to avoidworsening of hypokalemia.

Patient’s respiratory status, however, was closely monitored.Once SK reached 2.9mEq/L, insulin was cautiously givento avoid respiratory failure as patient exerted high work ofbreathing to compensate for the metabolic acidosis. Within12 hours of insulin administration, SAG, likely all reflectingketone bodies, decreased from 30mEq/L to 19mEq/L witha parallel increase in total CO

2from 6 to 14mEq/L. The

rapid inverse change in SAG and total CO2demonstrates

perfectly how sufficient fluid resuscitation, not excessive fluidadministration with resultant urinary loss of serum ketonebodies, can allow for preservation of serum ketone bodies,where rapid hepatic conversion to bicarbonate occurs withinsulin administration [6]. Patient’s respiratory status alsoimproved significantly with correction of metabolic acidosis.

Hyponatremiawas likely multifactorial and includes con-tinuing free water intake in the presence of enhanced secre-tion of antidiuretic hormone (ADH) with volume depletionand/or inappropriate ADH secretion in the setting of nau-sea, “beer potomania,” and small degree of hyperglycemia-induced extracellular free water shift. The major goal inhyponatremia correction is ODS prevention. This requiresboth setting an appropriate correction goal and recognizingand optimizing any concurrent factors that could potentiatethe risk of developing ODS [3, 9]. The correction goalwas determined to be 4 to a maximum of 6mEq/L/daybecause of patient’s ODS risks including severe hypona-tremia, hypokalemia, alcoholism, hypophosphatemia, hypo-magnesemia, glucose intolerance, and presumed thiaminedeficiency [3, 9]. Routine assessment of reversible ODS riskfactors is warranted because electrolytes such as phosphorusand magnesium are not routinely measured at many institu-tions, including our own (Table 2).

Case Reports in Nephrology 5

Table2:Teaching

pointsbo

x.

Generalteaching

points

Com

mentspertinenttocurrentcase

Treatm

ento

fone

electrolyteor

metabolicabno

rmality

cancritically

worsen

another.In

apatient

with

multip

ledistu

rbances,ac

omprehensiv

emanagem

entp

lan

mustp

rioritizethe

mosttoleastlife-th

reateningdistu

rbance

andtre

ataccordingly.

Additio

nally,con

siderationmustb

emadefor

allp

ossib

letre

atmentinteractio

ns,

particularlywhenthetreatmento

falesscriticalproblem

canexacerbatea

life-threateningcond

ition

(i)Hypokalem

iaandhypo

phosph

atem

iawerethe

twomostlife-th

reatening

cond

ition

sincurrentp

atient.Since

thetreatmento

fdiabetic

ketoacidosis(D

KA)

with

insulin

with

orwith

outg

lucose

supp

ortcou

ldhave

exacerbatedthes

evere

hypo

kalemiaandprecipitatecardiaca

rrest,such

treatmentw

asintentionally

delay

ed.A

ggressivep

otassiu

mreplacem

entw

ithbo

thKC

land

KPO4to

achievea

saferserum

potassium

levelw

asdo

nePR

IORto

thetreatmento

fDKA

Comprehensiv

eprotocolfor

them

anagem

ento

fhypon

atremia:

(i)Determineo

smoticdemyelin

ationris

ks(O

DS)

andapprop

riaterateof

correctio

n(ii)A

ssessa

ndtre

atallcorrectableODSris

ks(hypokalem

ia,hypom

agnesemia,

hypo

phosph

atem

ia,alteredglucosem

etabolism

,and

clinicaln

eedforthiam

ine)

(iii)Und

ersta

ndthatpo

tassium

canincrease

serum

sodium

exactly

asifthes

ame

amou

ntof

sodium

isbeingadministered

(iv)M

onito

rurin

eoutpu

tand

itscontento

fsod

ium

andpo

tassium

fora

nypo

ssible

aquaretic

phase

(i)Whilehypo

natre

miawas

beingcorrectedwith

KCland

KPO4infusio

ns,the

immediateplan

tomon

itora

ndcorrectfactors[hypop

hosphatemiaand

hypo

magnesemia]a

ssociatedwith

high

ODSris

ksledto

thep

rompt

recogn

ition

ofsevere

andlife-threateninghypo

phosph

atem

ia(ii)Inadditio

nto

thec

orrectionof

concurrent

electrolytedistu

rbances,thiamine

supp

lementatio

nshou

ldbe

considered

inpatie

ntsw

ithmalnu

trition

oralcoho

lism

asthiamined

eficiency

hasb

eenim

plicated

inincreasin

gther

iskforO

DS

(iii)Cu

rrentp

atient’sserum

sodium

concentrationim

proved

asplannedwith

only

potassium-con

tainingflu

ids

(iv)A

ggressivem

onito

ringof

both

urineo

utpu

tand

contento

feffectivee

lectrolytes

(sod

ium

andpo

tassium)a

llowsfor

prom

ptinterventio

nandthus

preventio

nof

rapidover

correctio

nof

hypo

natre

mia

KClisa

seffectivea

sNaC

lsolutionas

avolum

eexp

andera

ndmay

bepreferredor

even

requ

iredwhenpo

tassium

iscritically

deficient

(i)Th

esub

stitutio

nof

KClfor

NaC

lsolutionforv

olum

eexp

ansio

ncanon

lybe

givenin

caseso

fsevereh

ypokalem

ia.Th

eratea

ndconcentrationof

theK

Clsolutio

nMUST

beadjuste

dto

assure

asafer

ateo

fincreaseinserum

sodium

(ii)N

otethata

maxim

umof

20mEq

ofKC

lmay

becontinuo

uslyinfusedperh

our

throug

hac

entralveno

uscatheter

Respira

tory

hyperventilationandmetabolicacidosisassociated

with

diabetic

ketoacidosisalon

emay

beeasilyandprom

ptlyreversed

with

thea

dministratio

nof

insulin

.Persis

tent

abno

rmalities

shou

ldthus

prom

ptan

evaluatio

nforo

ther

underly

ingetiologies

(i)Fo

llowingthea

dministratio

nof

insulin

,our

patie

nt’srespira

tory

statusimproved

from

arespiratory

rateup

tomid-30’s

breathsp

erminuted

ownto

mid-20’s

with

in24

hours

(ii)S

imilarly

,patient’sserum

totalC

O2im

proved

from

6to

14mEq

/Lwith

in8ho

urs

(iii)Note,ho

wever,close

mon

itorin

gof

potassium

mustb

edon

efollowinginsulin

andglucoses

uppo

rttherapy.With

theinitia

tionof

insulin

therapy,patie

nt’sserum

potassium

decreasedfro

mah

ighof

3.2m

Eq/L

to2.7m

Eq/L

with

in7ho

urs


In terms of actual hyponatremia correction, the infu-sion of potassium-containing solutions alone was sufficient.Patient’s SNa improved daily at expected rates from thepredominant infusions of KCl and KPO

4solutions (Table 1).

Additionally, as per our routine hyponatremia managementprotocol, monitoring of urine output, sodium, and potassiumwas done at regular intervals. Patient indeed developeda significant aquaretic phase when electrolyte-free waterand DDAVP were promptly given to divert hyponatremiaovercorrection. Significant aquaresis during the treatment ofhyponatremia may occur in multiple clinical settings andgenerally stems from the rapid cessation of ADH secretionfollowing the correction of underlying stimuli that inducedADH secretion like correction of volume depletion, nausea,pain, among others [10]. In current case, the aquaretic phasewas likely due to the correction of volume depletion andnausea.

Hypomagnesemia was likely due to poor oral intake,gastrointestinal malabsorption, and possibly urinary lossassociated with diabetes mellitus [11]. Patient was monitoredclosely for hypomagnesemia and treated as needed.

Thiamine was also supplemented given history of alco-holism to minimize ODS risk [4].

Respiratory and metabolic alkalosis on presentation werelikely due to pain/anxiety and volume depletion, respectively.Both conditions resolved with comprehensive supportivecare.

4. Conclusions

Wepresent a complex case involvingmultiple life-threateningelectrolyte and metabolic disturbances which demonstratesthe critical need for prioritization for the treatment of eachabnormality and considerations for all interactions amongmultiple concurrent treatment plans.

Aggressive potassium replacement prior to the adminis-tration of insulin for the DKA is vital to prevent worsening oflife-threatening hypokalemia.

Both sodium and potassium are equivalent effectivesolutes. Hyponatremia can be corrected with the predomi-nant infusion of potassium. Similarly, volume expansion withrelatively isotonic KCl solution is as effective as NaCl incurrent case of severe hypokalemia.

The treatment of hyponatremia must incorporate correc-tion rate, monitoring, and treatment of all factors (potassium,phosphorus, magnesium, glucose, and thiamine) associatedwith increased ODS risks. Additionally, during the treatmentof hyponatremia, transient aquaresis may arise for variousreasons and must be anticipated and immediately treated toavoid rapid overcorrection [11].

Insulin effectively converts ketone bodies to bicarbonateif the former have not been lost in the urine with excessivefluid administration.

Despite multiple life-threatening electrolyte and meta-bolic disturbances, patient was discharged within twelve daysin good condition and continued to do well at one monthfollow-up.

Teaching points are summarized in Table 2.

Competing Interests

The authors declare that they have no competing interests.

References

[1] I. S. Edelman, J. Leibman, M. P. O’Meara, and L. W. Birkenfeld,“Interrelations between serum sodium concentration, serumosmolarity and total exchangeable sodium, total exchangeablepotassium and total body water,”The Journal of Clinical Investi-gation, vol. 37, no. 9, pp. 1236–1256, 1958.

[2] B. D. Rose, Ed., Clinical Physiology of Acid-Base and ElectrolyteDisorders, McGraw-Hill, New York, NY, USA, 4th edition, 1994.

[3] P.-M. T. Pham, P.-A. T. Pham, S. V. Pham, P.-T. T. Pham, P.-T.T. Pham, and P.-C. T. Pham, “Correction of hyponatremia andosmotic demyelinating syndrome: have we neglected to thinkintracellularly?” Clinical and Experimental Nephrology, vol. 19,no. 3, pp. 489–495, 2015.

[4] J. J. Freitag, K. J. Martin, M. B. Conrades et al., “Evidencefor skeletal resistance to parathyroid hormone in magnesiumdeficiency. Studies in isolated perfused bone,” Journal of ClinicalInvestigation, vol. 64, no. 5, pp. 1238–1244, 1979.

[5] N. Brautbar, H. Leibovici, and S. G. Massry, “On the mecha-nism of hypophosphatemia during acute hyperventilation: evi-dence for increased muscle glycolysis,” Mineral and ElectrolyteMetabolism, vol. 9, no. 1, pp. 45–50, 1983.

[6] P. Felig, “Diabetic ketoacidosis,” New England Journal ofMedicine, vol. 290, no. 24, pp. 1360–1363, 1974.

[7] L. R. Chase andE. Slatopolsky, “Secretion andmetabolic efficacyof parathyroid hormone in patients with severe hypomagne-semia,” Journal of Clinical Endocrinology and Metabolism, vol.38, no. 3, pp. 363–371, 1974.

[8] R. K. Rude, S. B. Oldham, and F. R. Singer, “Functionalhypoparathyroidism and parathyroid hormone end−organresistance in human magnesium deficiency,” ClinicalEndocrinology, vol. 5, no. 3, pp. 209–224, 1976.

[9] J. G. Verbalis, S. R. Goldsmith, A. Greenberg et al., “Diagnosis,evaluation, and treatment of hyponatremia: expert panel rec-ommendations,”TheAmerican Journal of Medicine, vol. 126, no.10, supplement 1, pp. S1–S42, 2013.

[10] P. C. Pham, P. V. Chen, and P. T. Pham, “Overcorrection ofhyponatremia: where do we go wrong?” American Journal ofKidney Diseases, vol. 36, no. 2, article no. E12, 2000.

[11] P.-C. T. Pham, P.-M. T. Pham, S. V. Pham, J. M. Miller, and P.-T. T. Pham, “Hypomagnesemia in patients with type 2 diabetes,”Clinical Journal of the American Society of Nephrology, vol. 2, no.2, pp. 366–373, 2007.

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