Hillary
Lawson



NUT
116BL

F
12
–
1PM

February
27,
2013

Case
Study
#3
Renal

1.


Lab

 Value
 Normal
Range
 Interpretation

 Case
Based
Interpretation
 Reference

with
CKD
ranges
(NTP
p.
532‐
533)

GFR
 15
mL/min
 Greater
than
90
 Extremely
Low
 15‐
29
mL/min

 Pocket

mL/min
 
 Kidney
damage:
severe
 Reference

reduction
of
GFR
 pg.109

(recommendation
for
kidney

replacement
dialysis)

BUN
 90mg/dL
 10‐20
mg/dL
 Greater
than
normal
 60‐80mg/dL
Hypercatabolism
Pocket

and
exceeding
CKD
 or
excessive
protein
intake,
 Reference

range
 inadequate
dialysis
(p.111)
 pg.71


 Waste
product
that
comes

from
the
protein
we
consume.

Normally
removed
by
the

kidneys,
a
high
BUN
shows

altered
kidney
function.


Serum
 14mg/dL
 .5
–
1.1
mg/dL
 Too
High,
but
with
 2‐15mg/dL
 Pocket

Creatinine
 CKD
Range

 Close
to
high
end
=
excess
 Reference
p.


 protein,
inadequate
dialysis,
 74

muscle
damage)
p.112

Creatinine
 17.0mL/min
 88‐188ml/min
 Extremely
Low
 Creatinine
is
a
waste
product
 

Clearance
 for
women
 in
the
blood
from
muscles,
it
is

normally
removed
by
the

kidneys.
When
kidney

function
is
slow
the
clearance

is
low.


Serum
 142mEq/L
 136
–
146
 WNL
 
 Pocket

Sodium

 mEq/L
 Reference

p.80

Serum
 5.7mEq/L
 3.5‐5.0mEq/L
 Excessive
K
in
the
 3.5‐6.0mEq/L
CKD,
 Pocket

Potassium
 diet,
renal
failure,
 inadequate
dialysis,
excessive
 Reference

renal
HTN
 oral
intake
(high
or
low
levels
 p.79,113

can
weaken
muscles
and

change
your
heartbeat)

Serum
 2.8g/dL
 
 Too
Low
 *ideal
is
greater
than

4.0
g/dL
Pocket

Albumin
 3.5‐5.0
g/dL
 *maybe
be
due
to
 (p.
111)
 Reference

dilution
 *Fluid
overload
(nephritic
 pg.71

syndrome)

Hgb/Hct
 11.5g/dL
/
 12‐
16
g/dl
 Both
are
too
low
and
10‐12g/dL/33‐36%
 Pocket

28%
 and

 indicate
anemia
 Renal
failure/
renal
artery
 Reference
p.

37
–
47%
 stenosis,
uremia.
 77,
112



(anemia
or
inadequate
ESA)


Serum
 155mg/dL
 250‐380mg/L
 Low
 Low
iron
stores
linked
to
 Pocket

Transferrin
 Anemia,
nephrosis
 anemia.

 Reference


p.81



BP
 160/100
 Lower
than
 High
 Indicates
arterial
narrowing
 NTP
p.289

standing,
right
120/80mmHg

 HTN
is
greater
than
 or
plaque
build‐up,
high

arm
 140/90mmHg

 volume
fluid

Urine
pH
 7.31
 4.6
to
8

 WNL
 A
pH
below
4.5
would
be
very
 


 acidic
and
cause
renal


 damage.




Serum
 5.0mg/dL
 3.0‐4.5mg/dL
 Too
high

 3.5‐5.5mg/dL
(within
range)
 NTP
532‐
Phosphorus
 CKD,
inadequate
P
binder
 533

(High
levels
can
lead
to
weak

bones
and
calcifications
in
the

blood
when
bound
to
serum

calcium)

PTH
 100pg/mL
 
 Too
High
 indicates
a
poor
balance
of
 Pocket

10‐65
pg/mL
 
 calcium
and
phosphorous
in
 Reference
p.

Renal
hypercalcemia
the
body
and
could
cause
 79

bone
disease.


Urine
Volume
450‐mL/24hr
 800‐ Low
urine
output
 Indicates
poor
kidney
function
NTP

2000ml/24hr
 (18.75ml/hr)
 and
CKD

(based
on
2L

normal
intake)


References:

http://www.kidney.org/kidneydisease/understandinglabvalues.cfm


























http://lifeoptions.org/kidneyinfo/labvalues.php

http://www.nlm.nih.gov/medlineplus/ency/article/003425.htm





2.
Type
II
Diabetes
Mellitus
is
one
of
the
most
common
causes
of
chronic
kidney
disease

due
to
its
affect
on
the
glomerulus
and
renal
solute
load.
It
typically
becomes
a
risk
with

increasingly
uncontrolled
glucose
levels.
A
patient
with
type
II
DM
has
a
thickening
of
the

glomerulus
of
the
kidney,
which
is
responsible
for
filtering
the
blood
and
consolidating
the

waste
products
into
urine
to
be
excreted
from
the
body.
As
the
thickening
of
the

glomerulus
worsens,
more
protein
than
normal
is
lost
through
urine.
After
an
increasing

number
of
glomeruli
are
destroyed,
the
amount
of
albumin
excreted
in
the
urine
increases,

which
decreases
the
serum
concentration
of
albumin.
The
amount
of
nephrons
declines

and
a
diminished
number
of
nephrons
are
left
to
handle
the
same
solute
load,
which
causes

a
limit
on
how
much
solute
is
filtered
at
a
time.
As
a
result,
the
body
fluid
concentration

increases
and
leaves
the
patient
susceptible
to
azotemia
and
uremia,
as
well
as
an
obvious

decrease
in
GFR,
which
is
a
hallmark
of
CKD
(NTP.
527).



3.
Although
BK
complains
of
anorexia
and
weight
loss,
she
has
gained
weight
due
to
her

high
fluid
consumption
and
inability
to
filter
and
urinate
out
the
additional
fluid.
Patients

with
chronic
kidney
disease
have
reduced
or
complete
loss
of
kidney
function
and
have
an

inability
to
filter
their
blood.
This
inability
causes
a
back
up
of
fluid
in
the
system
and
a

higher
volume
of
fluid
retained
in
the
body.
Patients
with
CKD
have
two
weights.
Their

“wet
weight”
is
the
weight
in
which
they
are
carrying
additional
fluid
that
is
not
urinated

out
or
filtered
through
dialysis;
the
“dry
weight”
is
the
weight
in
which
the
patient
has
no

excess
fluid
in
their
system
or
just
after
dialysis.
Excessive
fluid
in
a
patient
can
cause

abnormal
lab
values,
edema,
hypertension,
and
cardiac
stress.




4.

Which
foods
in
her
usual
diet
are
contributing
most
to:

a)
Phosphorous
levels:
Eggs,
Corn
Tortillas,
Ice
Cream,
Whole
Milk,
Cheese

(Quesadillas)

b)
Potassium
levels:
Tampico
(citrus
juice),
Orange
Juice,
Banana,
Whole
Milk,
Ice

Cream

Sources:


‐ http://www.davita.com/kidney‐disease/diet‐and‐nutrition/diet‐
basics/phosphorus‐and‐chronic‐kidney‐disease/e/5306

‐ http://www.davita.com/kidney‐disease/diet‐and‐
nutrition/diet%20basics/potassium‐and‐chronic‐kidney‐disease/e/5308



5.
Explain
the
rationale
for
the
following
interventions:

a) Phosphate
Binder
:
A
phosphate
binder
is
used
to
prevent
the
gastrointestinal

absorption
of
phosphorous
by
acting
like
a
sponge
and
binding
up
the
available

phosphorous
in
the
stomach.
Unbound
serum
phosphorous
can
calcify
with
Calcium.

Typically,
high
Calcium
foods
are
high
in
phosphorous
as
well;
when
these
foods
are

consumed,
the
excess
phosphorous
must
be
controlled
somehow.




b)
Calcium
Supplement:
A
Calcium
supplement
is
typically
given
to
a
CKD
patient
because

there
is
a
deficiency
in
the
active
form
of
vitamin
D
due
to
parathyroid
hormone(PTH)
loop

inhibition.
PTH
is
involved
with
the
regulation
of
calcium
in
the
body
by
stimulating

calcium
reabsorption,
phosphorous
excretion,
and
the
activation
of Vitamin
D,
which
then

stimulates
the
absorption
of
intestinal
Calcium.
When
damaged
kidneys
are
unable
to

convert
Vitamin
D
to
the
active
form,
the
PTH
loop
is
disabled,
and
bone/mineral
disorders

can
ensue.

High
calcium
foods
are
typically
high
in
phosphorous
as
well,
which
can
result

in
calcifications
in
serum.
Thus,
Calcium
supplements
in
conjunction
with
calcium
in
the

diet
are
used
to
meet
requirements
of
CKD
patients.
Calcium‐based
phosphate
binders
are

sometimes
used
to
increase
calcium
levels
in
patients
while
lowering
phosphate
to

maintain
bone/mineral
density
(NTP
524,541).



c)
Iron
and
EPO:

Iron
deficiency
is
common
among
CKD
patients
because
the
kidneys
are

unable
to
make
adequate
erythropoietin
(during
dialysis)
for
RBC
production.

Erythropoietin
is
made
by
the
renal
tubular
cells;
in
compromised
kidneys,
the
RBC

production
declines
in
the
bone
marrow
and
results
in
low
hemoglobin.
Recombinant

Human
Erythropoietin
is
used
to
supplement
CKD
patients
and
increase
RBC
production.

Typically,
the
effectiveness
of
erythropoietin
depends
on
iron
status
because
RBC

production
requires
a
great
deal
of
iron,
which
is
why
CKD
patients
are
often
given

supplements.

Untreated
anemia
can
result
in
cardiac
or
ventricular
hypertrophy,
angina,

CHF,
malnutrition
or
impaired
immunological
responses
(NTP544‐545).




d)
Vitamin
Supplement
containing
only
WSV:
Due
to
increased
losses
of
water
soluble

vitamins
during
dialysis,
anorexia,
or
poor
dietary
intake,
WSV
supplements
are
necessary.

The
renal
diet
is
also
very
low
in
fresh
fruits
and
vegetables,
whole
grains,
and
dairy;
these

groups
of
food
that
are
high
in
water‐soluble
vitamins.
Renal
WSV
supplements
typically

contain
B
vitamins,
folic
acid,
and
Vitamin
C;
fat‐soluble
vitamins
and
minerals
need
not
be

included
in
these
supplements
(NTP
549).




6.
Explain
the
purpose
of
each
of
the
following
interventions
and
list
the
data

indicating
the
need
for
treatment:
(NTP
p.532­33)

a)Protein
Restriction:
A
low
protein
diet
is
recommended
for
those
in
the
early
stages
of

CKD,
and
a
high
protein
diet
is
recommended
for
those
on
dialysis.
CKD
patients
on
a

protein
restriction
should
limit
their
protein
intake
because
their
kidneys
are
unable
to

filter
the
waste
products
of
protein
metabolism.
By
reducing
protein
intake,
it
reduces
the

workload
of
the
kidneys
as
well
as
the
risk
of
azotemia
and
uremia,
and
may
stifle
the

progression
of
the
disease.
However,
it
is
important
that
the
patients
on
limited
protein

consume
at
least
50%
high
bioavailable
protein
for
protein
sparing.
Low
albumin
(below

3.5
mg/dL)
and
high
protein
waste
values
(Creatinine,
CC,
BUN)
indicate
kidney
issues,
as

well
as
a
decreasing
GFR
rate
showing
a
decreasing
ability
to
filter.




b)
Phosphorous
Restriction:
Phosphorous
in
the
body
is
used
for
maintaining
and
building

strong
bones
and
teeth,
or
aiding
in
the
conversion
of
food
to
energy.
Kidney
disease
can

prevent
the
body
from
excreting
phosphorous,
causing
secondary
issues
affecting
the

bones
and
the
heart
binding
with
calcium
in
the
serum,
which
causes
calcifications
in
the

blood
and
possible
osteoporosis.
Phosphorous
restriction
is
used
to
control
the
amount
of

serum
phosphorous.
It
is
also
important
when
on
hemodialysis
to
limit
phosphorous,

because
when
there
is
excess
phosphorus
in
the
blood,
patients
have
complained
of
itching.


A
phosphorous
level
greater
than
4.5mg/dL
indicates
a
high
serum
level
and
inability
to

clear,
a
high
PTH
level
can
also
be
associated
with
high
phosphorous
and
Calcium
9greater

than
65pg/mL).



c)
Potassium
Restriction:
The
kidneys
are
responsible
for
potassium
regulation.
In
the
case

of
chronic
kidney
disease,
potassium
levels
cannot
be
controlled,
and
the
buildup
of

potassium
can
result
in
hyperkalemia
and
undesirable
cardiac
events.
Potassium

 restriction
is
important
to
maintain
electrolyte
balances
and
prevent
cardiac
events.

A

potassium
level
greater
than
5.0
mEq/L
can
indicate
a
need
for
treatment.




d)
Fluid
and/or
Sodium
Restriction:
Fluid
and
sodium
restrictions
are
used
to
control
blood

pressure
and
maintain
fluid
electrolyte
balances.
The
kidneys
are
responsible
for
filtering

toxins
from
the
blood
and
due
to
reduced
kidney
function
the
urine
output
is
decreased.
A

lower
urine
output
means
a
higher
fluid
load
on
the
vasculature
of
the
body
and
the
heart

to
pump.
In
order
to
reduce
the
workload
on
the
body
and
reduce
fluid
retention,
fluid
and

sodium
restrictions
are
important;
they
can
reduce
the
risk
of
edema,
hypertension
(a

common
cause
of
CKD),
shortness
of
breath,
cardiac
stress,
and
fatigue.

A
sodium
level

greater
than
146
mEq/L
with
edema
indicates
a
need
for
treatment.
Also,
a
low
urinary

output
of
less
than
500
mL
per
24
hours
indicates
a
need
for
treatment.




7.
Assessment:

Subjective:
Patient
is
42
yo
female
with
type
2
DM,
HTN,
hyperlipidemia,
and
CKD
that
has

progressed
from
stage
3
two
years
ago
to
now
where
the
patient
c/o
of
an
inability
to

urinate,
itching
(pruritus),
and
a
weight
gain
of
5kg
in
10
days.
The
patient
c/o
N/V,

secondary
anorexia,
edema,
and
worsened
SOB.
Patient
has
2
children
both
macrosomic
at

birth
and
finds
it
hard
to
adhere
to
DM
or
CKD
management
due
to
her
busy
lifestyle.




Objective:


Lab
Values:

Anthropometrics:

GFR:
15
ml/min
(indicating
near
 Calculations:

Edema‐Free
W:
71.81kg


ESRD)

 Recommended
Kcals
for

SW
(Med)
=
61kg

BUN:
90
mg/dL
=
High

 Weight
maintenance:

Adj.BW
=
EFW
+
(SW‐EFWx0.25)


Work:
65.36
kg=66.8
+((61‐66.8)
x0.25)
 Serum
Creatinine:
14mg/dL
=
high
 35kcals/kgBW/d
per
CKD

IBW:
50
kg
 CC:
17.0mL/min
=
low
 patients
<
65
yo

Ht:
1.575m
 Albumin
=
2.8
g/dL
=
Low
 ‐
2287.6
or
~2300kcal

%IBW:130.72%
(ABW)
 Hgb/Hct
=
indicate
anemia
@
11.5
 Protein:

BMI
(AdjBW):
26.5
(overweight)
 g/dL
and
28%
 Recommended
≥
1.2
g/kgBW

Recommended
weight
for
HD
patients:
Transferrin:
155
mg/dL
=
Low
 65.36
x
1.2
=
78.43
(~80g)
PRO

(PR
pg.
110)
 BP:
160/100
indicates
Stage
II
HTN
 Fluid:
Gains
between
HD:

A
BMI
of
23.6
for
women
for
increased
Phos:
5.0
mg/dL
=
High
 3.3
kg
WG
brown
HD
appt.

survival
rate
 PTH
100pg/mL
=
High
 Tx
Fluid
Plan:

58.54kg
or
~
129lbs
 Urine
output:
450
mL/24hr
=
low
 1.5L
restriction


Na:
WNL

K:
5.7
mEq/L
=
High


Diet
History:
 Recommendations
for
Diet:

‐
Sub
3500
kcal
 Sub
2300kcal


34%
Total
Fat

 CHO:
sub
56%
(~322g)

15%
Sat
Fat
(11%Mono
 PRO:
79g
(~80g)
or
greater
than
13.9%

5%Poly)
 Greater
than
50%
HBV

18%
Protein
 Fat:
less
than
30%
total
fat


Ca:
2082mg
 Less
than
77g


K:
4431mg

 Less
than
10%
Sat
Fat
(or
26g)


Phos:
2802mg
Na:
6450mg
 2gm
Na.



2gm
K.


1gm
Ph


Drugs:
 Purpose:
 Nutrient
Interactions:
 Side
Effects:


Metformin
 Oral
hypoglycemic
 Avoid
Alcohol
 Lactic
Acidosis,
GI


distress,
chest
pain,
loss

of
appetite
(PR
p160)

Lasix
 Treatment
for
edema,
 Avoid
alcohol,
 Jaundice,
anorexia,

loop
diuretic
 barbituates,
and
 paresthesias,
diarrhea,

narcotics
 N/V,
dizziness,
rash,

urticaria
etc.
9pdr.net)

Vasotec
 ACE
inhibitor
used
to
 Use
caution
with
K+
 Fatigue,
Headache,

decrease
BP
and
 containing
salt
 Dizziness
(pdr.net)

decrease
HTN
 substitutes
or

supplements




Diagnosis:

PES:
Unintended
weight
gain
(NC‐3.4)
R/T
progression
of
chronic
kidney
disease
AEB
5kg

weight
gain
in
10
days
counter
indicated
by
secondary
anorexia,
inability
to
urinate
(GFR

15mL/min,
Urine
Volume
450mL/24hr),
altered
lab
values
(Albumin
2.8g/dL,
CC
17.0

mL/min,
Creatinine
14
mg/dL,
PTH
100ph/mL),
pitting
edema
3+
with
BP
160/100,

worsened
SOB,
N/V
(Phosphorous
5.0mg/dL
[barely
normal],
5.7
mEq/L),
ronchi
with

rales,
and
fatigue.




*
I
chose
unintended
weight
gain
as
the
main
problem
due
to
the
fact
that
the
5kg

weight
is
possibly
due
to
BK’s
inability
to
adhere
to
recommendations
concerning

her
current
condition.
She
has
been
a
CKD
patient
for
2
years
and
a
T2DM
for
most
of

her
life.
The
added
weight
gain
more
than
likely
is
causing
the
exacerbated

symptoms
of
edema,
HTN,
dilution,
SOB,
fatigue,
etc.




State
of
Δ:
BK
is
in
the
contemplation
stage
of
the
transtheoretical
model
of
behavior

change.
BK
was
diagnosed
with
type
II
DM
at
the
age
of
12
with
a
FMH
of
the
disease
and

was
diagnosed
with
CKD
stage
3
two
years
ago,
yet
she
has
not
made
the
recommended

changes
to
her
diet
or
lifestyle
and
is
not
adherent
to
her
medication
regiment.
The
patient

is
aware
of
her
medical
conditions
but
neglects
to
follow
a
treatment
plan
or
make
small

changes.



Intervention:

‐
Meet
with
the
patient
3
times
a
week
before
HD
appointments
and
slow
the
imminent

progression
of
the
ESRD
to
mortality.

‐
Reeducate
the
patient
on
DM
and
CKD
as
it
relates
to
the
progression
of
BK's
CKD
stage
3

to
end
stage.


‐
Reintroduce
the
patient
to
the
Renal
diet
and
restrictions
on
sodium,
potassium,

phosphorous,
and
fluid.


‐
Recommend
the
patient
for
Hemodialysis
(3xwk,
4hrs)
and
educate
the
patient
on
the

nutrition
variations
specific
to
Hemodialysis;
specifically
fluid
restriction,
dry
versus
wet

weight,
electrolyte
restrictions
(K,
Na,
P),
and
high
protein
intake.


‐
Introduce
the
patient
to
phosphate
binders
and
stress
the
importance
of
maintaining
her

medications
regimen;
making
the
patient
aware
of
her
iron‐deficiency
anemia,
CKD
stage
5

and
electrolyte
importance,
and
mortality.


Goals:

1)
Recommend
the
patient
keep
a
food/fluid/weight
journal
while
adhering
to
the
Renal

diet
(as
long
as
the
patient
is
on
dialysis)
until
the
patient
is
able
to
unconditionally
follow

the
diet
and
maintain
electrolyte/weight/protein
related
markers
within
normal
CKD

ranges.


2)
Maintain
a
high
protein
diet
of
at
least
80
grams
of
protein
a
day
while
decreasing

weight
until
a
BMI
of
sub
24
is
reached
to
improve
QOL
and
effectiveness
of
HD.


3)
Decrease
fluid
intake
to
1.5
L
per
day
to
improve
efficiency
of
HD
and
control
weight

gain
between
treatments,
while
decreasing
soda
(Tampico)
and
other
electrolyte‐rich

fluids
(whole
milk
and
orange
juice).



Monitor/Evaluate:

‐
Meet
with
the
patient
3
times
a
week
before
HD
appointments
and
monitor
the
patient’s

adherence
to
the
Renal
diet
by
the
food/fluid/weight
journal
the
patient
will
keep.

‐
Monitor
electrolyte
levels
while
patient
is
on
Renal
diet
and
over
the
course
of
HD

treatments
pertaining
to
the
kidneys
(K,
P,
Na,
and
Ca),
protein/protein
waste
markers

(Albumin,
BUN,
Creatinine),
and
weight
before
and
after
HD
treatments.

‐
Evaluate
Patient’s
adherence
to
the
high
protein
diet
through
journal
and
the
use
of
UUN

in
the
nitrogen
balance
equation.

‐
Monitor
and
evaluate
the
patient’s
anemic
status
over
the
course
of
treatment

(Diet/HD/EPO/Iron)
for
improvement
(Hgb/Hct).













Printed
Name:
 
 
 
 
 
 Signature:



Date/Time:























 

Renal
Diet
Pattern:

2gm
Sodium,
2gm
Potassium,
1gm
Phosphorous,
and
1.5
L
Fluid

Food # of Choices Kcal Pro (g) Na (mg) K (mg) Phos (mg)

Meat (total of 8)
- Animal Protein HBV 400 (80) 35 (7) 375 (75) 250 (50) 250 (50)
(5)
- Vegetarian Protein (3) 300 (100) 18 (6) 150 (50) 300 (100) 240 (40)
Milk (1) 100 4.0 80 185 110

Bread/starch (8) 800 (100) 16 (2) 640 (80) 360 (40) 240 (30)

Vegetable
- Low (1) 50 2 45 75 50
- Medium (1) 50 2 45 150 50
- High (0) 0
Fruit
- Low (2) 150 (75) 2 (1) 50 (25) 100 (50) 50
- Medium (1) 75 1 25 160 50
- High (0)
Fat (5) 225 (45) trace 275(55) 50 (10) 25 (5)

Extra (2) 120 (60) trace 30 (15) 40 (20) 10 (5)

Fluids (1.5L)
Choices:
- use the milk option
Total 2270 80 1715 1670 1075

Sources: NTP p. 537 (NRD Nutrition Composition of Foods for People on Dialysis)
https://smartsite.ucdavis.edu/access/content/group/bc09b3ba‐c660‐4648‐bcf5‐
e8ac1577a1f7/week%206/HandoutRenalDietExchanges.pdf



Food
Options:
8.

Weight
fluctuations
between
hemodialysis
sessions
is
normal.
Hemodialysis
is
the

process
of
removing
fluid
and
waste
from
the
blood
as
it
is
filtered
through
an
artificial

kidney.
The
artificial
kidney
removes
waste
products
and
excess
fluid
via
diffusion,

ultrafiltration,
and
osmosis.
The
artificial
kidney
does
the
job
of
the
human
kidney,
but
only

during
sessions
at
a
limited
rate.
Typically,
a
patient
does
three
sessions
a
week
that
each

last
about
four
hours,
whereas
a
normal
kidney
is
working
24/7
filtering
the
blood.
In‐
between
sessions,
the
kidney
is
not
able
to
filter
the
blood
as
efficiently
or
at
all,
and
all
of

the
excess
fluid
consumed
and
waste
products
of
the
body
remain,
resulting
in
added

weight.
Because
the
body
retains
any
excess
fluid
between
HD
sessions,
fluid
and
sodium

restrictions
are
important
to
reduce
HTN,
edema,
cardiac
stress,
SOB,
etc.

(http://www.davita.com/kidney‐disease/diet‐and‐nutrition/diet‐basics/fluid‐control‐for‐
kidney‐disease‐patients‐on‐dialysis/e/5321)




9.

BK’s
protein
consumption
on
February
25th
reflected
69.375
grams
of
protein
ingested

and
71.25
grams
on
her
subsequent
visit
February
27.
BK
is
shy
of
consuming
the
amount

of
protein
I
recommended
for
her.
As
an
end
stage
renal
disease
patient
on
hemodialysis,

BK
requires
a
higher
protein
intake
in
order
to
replace
the
protein
that
is
lost
through

dialysis.
It
is
no
longer
recommended
that
BK
eat
low
protein
because
the
protein
waste
is

being
removed
via
dialysis
and
protein
is
important
in
order
for
BK
not
to
lose
muscle
mass

and
maintain
her
ability
to
fight
infection.
I
had
recommended
that
BK
consume
80
grams

of
protein
or
more
a
day,
roughly
1.2g/kg
BW/d.
The
patient
is
just
under
my

recommendation,
and
in
reality
I
would
like
her
to
be
consuming
80
or
more.















10.
Sodium
in
the
diet
is
important,
it
is
a
way
to
regulate
blood
pressure
and
volume,

transmit
impulse,
and
regulate
the
body’s
acid‐base
balance.
However,
in
a
patient
with

CKD,
consuming
too
much
causes
water
retention
with
such
complications
as
swelling,

cardiac
issues,
and
SOB
due
to
the
kidney’s
inability
to
excrete
the
excess
sodium.
With
a

patient
like
BK,
on
hemodialysis,
a
low
sodium
diet
is
recommended.
The
use
of
salt

substitutes
to
maintain
a
low
sodium
intake
would
not
be
recommended
because
some
salt

substitutes
contain
potassium,
which
also
needs
to
be
regulated
with
CKD
patients.
The

best
thing
for
BK
to
do
would
be
to
find
ways
to
remove
sodium
from
her
diet
as
opposed

to
using
salt
substitutes,
such
as
using
spices
to
boost
the
flavor
of
foods
or
reading
food

labels.


(http://www.davita.com/kidney‐disease/diet‐and‐nutrition/diet‐basics/sodium‐and‐
chronic‐kidney‐disease/e/5310)