J Am Soc Nephrob
DISEASE OF THE MONTH
Hyperkalemia:
A Potential
I. DAVID
Division
WEINER
Gainesville,
Hyperkalemia
ical
perkalemia
pathophysiologic
well
understood,
are
forward.
Clinical
pseudohyperkalemia,
and
institution
requires
and
silent,
The
of
Gainesville
and
potentially
factors
and
management
assessment
the
therapy.
of the etiology
Veterans
Affairs
dinto
Medical
plements,
medications
treatment
of recur-
blood
pressure
eta)
Pathophysiology
sium
Hyperkalemia
sium
develops
intake
and
extracellubar
tassium
vast
ports
potassium
lular
space,
total
body
body
the
and
(1).
The
from
its
potassium
potassium
extracellubar
suggest
is present
extracellular
Na-K-ATPase
space
ebectrochemical
fluid
that
in the
renal
icines
is present
into
the
gradient.
intracellular
is supplied
trans-
U).
space,
of
of total
with
2%
in
Pen-Vee
in usual
taut. Citrate
salt,
or
as
primary
means
Although
all foods
potassium
differ
highest
primary
of
1 summarizes
enteral
dietary
food
nutritional
will
may
close
patient
and
for
frequent
failure
patients
for
with
reevaluations
Another
a number
of
total
fre-
is also
The
a com-
potassium
hyperalimentation
renal
may
insufficiency;
be necessary
via
potassium
uli,
absolute
the
sufficiently
cause
to
Gainesville,
1046-6673/0908-
FL 32610-0224.
1 535$03.00/0
Journal of the American
Society of Nephrology
Copyright
0 1998 by the American
Society of Nephrobogy
the
Because
of
if one
attention
potassium
does
to
the
certain
potassium,
not
monitor
type
of
citrate
collecting
duct.
potassium
tassium
cell
although
stim-
secretion
is
is not
hot
lost
climates
in sweat
a
little
and
may
with
be signif-
to hypokalemia.
elimination
Although
is regulated
potassium
even
levels
(12,13).
to the
in the
mechanisms
potassium,
Figure
filtered
in
by the
of filtered
potassium
is
and the loop of Henbe
distal
face
predominantly
is freely
90%
tubule
delivery
constant
secretes
physiologic
quantitatively
in
of potassium
is
the
Although
secretion
contributes
(9), approximately
by the proximal
transport
by
potassium
is
for
(7,8).
potassium
Sweat
lead
1). Potassium
relatively
cipal
may
potassium
excretion
colonic
inadequate
homeostasis
of potassium
is responsible
is regulated
of
elimination,
and
colon
potassium
secretion
that
potassium
80 to 90%
The
magnitude
the amount
icant,
(10,1
of renal
conditions,
excretion.
hyperkalemia.
exertion
Renal
HypertenP.O. Box
renal
low
of
glomerulus
reabsorbed
100224,
close
of the remaining
colonic
the
Charles
S. Wingo,
Division
of Nephrology.
University
of Florida
College
of Medicine,
2 summarizes
amounts
develop
potassium
Excretion
majority
population.
Correspondence
to Dr.
sion, and Transplantation,
pay
Table
impor-
salt,
preparation.
eliminated
supplements
fluids.
and
a sodium
barge
may
salt, the potassium
preparations.
provide
The second
component
excretion.
Under normal
chloride
receiving
can
potassium
Potassium
supplements.
of
Potassium
recommended
excessive
monitoring
this
hyperkalemia.
nutrition
content
renal
of
serum
as an alternative
to be clinically
salt.
hyperkalemia
and
the
overlooked
substitutes.
nutritional
(1).
to have
potassium
salt
of hyperalimentation
usually
be
with
enteral
food
amounts
tend
A commonly
is enteral
Patients
develop
concentrations
the relative
vegetables
many
potassium
through
is through
substitutes;
of
the
sources.
component
fluids
is salt
potassium
support
quently
and
of potassium.
constituent
source
intake
potassium,
Fruits
source
Table
for
contain
greatly.
potassium
is the
mon
of potassium
concentrations
dietary
preparations
is likely
per 1,000,000
1.7 mEq
as either
citrate
This
Other common
medand citrate. Penicillin
G
is insufficient
of various
potas-
frequency
potassium
G is available
a sodium-potassium
(6),
increasing
K is also a potassium
doses
be supplied
content
significant
Intake
The
may
potassium
(2,3).
oral
and skel-
balance
if serum
(supplying
penicillin
in-
decreases
in the future.
monitored.
are penicillin
salt
other
of the
women
with
hypokalemia
potassium
Although
present
mineral
to
receiving
In view
of hyperkalemia
as a potassium
sodium
citrate
Potassium
supply
be
supplementation
prescribed
as a
sup-
administered
also
improve
not carefully
If necessary,
form.
intracel-
98%
that
in the
Estimates
approximately
be
po-
body.
potassium
may
may
are
frequently
may
in postmenopausal
for conditions
other than
to increase
the incidence
function
are
medicines
supplied
is potassium
to hyperkalemia.
and
and
potasintra-
1 summarizes
in the
body
ubiquitous
the
against
between
between
Figure
movement
of total
fluid
regulation
distribution
is disturbed.
majority
intracellular
the
or the
potassium
distribution
The
when
excretion
obvious
potassium
metabolism
supplements
those
most
who
that
(4,5)
calcium
These
predispose
evidence
Most
recognizing
The
KCI.
Medicine,
of potassium.
but
diuretics
that
creasing
rence.
as
receiving
of
Florida.
source
salt,
is important.
such
patients
another
as a sodium
salt
College
Gainesville,
are
are prepared
Florida
of
Center,
potassium
exclusion
of
for treatment,
prevention
University
Medications
hy-
is straight-
Long-term
and
S. WINGO
Transplantation,
bead
treatment
1998
Killer
and
lethal
that
requires
of the urgency
appropriate
identification
CHARLES
Hypertension,
Florida,
is a common,
condition.
and
of Nephrology,
Silent
9: 1535-1543,
convoluted
of widely
2 summarizes
in the
whereas
collecting
the
tubule
varying
the
is
systemic
major
duct.
intercalated
The
poprincell
I 536
Journal
of the American
Society
GI
J Am Soc
of Nephrology
Intake
(-100
mEq
also
mEq)
regulating
regulate
to yield
also present.
In addition
mEq)
(2500
reabsorbs
Liver
(250
mEq)
possess
mEq)
Renal
Excretion
(90-95
1. Summary
Figure
Adapted
of potassium
reference
I.
from
Table
Potassium
1.
content
Supplement
Ensure
Ensure
intake
and excretion
nutrition
apical
H-K-ATPase
(33).
of
nism
variety
mechanisms.
supplements
the
relative
Under
conditions,
tities
normal
of
which
Potassium
Sodium
Osmobality
(mEq)
(mEqIL)
(mosmollkg)
potassium.
serum
1.00
40
40
375
partments
Osmolite
Pulmocare
I .06
1.50
26
49
27
57
300
490
sium
Suplena
2.00
29
34
615
potassium
1.06
41
41
310
lecting
duct
1.00
20
20
630
The
colon
due
content
of various
citrate
excretion.
which
Potassium
(mEq/ml)
Bicitra
2
subtle
1
1
The
1
2
solution)
(14,
transports
potassium
against
the
peritubular
space
Under
most
the buminal
apical
mechanism
15).
potassium
may
Whether
this
parallel
K and
NatKATPase
the
principal
cell
cellular
potassium
its electrochemical
channel
also
basobateral
its electrochemical
into
circumstances,
fluid,
down
A
(17,18).
contribute
mechanism
An
apical
to potassium
represents
Cl transporters
a KCI
gradient
receptor,
from
cytoplasm
(16).
is secreted
into
gradient,
via an
KC1
cotransport
secretion
(
plays
be due
number
quanof KC1,
usual
daily
intake,
by less
than
1 mEqfL
in-
if
and extracellular
to
impaired
to either
renal
nephron
units
of
that
corn-
renal
potas-
insufficiency,
available
impair
the
rate
for
of cob-
secretion.
small
which
to the kidney.
amounts
this
Some
of potassium.
occurs
are
regulation
particularly
amounts
and
in renal
of potassium
cotransporter
a central
or
cell potasvia binding
role
can
difficult
majority
membrane
cause
less
of colonic
secretion
The
well
defined,
potassium
insufficiency,
adverse
effects
to those
that
to detect
of these
intracellular
mEqIL,
in stim-
whereas
approximately
4
resting
membrane
lular to extraceblular
cellular
potassium
lular to extracellular
in resting
important
I 9,20).
is unknown.
Several
factors
are known
to regulate
principal
sium secretion.
The minerabocorticoid
aldosterone,
to the mineralocorticoid
large
although
remain
low.
effects
are rebated
potential
that
are
to effects
or voltage.
range
from
life-threatening.
The
of potassium
primary
deter-
minant
of cell membrane
potential
in most cells is the ratio of
intracellular
to extracellular
potassium
concentration.
Nor1 20
potassium
basolateral
Effects
mally,
reabsorbs
the intrain part,
secretes
occurs,
by a
activity
potassium
excretion
mechanisms
all conditions,
hyperkalemia
not
at beast
may
through
on cellular
1
This
400 mEq
of
the
or to factors
also
Adverse
(mEq/ml)
Acid
2
Polycitra
also
cells
Citrate/Citric
Sodium
(mEq/ml)
(Shohl’s
than
and
can excrete
between
potassium
Hyperkalemia
Pobycitra-K
duct
exit.
ingestion
on average
the
secretion,
secretion
preparations
This
decreases
the absolute
Preparation
is
(27-30).
apical
the kidney
greater
is related,
but similar
Potassium
is
intercalated
pump
of the
daily
potassium
to redistribution
mechanisms
2.
collecting
reabsorption
is determined
apical
HtKtATPase
renal function
is normal
and
are intact (34). Under
almost
Glucerna
Table
rates
insufficiency
duct
to potassium
The
is severalfold
creases
470
690
TEN
the
ion
permeabilities
transporters
37
49
Vivonex
flow
oliguria
across
the apical
membrane
via a barium-sensimost likely a potassium
channel,
or exit across
membrane,
also via a barium-sensitive
mecha-
barium-sensitive
40
54
Ultracal
Urine
renal
Collecting
Net potassium
factors,
including
1.06
1.50
Plus
(2 1-23).
signaling
however,
unless
potassium,
(26).
an
and
of enteral
Calories/cc
mEq/d)
(5-10
to secreting
(24).
(25);
hyperkalemia
potassium
either recycle
tive transporter,
the basobateral
GI Excretion
mEq/d)
secretion
secretion
1998
transporter
uses ATP as an energy
source
for proton
secretion
and potassium
reabsorption
(3 1 ,32). Potassium
that enters
can
7
Bone (-300
potassium
potassium
insufficient
Muscle
9: 1535-1543,
ulating
cortical
collecting
duct potassium
secretion
Arachidonic
acid
metabolites
are an intracellular
per day)
molecule
RBC (-250
Nephrol
potassium
concentration
extracellular
mEqIL.
potential
potassium
The contribution
is related
to this
membrane
potential.
in all electrically
rate
(35-38).
myocardial
of repolarization.
concentration
is
of potassium
to
ratio of intracel-
potassium;
thus, small changes
in extracan result in large changes
in the intracelpotassium
ratio, and hence
barge changes
Resting
membrane
potential
is
active
cells,
including
neurons,
voluntary
muscles,
and involuntary
muscles.
The most prominent
effect of hyperkalemia
cardium
decrease
is approximately
is on the myo-
Decreases
in resting
membrane
potential
cell conduction
velocity
and increase
the
The
decreased
conduction
velocity
leads
J Am
Soc
Nephrol
9: 1535-1543,
Clinical
1998
Peritubu/ar
Lumen
space
the progression
lemia
from
benign
is unpredictable,
and
Aspects
of Hyperkalemia
to lethal
arrhythmias
the
presence
in hyperka-
of any
EKG
Na
of hyperkalemia
should
be considered
a medical
Treatment
methods
are described
below.
C1
Skeletal
resulting
Hyperkabemia
also
affects
muscles
are
in increased
rebated
to the
contraction
importance
to
cause
severe
cells
muscles.
hyperkalemia;
throughout
Smooth
for
muscles
has
depression
the
body.
hyperkalemia,
This
may
potential
hyperkalemia
respiratory
findings
emergency.
sensitive
to
and fatigue.
of membrane
of skeletal
sitive
other
particularly
weakness
1537
are
been
be
normal
also
sen-
reported
to
(39).
H
Evaluation
The
evaluation
perkalemia
vitro
verity
measurement
of
needed,
H
of hyperkabemia
is present
HCO3
not
condition
known
2. Summary
principal
concert
cell
with
porter
may
bated
secretes
basolateral
also
cell
of potassium
potassium
via
Na-K-AIPase.
be present
(A cell)
transport
and
in the collecting
an apical
the
B-type
cell.
peritubular
channel.
barium-sensitive
mechanism,
most
An apical
barium-sensitive
transporter,
allows
recycling
interca-
(B cell)
of
the
The
most
lysis,
and
level
pink
tinge
the
cells
necessary.
age.
increases
complex
ization
known
in the
interval
and
the
(EKG).
width
The
rate leads to an increased
height
as “peaked”
T waves.
A slowed
especially
in the
chance
that
sudden
death.
sion
from
presence
to severe
hyperkalemia,
associated
with
waves,
otherwise
Mild
system
an increased
by progressive
Under
ciently
sine-wave
so
with
delayed
the
interval
flattening
extreme
that
pattern.
of the
EKG
may
be
conditions,
it
merges
However,
conduction
and eventual
the
development
findings
and
can
34%
of
frequently
of the
hyperkalethe
T
His-
with
the
the
complex
T
wave,
correlation
resulting
between
in
is not precise,
and depends
patient
sensitivity
and the
of hyperkalemia.
Unfortunately,
noted
(e.g.
can
release
due
the
tourniquet
more
other
and
than
specimen
the
red
leak-
surrounding
closing
a hand)
2 mEqIL
(40).
than
to a
of hemoglobin
formed
predisposes
beading
to potassium
tight
cells
is hemo-
red
blood
can
cells
or platelets
(44lead to pseudohy-
degree
of
severity
at clinically
with
between
elevation
of the
of
serum
leukocytosis
frequent
reactive
levels
and
is a family
rare
are
It has
which
history
potassium
reports
been
and
leads
pseudohyperkalemia
Pseudohyperkalemia
to
excessive
exhibit
between
the
count
(47).
is important
or if conditions
or thrombocytosis
are
from
in association
and mononucleosis
(49).
red blood cell membrane
platelet
I ,000,000/cm3
of pseudohyperkalemia
described
is
of thrombocytosis;
of hyperkalemia
extreme
beukocytosis
unnecessary
treatment.
either
or thrombocytosis,
thrombocytosis
500,000/cm3
of
can
70,000/cm3,
also can
arthritis
(48)
have abnormal
ity,
artificially
laboratory
Centrifuging
opening
,
by
from
in the
from
cells.
greater
than
1 ,000,000/cm3,
patients
There
a
blood
(41-43),
than
associated
with
present
to avoid
causes.
absolute
of
numbers
occur
if there
suffi-
to clot,
release
pseudohyperkalemia,
with a significant
correlation
degree
of pseudohyperkalemia
and the platelet
Verifying
that pseudohyperkalemia
is not present
of the P waves.
widens
that has been allowed
the serum.
Potassium
Excessive
The
counts
unpredictable.
a
levels
resulting
potassium
to the
but progres-
through
absence
QRS
related
in some
levels,
pseudohyperkalemia.
perkalemia.
to
ventricular
myocardium,
resulting
in
and a longer
QRS interval,
followed
potassium
levels and EKG findings
on a number
of factors,
including
rapidity
the
observed,
to
and
PR
between
is often
leukocytes
46), greater
hyper-
high
of pseudohyperkalemia
blood
release
treatment
potassium
t’ivo
in
se-
Potassium
an excessively
plasma
cause
of
hy-
bevel.
easily
extremity
that
led to the
be artificially
in
clot has completely
to membrane
damage,
Potassium
also
the
beading
6.0 mEq/L,
is more
a balanced
increase
in the height
known
as “tenting.”
More severe
is associated
QRS
repolar-
increases
develop,
hyperkabemia
5.5
the
of the T wave,
also
conduction
velocity,
may
correlation
of hyperkalemia
of
increased
T waves,
fibrillation
A rough
mild
Purkinje
of peaked
ventricular
and the degree
mia
PR
on electrocardiogram
rapidity
that
elements
cause
red
Alternatively,
increase
may
potassium
is usually
an exercising
to
cellular
to the plasma
before
blood
a
the
actual
in blood
to obtain
common
likely
a potassium
most likely a potas-
with
the
this
the
as “pseudohyperkalemia.”
serum
damaged
in concert
when
both
any
elevate
from
H-K-ATPase
potassium
A-type
cell
potassium
channel,
The
intercalated
reabsorb
sium
via an apical
potassium
channel
in
apical
KCI cotrans-
An
in the principal
from
duct. The
determining
condition(s)
reflect
are measured
typically
and then centrifuged
Figure
and
the
potassium
and
of the
potassium),
hyperkalemia
conditions
an artifact
serum
correcting
kalemia.
The plasma
verifying
is not
(and
of
the
and
involves
in vivo
with
Occasional
potassium
potassium
leakage
excluded
by
families
permeabilrates
(50-52).
can
be
other
rheumatoid
simultaneously
and
1538
Journal
measuring
of the
plasma
Plasma
can
specimen,
syringe.”
perkalemia
should
more
be
than
be
tube
a heparinized
and
0.3
then
mEqIL,
on
all
the
Several
classification
methods
of “true”
based
on
the
mechanisms
utilizing
between
the
inadequate
from
intra-
examination
A
is sufficient
Excess
fluid
careful
to differentiate
hy-
and
most
causes.
or
physical
potassium
hyperkalemia
above,
lents
ingestion
without
other
the normal
kidney
potassium
daily
of
excretion
or
produce
other
receiving
perkalemia
potassium
(53).
of potassium
enteral
nutrition
products
administration
of
potassium
or 200
100
intake
of
studies
estimate
related
to potassium
mEq
of
40
approximately
that
100
of
50%
mEqfL
all
mEq
cases
supplements
of
vast
majority
of total
intracellular
fluid
compartment;
between
intra-
result
in marked
ditions
are
dosis,
if due
trast,
metabolic
acid
hyperkalemia
mineral
(58,59).
acids
in cellular
or
on plasma
potassium
Mineral
acids
acid,
The
contrasting
potassium
release.
Many
or
more;
can
result
per
day.
increased
a
ing
are
lular
acidification
in membrane
potassium
completely
dissociated
undissociated
state
are
attributed
In
contrast,
conaci-
responsiveness,
increase
as
such
acid,
and
uptake,
organic
relatively
across
membranes.
as
f3-hy-
cause
of
organic
and
but
not
cause
intraceb-
which
results
gradient
for
are in-
acids
permeable
This
such
insulin,
do
results
and
may
distribution
lular
fluid
potassium
or
glucose
lead
to
cell
in
sterone
lack
with
caused
con-
Mannitol
is the
whereas
or
hyinsulin
cause.
by
The
effective
increases
intra-
potassium
cross
exit.
plasma
presence
and
of
do
memsufficient
not
with
bead
diabetic
significant
to
ke-
increase
in response
the
hormonal
between
compartments.
increase
which
to the
occurs
of potassium
The
when
potassium
to the
in
hyper-
of insulin.
interfere
is increased
can
(65).
associated
that
direct
is hy-
caused
rapidly
result-
hyperkalemia
stimulates
in the
be related
the
reflect
insulin
shrinkage,
hyperkalemia
in part,
distribution
agonists.
that
urea
osmolality
the
intake
those
as
may,
Drugs
and
not
The
toacidosis
gic
are
ammonia-
endogenous
shrinkage,
duct
by ammonium
when
concentration
hyperkalemia.
it may
osmole,
common
to cell
to
and
sufficient
osmolality,
osmoles
branes,
in
most
is attributed
potassium
Ineffective
re-
of
is the
glycemia
lactic
potassium
exogenous
absence
due
(64)
(66-69).
the
in extracellular
extracellular
to differences
favorable
and
HC1 or
In con-
or more
and
collecting
extracellular
administered
in
potassium
osmolality,
increase
1 to 2 mEqIL
commonly
osmoles,
extracellular
of
cellular
in solution
cell
can
most
include
infrequent
effects
a more
in extracellular
osmoles,
perglycemia,
or
of redistribution-induced
Increases
the
be
channel
by effective
by
inhibit
may
pertonicity.
centration
decrease
reabsorption
potassium
stimu-
respiratory
ammoniagenesis,
secretion,
apical
cause
should
effect
potassium
of the
can
in
clinical
acids,
such
hyperkalemia.
an
proton
and
exit.
regulation
cellular
dissociated
by electrogenic
conductive
and
is
causes
largely
depolarization
in the
This
to
and
and intracellular
acidosis
of collecting
duct apical
levels
of sodium
for
and
in addition
(P0)
ammonia
inhibition
gradient
dietary
basolaterally
metabolic
acidosis,
probability
secretion.
mediated
in-
membrane,
whereas
exit
secretion
Both
intracellular
open
extraceblubar
potassium
in
Some
changes
acids,
potassium
stimulates
(54).
apical
reabsorption,
reabsorption.
cause
is the
loads
(33)
inhibits
potassium
mecha-
potassium
potassium
which
These
Hydrochloric
acid,
are
reabsorption
potassium
enhances
exit
membranes
the
(62,63),
common
to organic
lactic
f3-hydroxybutyric
lease.
the
due
or
potassium
across
acidosis
osmoles.”
due to mineral
associated
with
net
restriction
acidosis
dietary
Chronic
compartments
anesthetics,
acidosis
droxybutyric
small
Several
to “effective
Metabolic
acidosis
NH4C1,
is commonly
decreasing
Increased
exits
of hyper-
potassium
basolateral
recycling
potassium
development
and
channels
is located
redistribution.
membrane-depolarizing
hypertonicity
acid
even
to cause
thereby
Another
and extracellular
hyperkalemia.
known
potassium
(27,28,30).
if potassium
to the
secretion.
hyperkalemia
potassium
intake.
increases
membrane
to regulate
apical
reabsorption
acidosis
reabsorption
known
a significant
potassium
apical
contribute
at the
crease
(46,55-57).
body
distribution
potassium
the
than
of collect-
to
by
potassium
Redistribution
The
prior
and
potassium
can
factor
membrane
HtKATPase
across
hyperkalemia
complicated
contributes
hy-
KCI
products
One
and
10 to 13 mEq
develop
of
cel-
potassium-reabsorbing
in the apical
secretion
of
A
the
per tablespoon
such
are
acid
and
present
whether
more
much
load.
cells,
in net
Acidosis
as 4%
membrane
conductive
are
decreases
supplements
contain
mlIh
many
contain
results
lating
can
the
predomi-
molecule,
prevents
1998
and
step
determine
acid
reabsorption
nisms
insuffi-
intake
As
salt substitutes
per gram,
renal
of hyperkalemia
substitutes.
chloride
Typical
potassium
potassium
causes
salt
described
renal
drugs,
excess
Common
and
As
of
of milliequiva-
if
through
then
cause
factors.
hundreds
of
kalemia.
infrequent
However,
whether
causes,
supplements
patients
contributing
(34).
hyperkalemia.
potassium
an
can excrete
is impaired,
ciency,
is
This
the
Stimulation
basolaterally,
Intake
Excessive
of
intercalated
potassium
compartments,
that
is present
duct
(31,32).
redistribution
history
ing
uptake
which
to acidosis
nature
component
schema,
intake,
extraceblubar
excretion.
is
homeostasis,
In this
excess
that
to protons
acid
of a neutral
the factors
HtK4ATPase
for the
one
potassium
principles.
either
and
renal
developed
recommend
govern
clinical
results
been
We
that
common
perkalemia
have
hyperkalemia.
the
dissociation
unaffected,
in response
just
9: 1535-1543,
exit.
In practice,
value.
evaluation
potassium
Soc Nephrol
this
diffusion
is largely
occurs
plasma
subsequent
Because
involves
lular
potassium
the
with
(60,61).
potential
the
pseudohy-
of
base
nantly
exceeds
further
basis
uptake
weak
or in a “blood-gas
is abnormal
and
made
cellular
concentrations.
by obtaining
diagnosed,
should
potassium
potassium
potassium
by
measurements
serum
J Am
of Nephrology
in a “green-top”
serum
potassium
Society
be measured
either
If the
plasma
but
and
potassium
blood
American
The
are
normal
synthesis,
intracellular
that
intra-
to
increased
potassium
extracel-
that
and
and
regulate
and
hormones
aldosterone,
response
aldosterone
the
major
insulin,
systems
the
regulate
3-adrener-
potassium
increased
content.
aldo-
Inhi-
J Am Soc
bition
Nephrol
of
cant
9: 1535-1543.
aldosterone
1998
production
hyperkabemia,
at
atrial
natriuretic
peptide
zyme
inhibitors,
and angiotensin
inhibiting
cellular
hyperkalemia
bution
of adrenal
production.
Drugs
any
through
Inhiband
en-
aldosterone
of
these
action
classes
alterations
can
in the cellular
a
mEq/L
(77),
mild
(77-80).
increase
and
in
with
insufficiency
when
receiving
cell
basolateral
with
digitalis
its
analogues,
(83,84)
even
in the
at the
(85).
This
by
cause
impaired
distri-
deaths
occurring
inhibiting
the
elderly
may
conventional
doses
been
digoxin,
both
can
sodium
may
with
of a cardiac
renal
uptake
glycoside
excretion
of potassium.
and
that
have
to
Some
to bufadienolides,
steroids
cause
reabsorption
cause
hyperkalemia
in
end-stage
renal failure,
impaired
attributed
cardioactive
Na4KtATPase
as
ingestion
to both
cellular
have
and
such
of toxic
relate
extrarenal
soning
of potassium.
absence
may
hyperkalemia
(81,82).
principal
and
1. I
averaging
in severe
even
of sulfamethoxazole-trimethoprim
the
1539
potassium,
results
renal
hyperkalemia
Inhibiting
of Hyperkalemia
serum
occasionally
Those
develop
Aspects
and potassium
secretion.
Digoxin
predisposed
patients,
such as those
syn-
thereby
a mineralo-
aldosterone
causes
hyperkalemia
inhibit
synthase,
Spironolactone,
inhibits
from
in part
affect aldosteis regulated
in
antagonists,
aldosterone
antagonist,
level.
cellular
II receptor
adrenal
abdosterone
to signifi-
angiotensin-converting
stimulation
inhibits
receptor
lead
to decreased
angiotensin
II production.
as 3-adrenergic
antagonists
analogues,
Il-mediated
corticoid
can
due
drugs
in common
use
Abdosterone
synthesis
part by renin-stimubated
of renin secretion,
such
Heparin
action
in part,
large
itors
thesis.
or
least
potassium
uptake.
Many
rone synthesis
or action.
angiotensin
Clinical
poi-
naturally
digoxin-like
effects
(86).
Renal
Potassium
The
kidney
large
Secretion
possesses
amounts
Obstructive
such
a remarkable
of potassium
that
chronic
that
via potassium
affect
those
secretion
potassium
due
collecting
ducts)
renal
failure,
and
a significantly
number
collecting
duct
potassium
tassium
distribution.
or
secretion.
Any
effect
in clinical
interact
Aldosterone
of its effects
that
with
interferes
inhibit
collecting
duct
potassium
their
necessity
acid
metabobites
for
secretion.
an
po-
potassium
This
important
may
potassium
be due
and
in cob-
in part
to
mechanism
collecting
duct
reabsorption
essential
sodium
reabsorption.
increases
potassium
nal electronegativity,
gradient
for potassium
thereby
secretion.
inhibit
apical
sodium
sodium
reabsorption
channel.
ride and triamterene
channel
(70). More
The
acid metabolite
P, thereby
decausing
potassium
Collecting
hyperka-
increasing
Several
duct
the
drugs
blocking
azole
to
treat
Pneumocvstis
carinii
hyperkaleto several
up
of the obstruction.
for
hyperkalemia
the cardiac
uptake
potassium,
and
can
effects
that
be
divided
into
of hyperkabemia,
by cells
those
resulting
those
those
that
in a decrease
remove
potassium
that
induce
in plasma
from
Blocking
Cardiac
Effects
Intravenous
calcium
admini
stration
specifically
the
on
myocardial
effects
of
hyperkalemia
on
myocardial
way
to treat
and
most
rapid
normocalcemic
used
is
sodium
lumi-
gluconate
the
repolarization
the body.
Calcium
and
can
conduction
Calcium
is the
is effective
even
be administered
in
as either
with
pneumonia,
sulfamethoxroutinely
10 mm.
Because
calcium
mic
potentiate
patients
infusion
because
that
CaCO3
precipitation
occurs
during
rapid
digoxin
Potassium
second
fastest
potassium
distribution
or ,-adrenergic
toxicity
should
20 to 30 mm
Cellular
The
insulin
be administered
the myocardial
taking
over
not
to avoid
Uptake
way to treat
by increasing
agonist
with
of the
EKG
ab-
intravenous
con-
can occur.
Seccalcium
infusion
of digitalis.
be given
via
administration
in solutions
it should
may
cell apical
(74-76).
to
with
First,
use
sodium
and
5
be given
calcium.
cell
of this
trimethoprim
and should
should
be the initial
treatment
for individuals
normalities
related
to hyperkalemia.
Several
precautions
should
be observed
principal
amilo-
chloride,
be given if no effect is seen within
rapid
onset
of its effect,
intravenous
taming
NaHCO3
ond, hypercalcemia
diuretics
or calcium
antagonizes
(89).
hyperkalemia,
patients.
electrochemical
in common
the
potassium-sparing
frequently
secretion
by increasing
are specific
inhibitors
recently,
the antibiotics
trimethoprim,
uropathy-induced
for periods
of
is
(87,88).
an intravenous
route.
Effects
can be documented
on the EKG
within
1 to 3 mm, and last for 30 to 60 mm. A second
dose may
pentamidine
have been found to block the principal
sodium
channel
(71-73)
and lead to hyperkalemia
High-dose
or
is unclear
calcium
secretion
by
that occurs
nonsteroidal
potentially
for renal
of minerabocordeficiency
channels;
lemia.
A third
nephritis
a degree
a receptor
Arachidonic
reduce
arachidonic
potassium
channel
secretion
role
is
hyperacido-
release.
of renin
regulate
drugs
decrease
potassium
play
stimulation
also
anti-inflammatory
production
and
creasing
metabolites
relief
potassium
system
acid
have
this
but
(87,88).
The
with metabolic
inon
aldosterone
duct
after
Therapies
with
directly
independent
drug
will
use
patients
whether
to the interstitial
minimize
have
to hyperkalemia,
Therapy
renal
of hyperkalemia.
secretion,
Arachidonic
lecting
risk
These
resistance;
weeks
potassium
function
leads
Many
patients
with obstructive
mia will remain
hyperkalemic
ducts
is directly
insufficiency
or
renal
frequently
is incompletely
understood
occur either in association
or separately.
sis
related
into
to impaired
uropathy
the mechanism
kalemia
may
ticoid
of functioning
leads
impaired
of medications
potassium
creases
production
secretion.
with
is
factors
be classified
of active
or chronic,
Patients
greater
A large
impairment
is al-
secretion
potassium
duct,
(number
number
of collecting
filtration
rate, renal
acute
secretion.
can
mass
intrinsic
whether
potassium
generally
nephron
secretion.
Because
the
related
to the gbomerubar
potassium
regulates
in the collecting
excretion
to reduced
to excrete
hyperkalemia
most impossible
to produce
unless renal
impaired.
Because
the kidney
primarily
excretion
ability
Hyperkale-
calcium
as a slow
hypercalcemia.
hyperkalemia
cellular
administration.
is to alter
uptake
with
Insulin
either
rapidly
1540
Journal
stimulates
of the
cellular
marily
and
should
be administered
sistent
bioavailabibity,
levels
within
10 to 20
and
will
mm,
by
with
extrarenal
(90,91).
Ten
and con-
serum
lasting
potassium
for 4 to 6 h (91).
to avoid
due
to
hypertonicity-induced
effective
administration.
lates
treatment
potassium
uptake
approximately
nous
use
used,
however.
of
0.98
mEqIL,
and
can
1 mEqIL
(92),
United
States.
in the
dose
albuterob,
Albuterol,
10 or 20
mg,
is not
an
at 90 to 120 mm
therapy
include
intravenously
and
patients
may
when
given
decrease
abysis
albuterol
by
administered
kalemia,
by
metered
combined
effective
and
dose
therapy
than
Bicarbonate
when
the dose
nebulizer
either
in
to
or
to
33%
severe
albuterol
Table
3.
Potassium
treatment
worsen
hypertension
hyper-
may
be
and
not
chronic,
bicarbonate
may
be a prefer-
than
normal
saline
be
cause
EKG
sodium
for
of
either
loop
or thiazide
is generally
the
rate
Most
of
not
patients
condition
with
with
elimination
sulfonate.
contrib-
4 h for
the
the use
resin
exchanges
gastrointestinal
In
removes
full
close
contin-
is with
This
general,
approximately
tract,
1 g
0.5
effect.
When
given
Dose
Calcium
effects
gluconate,
solution,
10%
10 ml iv.
of
sodium
to 1 .0 mEq
It can
enema.
requiring
orally,
sodium
Onset
Duration
1 to 3 mm
30 to 60 mm
30 mm
4 to 6 h
30
mm
2 to 4 h
1 to 2 h
4 to 6 h
Immediate
Until
over
10 mm
Cellular
potassium
Insulin
Regular
iv.,
uptake
50
insulin, 10 U
with dextrose,
50%,
ml if plasma
glucose
is <250
Nebulized
/32-adrenergic
agonist
Potassium
removal
Sodium
sulfonate
polystyrene
Kayexalate,
20%
mg/dl
albuterol,
10 mg
60 g p.o.
sorbitob,
Kayexalate,
retention
in
or
60 g per
enema,
without
sorbitol
Hemodialysis
a
iv.,
dialysis
completed
intravenously:
p.o.,
postoperatively.
of
thereby
of potassium
in exchange
for 2 to 3 mEq of sodium.
administered
either orally or per rectum
as a retention
The rate of potassium
removal
is relatively
slow,
approximately
re-
as obstructive
in association
elimination.
sulfonate
factor
If a rapidly
be adequate.
polystyrene
in
hyperkalemia
such
of the underlying
potassium
opti-
excretion
with
is identified,
may
treated
a contributing
of diuretics.
level
diuretics
potassium
as
of potassium
potassium
polystyrene
stimulation
potassium
mode
sodium
of
hyperkalemia,
failure
observation
cases,
mild
effectiveness
treatment
of the
In selected
for treatment
insufficiency
of renal
then
removal.
of
3 summarizes
be adequate
adequate.
the
removal
is
Table
may
with
renal
a resin,
Therapy
Calcium
membrane
sodium
options’
Mechanism
Antagonize
metabolic
dextrose
5%
hyperkalemia
potassium
excretion
limiting
A second
show
bicarthe
may
With
will
uous
dose
for
elimination
underlying
uropathy,
either /3-agonist
administration
or insulin.
Recent
studies
that the changes
in serum
potassium
with intravenous
bonate
are small
and inconsistent
(98-100).
Moreover,
load
mEqIL
1 L D5W)
individual.
because
allowing
less
options
observation
that
the
for
hyperkalemia
versible
than
sodium
with
1998
failure.
At
bicarbon-
hyperkalemia,
rehydration
affected
Acute
(101),
hemodi-
the
diuretics
have
of
effective
associated
for
with
usually
(97).
is probably
150
in
suffice.
mally
albuterol
times
from
potassium
may
nebulized
In
and
of
bicarbonate
potassium
renal
bimigiven
is 2 to 8 times
100
(96).
insulin
alone
20
subsequent
required
addition
solution
hyperkalemia.
at a
primary
when
administering
50
the
available
renal
of action
In addition,
inhalers
with
administration
(93). The
tachycardia
the
be
by 0.62
onset
during
mistake
by
can
potassium
(93,94).
with
of sodium
potassium
intrave-
by nebubizer
response
removal
A frequent
given
of
by nebulizer
is underdosage;
usually
more
lack
potassium
(95).
for
immediate
and maximal
effect
tations
of ,-agonist
(92)
potassium
,-agonists
serum
with
rehydration
volume
Potassium
Removal
The definitive
treatment
stimu-
serum
administered
decreases
rapidly
approved
Nebulized
with
depletion,
and
able intravenous
solutions.
is n-agonist
mg,
decrease
but
when
respectively,
0.5
9: 1535-1543,
potas-
for hyperkabemia
Intravenous
In patients
acidosis,
(3 amps
redistribution.
A second
ate for hyperkalemia.
solutions
hypoglycemia,
to hyperglycemic
individuals.
Glucosecan lead to further
increases
in the
concentration
Soc Nephrol
ute to the development
of acute congestive
heart
present
we do not recommend
routine
use of sodium
pri-
of insulin
rapid
to affect
effects
cells,
units
to ensure
begin
coadministered
but should
not be given
induced
hyperglycemia
sium
uptake
myocytes
J Am
of Nephrology
intravenously
is generally
potassium
Society
potassium
hepatocytes
Glucose
American
be
J Am
Soc Nephrol
polystyrene
bitob
9: 1535-1543,
sulfonate
to avoid
Clinical
1998
is generally
constipation.
use of sorbitol
may
suggest
an association
sodium
polystyrene
administered
If given
with
as an enema,
20%
sor-
avoiding
Animal
models
suggest
the colonic
perforation,
possibly
related
due
to mucosal
lumen
Dialysis
sium
removal
serum
be considered
when
renal
the primary
function
is absent
and
is the
most
If a potassium-free
may
decrease
plasma
potassium
the
of 0 or 1 mEq/L
dialysis
but
is the
rapid
Specific
hyperkalemia.
in
with
tract
example,
many
may
be
latter
may
potassium
is used,
to treat
in certain
of
Fab
digitalis
hy-
treated
the rate
be
0, Kbose
potassium
with
relief
variable,
frequent
of
Orloffi,
in
RD.,
provided
the information
National
by
the
excretion
metabolism.
edited
In:
by
GB,
man.
AM:
Invest
health:
Effects
206-212,
blood
function
Electron
Microsc
the rabbit
17. Koeppen
and
RA,
New
York,
Lin
Total
244:
BN,
DH,
of age,
sodium,
potassium,
Phillips
Liv-
sex,
and chloride
height,
and
fat. Am
potassium
J Phvsiol
in
CS:
pressure
D, Kbag
and
J Ani
Jiang
MJ:
PE,
Svetkey
causes
LP:
Potassium
natriuresis
in older
Soc Nephrol
2: 1302-1
H, Cutler
JA, Brancati
Effects
of oral
chloride
226:
potassium
lowers
patients
309,
1992
FL,
Appel
.
on blood
with
Foll-
pressure:
acidification
of
8, Renal
in col-
Physiology,
DC, American
transport:
In:
edited
by
Physiological
Morphological
257:
and func-
R989-R997,
Tisher
CC:
1989
Relationship
tubule
9: 187-208,
and
between
collecting
J
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