Chronic  
Chronic KKidney
idney  D isease  ((CKD)
Disease CKD)  aand
nd  D iet:  
Diet:
Assessment,  Management,  and  Treatment  
Assessment, Management,
 
and Treatment
Treating  CKD  Patients  W
  ho  Are  Not  on  Dialysis  
Treating CKD Patients Who Are Not on Dialysis
  An  
An O verview  G
Overview uide  ffor
Guide or  DDietitians
ietitians    
 
 
 
   
Revised  
Revised M   arch  2
March 011  
2011
 
 
 

NKDEP
National Kidney Disease
Education Program
  

Table  
Table o off  CContents
ontents  
 
 

I.I.   About  
About C KD............................................................................................1  
CKD 1

I I .      A
II. ssess  KKidney
Assess idney  FFunction
unction  aand
nd  DDamage
amage ...................................................2  
2

III.
I I I .      SSlow
low  PProgression
rogression..................................................................................3  
3

IV.
I V .      Prevent,  
Prevent, M onitor,  aand
Monitor, nd  TTreat
reat  CComplications
omplications ........................................5  
5

V.  
V .    PPatient
atient  EEducation
ducation  M aterials...............................................................11  
Materials 11

VI.  
V I .  RReferences
eferences .........................................................................................12  
12

CKD  
CKDaand nd  DDiet
iet  ||  AAssessment,
ssessment,  M anagement,  aand
Management, reatment  Page10
nd  TTreatment
 
This document, developed by the National Kidney Disease Education Program (NKDEP), is intended to help registered dietitians (RDs) provide
effective medical nutrition therapy (MNT) to CKD patients who are not on dialysis.

I. About CKD
The kidneys regulate the composition and volume of blood,
remove metabolic wastes in the urine, and help control the
acid/base balance in the body. They activate vitamin D needed for
calcium absorption and produce erythropoietin needed for red-
CKD RISK FACTORS
blood-cell synthesis. Diabetes
Hypertension
CKD is typically a progressive disease. It is defined as: Family history of kidney failure
• Reduction of kidney function—defined as an estimated Cardiovascular disease
glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2 Recurrent urinary tract infections
and/or HIV infection
• Evidence of kidney damage, including persistent Immunological diseases
albuminuria—defined as ≥ 30 mg of urine albumin per gram
of urine creatinine

Kidney failure is typically defined as an eGFR < 15 mL/min/1.73 m2.
CKD is detected and monitored by two tests:
• Estimated glomerular filtration rate (eGFR) and
• Urine albumin-to-creatinine ratio (UACR)
The purpose of diet therapy for CKD is to maintain good nutritional
status, slow progression, and to treat complications.
The key diet components to slowing progression of CKD are:
• Controlling blood pressure by reducing sodium intake
• Reducing protein intake, if excessive
• Managing diabetes
As eGFR declines, complications occur more commonly and are
more severe. These may include:
• Malnutrition
• Metabolic acidosis due to reduced acid (hydrogen ion)
excretion
• Hyperkalemia
• Mineral imbalance and bone disorder (calcium, phosphorus,
and vitamin D)
• Anemia due to impaired erythropoiesis and low iron stores
• Cardiovascular disease (CVD) (dyslipidemia)

CKD and Diet | Assessment, Management, and Treatment Page 1

II.  
II. A ssess  KKidney
Assess idney  FFunction
unction  aand
nd  D amage  
Damage
 

Test  
Test a nd  IIts
and ts  RRelevance
elevance   Results  
Results Assessment  
Assessment

Estimated  
Estimated G lomerular  
Glomerular •• Evaluate  
Evaluate eeGFR
GFR  tto  
o aassess
ssess  kkidney
idney  ffunction;
unction;  ttrack
rack  oover  
v e rttime  
i m e tto  
om monitor  
o n i t o r eeffectiveness
ffectiveness  ooff  ddiet
iet  therapy.  
therapy.  
2
eGFR  
eGFR ((mL/min/1.73m
m L / m i n / 1 . 7 3 m 2 )  
) •• Stable  
Stable eeGFR
GFR  mmay
ay  indicate  
indicate ttherapy  
h e r a p y is  
iswworking.
orking.  
Filtration  
Filtration R ate  ((eGFR)
Rate eGFR)    
eGFR  
eGFR e stimates  kkidney
estimates idney  ffunction.
unction.     Normal  
Normal > >  6
600     •• Decline  
Decline ooff  eeGFR
GFR  rreflects
eflects  pprogression KD.    
rogression  ooff  CCKD.
As  
As e GFR  ddeclines,
eGFR eclines,  ccomplications
omplications   CKD  
CKD 115–60  
5 - 6 0  
are  
are m ore  llikely
more ikely  aand
nd  m ore  ssevere.
more evere.   Kidney  
Kidney ffailure
ailure  <<  1155   Additional  
Additional IInformation
nformation    
  Each  
Each ffiltering
iltering  uunit nit  ooff  tt hhe  
e kkidney,
idney,  oorr  nnephron,
ephron,  ffilters
ilters  aa  ttiny
iny  aamount  
mount o off  p lasma  eeach
plasma ach  m inute.    eeGFR
minute. GFR  
  reflects  
reflects tthhe  e tt ootal  
t a l ff iltration  
iltration o off  a ll  ttw
all wo  
o m illion  nnephrons.
million ephrons.    A Ass  n ephrons  aare
nephrons re  ddamaged
amaged  oorr  ddestroyed,
estroyed,  eeGFR GFR  
declines.  
declines.  The The  qquantity
uantity  oorr  vv olume  
olume o off  u rine  m
urine may ay  nnotot  cchange
hange  ssignificantly
ignificantly  aass  eeGFR
GFR  ddeclines.
eclines.    HHowever,
owever,  
what  
w h a t iiss  e xcreted  iinto
excreted nto  tt hhe  
e u rine  ddoes
urine oes  cchange.
hange.    RRapidly
apidly  ddeclining
eclining  eeGFRGFR  m ay  w
may w aarrant  
r r a n t aappropriate
ppropriate  
discussion  
discussion o off  rrenal
enal  rreplacement
eplacement  ttherapies. herapies.    
 
In  
In a dults,  tt hhe  
adults, e b est  eequation
best quation  ff or   or e stimating  eeGFR
estimating GFR  ff rom  
r o m sserum
erum  ccreatinine
reatinine  iiss  tt hhe  
e M M oodification  
dification o off  D iet  iin
Diet n  
Renal  
Renal D isease  ((MDRD)
Disease MDRD)  SStudy tudy  eequation
quation  ((Levey, Levey,  11999).
999).  N KDEP  ooffers
NKDEP ffers  ccalculators
alculators  oonline nline  aand
nd  aass  
downloadable  
downloadable a pplications  ffor
applications or  eestimating
stimating  G FR.    SSerum
GFR. erum  ccreatinine
reatinine  llevel,
evel,  aage,ge,  ggender,
ender,  aand nd  rrace
ace  aarere  
needed.  
needed.  M Manyany  llaboratories
aboratories  rroutinely outinely  rreport eport  eeGFR
GFR  w w iith  
th a ll  sserum
all erum  ccreatinine eterminations.  
reatinine  ddeterminations.

Urine  
Urine A lbumin-­‐to-­‐
Albumin-to- •• Evaluate  
Evaluate UUACR
ACR  oover
ver  ttime  
i m e tto  
o aassess
ssess  rresponse
esponse  tto  
o ttherapy  
h e r a p y aand
nd  mmonitor  
o n i t o r pprogression
rogression  ooff  CCKD.
KD.    
UACR  
UACR ((mg/g)
mg/g)  
Creatinine  
Creatinine R atio  
Ratio Normal  
Normal 00–29  
- 2 9  
•• Change  
Change in  
in aalbuminuria
lbuminuria  mmay
ay  rreflect
eflect  rresponse
esponse  tto  
o ttherapy  
h e r a p y aand
nd  rrisk
isk  ffor
or  pprogression.
rogression.  

(UACR)  
(UACR)   Albuminuria  
Albuminuria > >  330
0   •• A  
Addecrease
ecrease  in  
inuurine
rine  aalbumin
lbumin  mmay
ay  bbe
e  aassociated
ssociated  wwith  
i t h improved  
improved rrenal
enal  aand
nd    
UACR  
UACR iiss  tthhe  
e p referred  m
preferred easure  
measure   cardiovascular  
cardiovascular ooutcomes.utcomes.  
for  
for sscreening,
creening,  aassessing,
ssessing,  aand nd    
monitoring  
m o n i t o r i n g kkidney
idney  ddamage.
amage.       Additional  
Additional IInformation
nformation  
UACR  
UACR e stimates  224-hour
estimates 4-­‐hour  uurine
rine     Normally  
Normally ffunctioning
unctioning  kkidneysidneys  eexcrete xcrete  very
very  ssmall
mall  aamounts
mounts  ooff  aalbumin
lbumin  iinto nto  tt hhe  
e u rine.    AAlbuminuria
urine. lbuminuria  
albumin  
albumin e xcretion.    U
excretion. nlike  aa  
Unlike
usually  
usually rreflects
eflects  ddamageamage  ttoo  tthhe  
e g lomerulus—the  “" filter”  
glomerulus—the filter" o
off  tt h
he  
e n ephron.    A
nephron. lbuminuria  iiss  aan
Albuminuria n  
dipstick  
dipstick test test  ff or  
or u rine  aalbumin,
urine lbumin,   independent  
independent rrisk isk  ffactor
actor  ffor
or  CCKD
KD  pprogression
rogression  ((Hemmelgarn,
Hemmelgarn,  22010) 010)  aand
nd  iiss  cconsidered
onsidered  aa  m arker  ffor
marker or  CCVD
VD  
UACR  
UACR iiss  u naffected  bbyy  vvariation
unaffected ariation  iin
n   and  
and m ortality  iinn  hhypertension.
mortality ypertension.    RReducing
educing  uurine
rine  aalbumin
lbumin  ttoo  nnormal
ormal  oorr  nnear-normal
ear-­‐normal  llevelsevels  m may ay  iimprove
mprove  
urine  
urine cconcentration.
oncentration.   cardiovascular  
cardiovascular pprognoses. rognoses.  
 
 

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 2 2  
 
III.  
III. S low  PProgression
Slow rogression    
 
Therapeutic  
Therapeutic G oal  aand
Goal nd  
Ranges/Goals  
Ranges/Goals Dietary  
Dietary IIntervention
ntervention  
Its  
Its R elevance  
Relevance
Control  
Control B lood  PPressure
Blood ressure   •• Limit  
Limit ssodium
odium  intake  
intake tto  
o 11,500
,500  mmg
g  aa  dday
ay  oor
r  less  
less(USDA  
(USDA &&  UUS
S  DDHHS,
HHS,  22010).
010).  
Goal  
Goal < <  1 30/80  m
130/80 m m  
m H g  
Hg
Blood  
Blood p ressure  ccontrol
pressure ontrol  sslows
lows   •• Weight  
Weight rreduction
eduction  mmay
ay  bbe
e  bbeneficial.
eneficial.    
progression  
progression o off  CCKD KD  aand
nd  llowers
owers    
CVD  
CVD rrisk.isk.   •• Monitor  
M o n i t o r sserum
erum  ppotassium
otassium  in  
in ppatients
atients  oon
n  rrenin
enin  aangiotensin
ngiotensin  ssystem
ystem  (RAS)  
(RAS) aantagonists;
ntagonists;  limit  
limit ddietary
ietary  
   
  potassium  
potassium iintake ntake  w
w hhen  
e n sserum
erum  ppotassium
otassium  >>  55  m Eq/L.    
mEq/L.
 
Sodium  
Sodium p lays  aa  llarge
plays arge  rrole
ole  iinn  bblood
lood  
pressure  
pressure ccontrol ontrol  iinn  CCKD KD  aass  aa  rresult
esult  
of  
of a lterations  iinn  ssodium
alterations odium  eexcretion
xcretion   Additional  
Additional IInformation
nformation  
by  
by tth he  
e kkidneys.
idneys.   For  
For p atients  w
patients w iith  
th h ypertension,  rreduction
hypertension, eduction  ooff  ddietary
ietary  ssodium
odium  hhasas  bbeen
een  aassociated
ssociated  ww iith  
t h iimproved
mproved  bblood lood  
  pressure  
pressure ccontrol
ontrol  iinn  cclinical
linical  ttrials
rials  aand
nd  eepidemiological
pidemiological  sstudies. tudies.  
 
Multiple  
Multiple m edications  m
medications ay  bbee  rrequired
may equired  tt oo  ccontrol
ontrol  bblood
lood  ppressure.
ressure.    RRAS
AS  aantagonists,
ntagonists,  ssuch uch  aass  
angiotensin-­‐converting  
angiotensin-converting e nzyme  iinhibitors
enzyme nhibitors  ((ACEi)
ACEi)  oorr  aangiotensin
ngiotensin  rreceptor
eceptor  bblockers
lockers  ((ARBs),
ARBs),  aare re    
often  
often u sed  ttoo  ccontrol
used ontrol  bblood
lood  ppressure,
ressure,  ddelayelay  pprogression,
rogression,  rreduce educe  aalbuminuria,
lbuminuria,  aand nd  pprotect
rotect  aagainst
gainst    
heart  
heart ddisease.
isease.  
 
Diuretics  
Diuretics a re  pprescribed
are rescribed  tt oo  tt rreat  
e a t ffluid
luid  ooverload
verload  aand
nd  hhigh igh  bblood
lood  ppressure,
ressure,  aand nd  m ay  hhelp
may elp  ccontrol
ontrol  sserum erum  
potassium  
potassium llevels.evels.  

Reduce  
Reduce A lbuminuria  
Albuminuria Reduce  
Reduce o orr  sstabilize
tabilize  tt hhe  
e aamount  
mount
Limit  
Limit e xcessive  ddietary
excessive ietary  pprotein
rotein  aass  ffollows:
ollows:  
Decreased  
Decreased a lbuminuria  iiss  
albuminuria of  
of a lbumin  llost
albumin ost  iinn  tthhe  
e uurine
rine     •• Nondiabetic:  
Nondiabetic:  00.8
.8  gg  pprotein/kg/day  
rotein/kg/day
associated  
associated w w iith  
t h sslower
lower   (see  
(see U ACR  aabove
UACR bove  oonn  ppage age  22).
).  
progression  
progression o off  C KD,  pparticularly
CKD, articularly  iin n   •• Diabetic:  
Diabetic:  00.8-1.0 r o t e i n / k g / d a y  
.8-­‐1.0  gg  pprotein/kg/day
diabetics.  
diabetics.  LLimiting
imiting  ddietary rotein    
ietary  pprotein Evidence  
Evidence ssuggests
uggests  tt hhat  
a t ff urther  
u r t h e r llowering
owering  ttoo  00.6
.6  gg  pprotein/kg/day  
r o t e i n / k g / d a y iin
n  nnondiabetic
ondiabetic  ppatients
atients  mmay ay  bbe
e  
may  
may rreduce
educe  aalbuminuria
lbuminuria  aand nd         beneficial,  
beneficial,bbutut  aadherence
dherence  is   isddifficult.
ifficult.    SSome
ome  ppatients
atients  mmay ay  bbe
e  aable
ble  tto  
o aachieve
chieve  tthis
his  level  
level w with  
i t h intensive  
intensive
improve  
improve b lood  gglucose
blood lucose  ccontrol,
ontrol,   counseling.  
counseling.
hyperlipidemia,  
hyperlipidemia, b lood  ppressure,
blood ressure,  
renal  
renal b one  ddisease,
bone isease,  aand nd  m etabolic  
metabolic  
acidosis.  
acidosis.
  Additional  
Additional IInformation
nformation  
Limiting  
Limiting e xcessive  pprotein
excessive rotein  m ay  aactivate
may ctivate  aadaptive
daptive  rresponses
esponses  tthhat   at d ecrease  aalbuminuria
decrease lbuminuria  aand
nd  iincrease
ncrease  
serum  
serum a lbumin,  w
albumin, w iithout  
t h o u t iincreasing
ncreasing  rrisk
isk  ffor
or  pprotein
rotein  m a l n u t r i t i o n .  
malnutrition.

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 3 3    
 
III.  
III. S low  PProgression
Slow rogression  (continued)
(continued)  
 
Therapeutic  
Therapeutic G oal  aand
Goal nd  
Ranges/Goals  
Ranges/Goals Dietary  
Dietary IIntervention
ntervention  
Its  
Its R elevance  
Relevance
Manage  
Manage D iabetes  
Diabetes •• Consider  
Consider less-­‐stringent  
less-stringent ccontrol ontrol  ffor  
o r ppatients
atients  wwith  
i t h hhistories
istories  ooff  hhypoglycemia,
ypoglycemia,  tthe  
h e eelderly,
lderly,  aand
nd  
A1C  
A1C ≤ <  7 .0%  
7.0%
patients  
patients w w iith  
th m ultiple  cco-morbid
multiple o-­‐morbid  cconditions.
onditions.  
Blood  
Blood g lucose  ccontrol
glucose ontrol  m ay  hhelp
may elp    
slow  
slow p rogression  ooff  CCKD
progression KD     •• Instruct  
Instruct ppatients
atients  tto  
o ttreat  
r e a t hhypoglycemia
ypoglycemia  wwith  
i t h ccranberry
ranberry  jjuice
uice  ccocktail,
ocktail,  ggrape
rape  oor
r  aapple
pple  jjuice,
uice,  gglucose
lucose  
(DCCT,1993;  
(DCCT,1993; U KPDS,1998)  
UKPDS,1998) tablets,  oorr  1100  jelly
jelly  bbeans
eans  tt oo  pprevent yperkalemia.  
revent  hhyperkalemia.
  tablets,
 
Additional  
Additional IInformation
nformation  
As  
As e GFR  ddeclines,
eGFR eclines,  rrenalenal  m etabolism  ooff  iinsulin
metabolism nsulin  aand
nd  ccertain
ertain  ooral
ral  ddiabetes
iabetes  m edications  aare
medications re  rreduced,
educed,  
potentially  
potentially ccausing ausing  hhypoglycemia
ypoglycemia  iinn  ddiabetes
iabetes  ((Snyder,Snyder,  22004).
004).    U nexplained  iimprovement  
Unexplained m p r o v e m e n t iin n  gglucose
lucose  
control  
control m may ay  rreflect
eflect  pprogression
rogression  ooff  CCKD.
KD.  
 
Low-­‐protein  
Low-protein d iets  hhave
diets ave  bbeen
een  aassociated
ssociated  w w iith  
t h iimproved
mproved  iinsulin
nsulin  ssensitivity
ensitivity  aand
nd  ffasting
asting  sserum
erum  iinsulin
nsulin  
levels,  
levels, llower
ower  iinsulin
nsulin  rrequirements
equirements  aand nd  bblood
lood  gglucose
lucose  llevels,
evels,  aand
nd  aa  ddecrease
ecrease  iinn  eendogenous
ndogenous  gglucose lucose  
production  
production iin n  ppatients
atients  ww iith   iabetes.  
t h ddiabetes.

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 4 4  
 
IV.  
IV. P revent,  M
Prevent, onitor,  aand
Monitor, nd  TTreat
reat  CComplications
omplications  
 
Data  
Data iiss  llimited
imited  ffor
or  CCKD.
KD.    M any  ooff  tthe
Many he  rrecommendations
ecommendations  ffor
or  CCKD
KD  aare
re  eextrapolated
xtrapolated  from
from  rrenal
enal  rreplacement
eplacement  ttherapies
herapies  lliterature.
iterature.  
 
Complication  
Complication a nd  IIts
and ts  
Ranges/Goals*  
Ranges/Goals* Dietary  
Dietary IIntervention
ntervention  
Relevance  
Relevance
Malnutrition  
Malnutrition •• Manage  
Manage w with  
i t h aadequate
dequate  ccalories
alories  aand
nd  nnutrients.
utrients.  
Albumin  
Albumin > >  4 .0  gg/dL
4.0 /dL  
Malnutrition  
M a l n u t r i t i o n iis s  ccommon  
o m m o n iin n  CCKD;
KD;   Normal  
Normal rrange:
ange:    33 .4–5.0  
. 4 - 5 . 0 gg/dL
/dL   •• Water-­‐soluble  
Water-soluble vvitamin   i t a m i n ssupplementation  
upplementation m ay  bbe
may e  indicated  
indicated ddue ue  tto  
o tthe  
h e rrestricted
estricted  pprotein rotein  intake.  
intake.  
as  
as e GFR  ddeclines,
eGFR eclines,  ssoo  m ay  
may Vitamin  
Vitamin C C  iis
s  typically
typically  nnot ot  ssupplemented  
upplemented a bove  tthhe  
above e D ietary  RReference
Dietary eference  IIntake,ntake,  aass  iitt  m ay  ccause
may ause  
appetite.  
appetite.  M M aalnutrition  
l n u t r i t i o n iin
n  CCKD
KD   Serum  
Serum a lbumin  <<  44.0
albumin .0  gg/dL,
/dL,  pprior
rior  
oxalosis.  
oxalosis.  V itamins  A
Vitamins A,,  E
E,,  a nd  KK  ccan
and an  aaccumulate
ccumulate  m moreore  rrapidly
apidly  iinn  CCKD
KD  aand
nd  aare
re  nnot
ot  rrecommended  
e c o m m e n d e d ffor
or  
tto  
o iinitiation
nitiation  ooff  ddialysis,
ialysis,  m ay  
may
patients  
patients iis s  aassociated
ssociated  w with  
ith supplementation.  
s u p p l e m e n t a t i o n .  S pecific  rrenal
Specific enal  vv itamin  
i t a m i n fformulas
ormulas  aare re  aavailable
vailable  fforor  ddialysis atients.  
ialysis  ppatients.
increased  
increased m m orbidity  
o r b i d i t y aandnd   predict  
predict m m orbidity  
orbidity a nd  m
and ortality  
mortality

mortality.  
mortality. (Lowrie,  
(Lowrie, 11990).
990).    
 
Additional  
Additional IInformation
nformation  
Blood  
Blood u rea  nnitrogen
urea itrogen  ((BUN)
BUN)                  
Serum  
Serum a lbumin  iiss  uused
albumin sed  ttoo  m
m onitor  
onitor n utritional  sstatus.
nutritional tatus.    H ypoalbuminemia  m
Hypoalbuminemia ay  rresult
may esult  ff rom  
r o m rreduced
educed  
<  
<2 0  m
20 g/dL  
mg/dL
protein  
protein a and/or  
n d / o r ccalorie
alorie  iintake,
ntake,  uuremia,
remia,  m etabolic  aacidosis,
metabolic cidosis,  aalbuminuria,
lbuminuria,  iinflammation,
nflammation,  oorr  iinfection.
nfection.  
 
 
Although  
Although n ot  uused
not sed  tt oo  iindicate
ndicate  nnutritional
utritional  sstatus,
tatus,  eelevated
levated  BBUN UN  m ay  bbee  aassociated
may ssociated  w w iith  
th a version  tto  
aversion o
certain  
certain h igh-­‐biological-­‐value  pprotein
high-biological-value rotein  ffoods.
oods.    A ppetite  m
Appetite mayay  iimprove
mprove  iinn  rrenal
enal  ffailure
ailure  w
w iith  
th a dequate  rrenal
adequate enal  
replacement  
replacement tt hherapy  
e r a p y ((i.e., i.e.,  ddialysis
ialysis  tt rreatment  
eatment o orr  kkidney ransplantation).  
idney  ttransplantation).

Metabolic  
Metabolic A cidosis  
Acidosis •• Dietary  
Dietary pprotein
rotein  is  
isaa  ssource
ource  ooff  mmetabolic
etabolic  aacid.
cid.    SSerum
erum  bbicarbonate
icarbonate  levels  
levels m ay  increase  
may increase w with  
i t h ddietary
ietary  
Bicarbonate  
Bicarbonate ((C0CO22))  >>  2222  m Eq/L  
mEq/L
protein  
protein rrestriction.
estriction.  
Patients  
Patients w w iith  
th C KD  aare
CKD re  aatt  rrisk
isk  ffor
or  
Normal  
Normal rrange:
ange:    22 1–28  
1-28 m Eq/L  
mEq/L
metabolic  
metabolic a cidosis  aass  aa  rresult
acidosis esult  ooff   •• Sodium  
Sodium bbicarbonate
icarbonate  ssupplementation   upplementation m ay  bbe
may e  pprescribed
rescribed  tto  
o improve  
improve nnutritional
utritional  pparameters
arameters  aand nd  
reduced  
reduced e xcretion  ooff  aacid
excretion oad.  
cid  lload. slow  
slow rrate
ate  ooff  CCKDKD  pprogression
rogression  ((de de  BBrito-Ashurst,
rito-­‐Ashurst,  22009).
009).    M
Moonitor  
nitor b lood  ppressure
blood ressure  cclosely
losely  w
w hhen  
e n tthis
his  
medication  
medication iis s  uused,
sed,  aass  ssome
ome  ppatients
atients  mmayay  eexperience
xperience  eelevated
levated  bblood
lood  ppressure
ressure  aassociated
ssociated  w with  
ith
increased  
increased ssodium odium  lload. oad.  

Additional  
Additional IInformation
nformation  
Metabolic  
Metabolic a cidosis  iiss  tt hhought  
acidosis o u g h t tt o
o  rresult
esult  iinn  lloss
oss  ooff  bbone
one  aand
nd  m uscle  m
muscle ass,  nnegative
mass, egative  nnitrogen
itrogen  bbalance,
alance,  
increased  
increased p rotein  ccatabolism,
protein atabolism,  aand nd  ddecreased
ecreased  pprotein rotein  ssynthesis ibid).  
ynthesis  ((ibid).

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 5 5  
 
IV.  
IV. P revent,  M
Prevent, onitor,  aand
Monitor, nd  TTreat
reat  CComplications
omplications  ((continued)
continued)  
 
Complication  
Complication a nd  IIts
and ts  
Ranges/Goals*  
Ranges/Goals* Dietary  
Dietary IIntervention
ntervention  
Relevance  
Relevance
Hyperkalemia
Hyperkalemia   Potassium  
Potassium 3 3 .5–5.0  
.5-5.0 m Eq/L  
mEq/L •• Counsel  
Counsel ppatients
atients  tto  
o rrestrict
estrict  ddietary
ietary  ppotassium
otassium  wwhen  
h e n sserum
erum  level  
level is  
is55.0
.0  mmEq/L
Eq/L  oor
r  hhigher.
igher.  
Patients  
Patients w w iith  
th C KD  aare
CKD re  aatt  rrisk
isk  ffor
or   Hyperkalemia  
Hyperkalemia iiss  u sually  nnot
usually ot  sseen
een   •• Caution  
Caution ppatients
atients  tto  
o aavoid
void  ppotassium-containing
otassium-­‐containing  ssalt
alt  ssubstitutes.
ubstitutes.  
hyperkalemia  
hyperkalemia a ass  aa  rresult
esult  ooff   until  
until C KD  iiss  aadvanced,
CKD dvanced,  bbut ut  mmayay  
reduced  
reduced p otassium  eexcretion,
xcretion,   •• Instruct  
Instruct ppatients
atients  wwith  
i t h ddiabetes
iabetes  tto  
o ttreat  
r e a t hhypoglycemia
ypoglycemia  wwith  
i t h ccranberry
ranberry  jjuice
uice  ccocktail,
ocktail,  ggrape
rape  oor
r  aapple
pple  
potassium be  
be sseen
een  aatt  hhigher
igher  eeGFRs
GFRs  iin
n  
intake  
intake o off  h igh-­‐potassium  ffoods, oods,   juice,  gglucose
juice, lucose  tablets,
tablets,  oorr  1100  jelly
jelly  bbeans
eans  ttoo  pprevent
revent  hhyperkalemia.
yperkalemia.  
high-potassium diabetics.  
diabetics.
metabolic  
metabolic a cidosis,  aand
acidosis, nd     •• Counsel  
Counsel ppatients
atients  tto  
o aadhere
dhere  tto  
o ssodium
odium  bbicarbonate
icarbonate  ttherapy,
herapy,  if  ifpprescribed.
rescribed.    CCorrection
orrection  ooff  aacidosis
cidosis  
medications  
medications tt h hat  
a t iinhibit
nhibit     may  
may llower otassium.  
ower  ppotassium.
potassium  
potassium e xcretion,  ssuch
excretion, uch  aass  RRASAS  
 
antagonists  
antagonists ffor or  bblood
lood  ppressure
ressure  
control.  
Additional  
Additional IInformation
nformation  
control.

The  ppotassium
The otassium  ccontent
ontent  ooff  m ost  vvegetables
most egetables  ccan
an  bbee  ddecreased
ecreased  tt hhrough  
rough a a  p rocess  ooff  lleaching.
process eaching.    LLeaching
eaching  
entails  
entails sslicing
licing  aand nd  ssoaking
oaking  tthhe  
e v egetable  oovernight
vegetable vernight  iinn  ww aater,  
t e r , tth
hen  
en d raining  aand
draining nd  bboiling
oiling  tt hhe   vegetable  iin
e vegetable n  
new  
new w w aater.  
t e r .  A
A  rrecent
ecent  sstudy,
tudy,  hhowever,
owever,  sshows hows  tt hhat  
at w w hhite  
ite p otatoes  ddoo  nnot
potatoes ot  nneed
eed  ttoo  bbee  ssoaked
oaked  oovernight
vernight  
(Bethke  
(Bethke & &  Jansky,
Jansky,  22008). 008).    The
The  ppotassium
otassium  ccontentontent  ooff  oo ther  
t h e r ttuuberous  
b e r o u s rroot
oot  vegetables
vegetables  ccommonly ommonly  eeatenaten  iin
n  
tthe  
he C aribbean  aand
Caribbean nd  SSouth
outh  A merica  hhas
America as  bbeen
een  sshown
hown  ttoo  bbee  rreduced
educed  ssomewhat  
omewhat b y  ddouble-cooking,
by ouble-­‐cooking,  
however,  
however, m mostost  sstilltill  rremained
emained  hhigher igher  tthhan  
an 2 00  m
200 mgg  pper
er  sserving
erving  ((Burrowes
Burrowes  & &  R 006).  
amer,  22006).
Ramer,  

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 6
 
IV.  
IV. P revent,  M
Prevent, onitor,  aand
Monitor, nd  TTreat
reat  CComplications
omplications  ((continued)
continued)  
 
Complication  
Complication a nd  IIts
and ts  
Ranges*/Goals  
Ranges*/Goals Dietary  
Dietary IIntervention
ntervention  
Relevance  
Relevance
CKD  
CKD M ineral  aand
Mineral nd     See  
See ssections
ections  oonn  ccalcium,
alcium,  
Existing  
Existing g uidelines  oonn  m
guidelines anagement  ooff  CCKD-MBD
management KD-­‐MBD  rreflect
eflect  cconsensus
onsensus  rrather ather  tt hhan  
an h igh-­‐grade  eevidence.
high-grade vidence.    
Early  
Early iintervention
ntervention  m ay  hhelp
may elp  pprevent
revent  vvascular
ascular  ccalcification
alcification  aand nd  ssecondary
econdary  hhyperparathyroidism.
yperparathyroidism.  
Bone  
Bone D isorder                
Disorder phosphorus,  
phosphorus, pparathyroid
arathyroid  
 
hormone  
h o r m o n e ((PTH),
PTH),  aand
nd    
(CKD-­‐MBD)  
(CKD-MBD) vvitamin  
itamin D D..  
The  kkidneys
The idneys  m aintain  ccalcium
maintain alcium  aand nd  pphosphorus
hosphorus  llevels evels  aand nd  aactivate
ctivate  vv itamin  
itamin D D..    A
Ass  kkidney
idney  ffunction  
unction

CKD-­‐MBD  
CKD-MBD iiss  rrenal
enal  bbone
one  ddisease
isease   declines,  
declines, ccomplex
omplex  iinteractions
nteractions  ooccur ccur  tt hhat  
at a ffect  ccalcium,
affect alcium,  pphosphorus,
hosphorus,  vv itamin  
itamin D D,,  a nd  tthhe  
and e pparathyroid
arathyroid  
tthat  
hat o ccurs  w
occurs w hhen  
e n tthhe  
e kkidneys
idneys  ffail
ail   gland.  
gland.  A
A bnormal  
b n o r m a l llevels
evels  ooff  PPTH
TH  ((measured
measured  aass  iintactntact  oorr  iiPTH)
PTH)  mmayay  bbee  sseen.
een.    M ineral  aand
Mineral nd  bbone
one  ddisorders
isorders  
may  
may rresult
esult  ff rom   these  iinteractions.
r o m these nteractions.    SSee ee  tt hhe  
e sspecific
pecific  ssections
ections  tthhat   o l l o w .  
a t ffollow.
tto  
o m aintain  sserum
maintain erum  ccalcium
alcium  aand
nd  
phosphorus  
phosphorus llevels.
evels.  
  Additional  
Additional IInformation
nformation  
Depending  
Depending o n  tthhe  
on e tt yype  
pe o off  rrenal
enal  bbone
one  ddisease,
isease,  ccalcium,
alcium,  pphosphorus,
hosphorus,  aand
nd  iiPTH
PTH  m ay  bbee  nnormal,
may ormal,  
decreased,  
decreased, o orr  eelevated.
levated.  
•• Secondary  
Secondary hhyperparathyroidism
yperparathyroidism  iiss  aassociated
ssociated  w
w iith  
th h igh  bbone
high one  tt uurnover,  
rnover, a nd  eelevated
and levated  llevels
evels  ooff  
calcium,  
calcium, p hosphorus,  iiPTH,
phosphorus, PTH,  aand
nd  aalkaline
lkaline  pphosphatase.
hosphatase.  
•• Osteomalacia  
Osteomalacia rresults
esults  iin
n  llow
ow  bbone
one  tt urnover  
urnover w w ith  
ith e levated  sserum
elevated erum  ccalcium
alcium  llevels
evels  aand
nd  nnormal-to­
ormal-­‐to-­‐
decreased  
decreased sserum
erum  pphosphorus,
hosphorus,  iiPTH,PTH,  aandnd  aalkaline
lkaline  pphosphatase.
hosphatase.  
•• Adynamic  
Adynamic bbone one  ddisease
isease  rresults
esults  iin
n  llow
ow  bbone
one  tt uurnover  
rnover a nd  m
and ay  bbee  ccharacterized
may haracterized  bbyy  nnormal-­‐to-­‐low  
ormal-to-low
iPTH  
iPTH a nd  aalkaline
and lkaline  pphosphatase.
hosphatase.    SSerum
erum  ccalcium
alcium  aandnd  pphosphorus
hosphorus  m may ay  bbee  nnormal
ormal  tt oo  eelevated.
levated.  
•• Mixed  
M i x e d bbone
one  ddisease,
isease,  aass  tt he  
h e nname
ame  iimplies,
mplies,  hhas
as  ffeatures
eatures  ooff  bboth
oth  llow
ow  aand
nd  hhigh
igh  bbone u r n o v e r .  
one  tturnover.

Calcium  
Calcium
Calciu m Calcium  
Calcium 8 8 .5–10.2  
.5-10.2 m g/dL  
mg/dL •• Dietary  
Dietary ccalcium
alcium  
calciu m rrecommendation
ecommendations  
s ffo
recommendations or  
rC
for KD  
D hhav
CKD
CK ave  
e yye
have et  
t tt o  
yet ob be  
e eestablished
stablished.  .
established.

Control  
Controll o
Contro o f  
f ccalcium
alcium  
calciu m aand nd  
an d   •• Calcium-­‐based  
Calcium-based pphosphate-bindin
Calcium-based
Calcium-base hosphate-­‐binding  
phosphate-binding g m edications  
medications
medication s cca an  
n iincrease
can ncrease  
increas e tt otal  
otal d aily  
dail
dailyy iintak
ntake  
e aan
intake nd  
d eelevate
and levate  
elevat e
phosphorus  
phosphoruss llevels
phosphoru evels  
level sh elps  
helps
help s ccontrol
ontrol  l
contro calcium.  
calcium .  
calcium.
PTH.  
PTH
PTH..
Maintain  
Maintain within  
within normal  
normal range.  
range.
• Supplementation  with  active  vitamin   D  increases  the  
• Supplementatio
Supplementation n rw isk  
i t hfor  
activ
activehypercalcemia.  
e v i t a m i n D increase
increasess t h e risk
ris k fo
forr hypercalcemia
hypercalcemia..
   
• Use  formula  to  correct  calcium  with  
• hypoalbuminemia:     Use
Us e f o r m u l a t o correct
correc t calcium
calciu m w i t h hypoalbuminemia
hypoalbuminemia::
 
Corrected  
Correcte
Corrected d ccalcium
alcium  
calciu m ((mg/dL)
mg/dL)  
(mg/dL ) ==  sseru
erum  
serumm ccalcium
alcium  
calciu m ((mg/dL)
mg/dL)  
(mg/dL ) + +  0
0..8  
0.88 ((4.04.0  
(4. 0 -­‐-  sseru
erum  
serum m a lbumin  
albumin
albumi /dL))  
n gg/dL)
g/dL

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 7 7  
 
IV.  
IV. P revent,  M
Prevent, onitor,  aand
Monitor, nd  TTreat
reat  CComplications
omplications  ((continued)
continued)  
Complication  
Complication a nd  IIts
and ts  
Ranges*/Goals  
Ranges*/Goals Dietary  
Dietary IIntervention
ntervention  
Relevance  
Relevance
Phosphorus  
Phosphorus •• If  Ifsserum
erum  pphosphorus
hosphorus  is  
iseelevated,
levated,  ddietary
ietary  pphosphorus
hosphorus  rrestriction estriction  mmay ay  bbe
e  indicated.  
indicated.  TThe
he  
Phosphorus  
Phosphorus 2 .7–4.6  m
2.7-4.6 g/dL  
mg/dL
recommended  
r e c o m m e n d e d llevel
evel  ooff  rrestriction
estriction  hhas
as  yyet
et  tt oo  bbee  dd etermined  
e t e r m i n e d iin
n  CCKD.
KD.  
Control  
Control o off  p hosphorus  aand
phosphorus nd  
calcium  
calcium llevels
evels  hhelps
elps  ccontrol
ontrol  PPTH.
TH.   Maintain  
Maintain w w iithin  
thin n ormal  rrange.
normal ange.    
•• Dietary  
Dietary pprotein
rotein  rrestriction
estriction  ddecreases
ecreases  pphosphorus
hosphorus  intake.  
intake.  If  
Ifffurther  
u r t h e r rrestriction
estriction  is  
isnneeded,
eeded,  ccounsel
ounsel  
Serum  
Serum p hosphorus  llevels
phosphorus evels  m ay  
may patients  
patients tto o  rreduce
educe  iintake
ntake  ooff  ffoods
oods  w
w iith  
th a dded  pphosphorus.
added hosphorus.  ((Uribarri,
Uribarri,  22007)
007)  
be  
be “" n
normal”  
ormal" u ntil  CCKD
until KD  iiss  
•• Counsel  
Counsel ppatients
atients  tto  
o rread
ead  ingredient  
ingredient lists  
lists ffor  
o r “"phos”  
p h o s " tto  
o identify  
identify ffoods
oods  wwith  
i t h pphosphate
hosphate  aadditives,
dditives,  aas
s  
advanced.  
advanced.
these  aadditives
these dditives  m ay  bbee  aabsorbed
may bsorbed  m ore  eefficiently
more fficiently  tthhan  
a n ff ood  
o o d ssources.
ources.  
 
  •• Limiting  
Limiting w whole  
h o l e ggrains
rains  mmay
ay  hhelp
elp  if  ifffurther  
u r t h e r rreduction
eduction  is  
isnneeded.
eeded.  
•• Phosphorus  
Phosphorus bbinders inders  mmay ay  bbe
e  pprescribed
rescribed  tto  
o lower  
lower pphosphorus
hosphorus  levels.  
levels.  CCounsel
ounsel  ppatients
atients  tto  
o take  
take
binders  
binders w w iith  
th m eals  ttoo  hhelp
meals elp  llimit
imit  aabsorption
bsorption  ooff  pphosphorus
hosphorus  ff rom  
r o m ff ood  
ood a nd  bbeverages.
and everages.  

Additional  
Additional IInformation
nformation  
Calcium  
Calcium a cetate  aand
acetate nd  ccalcium
alcium  ccarbonate
arbonate  aare re  ccommon  
o m m o n ccalcium-containing
alcium-­‐containing  pphosphate
hosphate  bbinders. inders.    CCalcium
alcium  
citrate  
citrate iis s  nnot
ot  rrecommended  
ecommended a ass  a
a  p hosphate  bbinder
phosphate inder  ffor
or  CCKD
KD  ppatients
atients  bbecause
ecause  iitt  m ay  iincrease
may ncrease  aaluminum  
luminum
absorption.  
absorption.  O Otherther  bbinders,
inders,  uused
sed  m ore  ooften
more ften  iinn  rrenal
enal  rreplacement
eplacement  ttherapy,
herapy,  aare
re  typically
typically  ccomposed
omposed  ooff  
resins  
resins ((sevelamer
sevelamer  ccarbonate)arbonate)  aand nd  eearth
arth  m etals  ((lanthanum
metals lanthanum  ccarbonate).
arbonate).  

Parathyroid  
Parathyroid H ormone  
Hormone Normal  
Normal P TH  <<  6655  ppg/mL  
PTH g/mL Dietary  
Dietary p hosphorus  rrestriction
phosphorus estriction  aand
nd  uuse
se  ooff  aactive
ctive  vvitamin  
itamin D D  o
orr  iits
ts  aanalogs
nalogs  m ay  hhelp
may elp  ccontrol
ontrol  PPTH
TH  llevels
evels  iin
n  
CKD.  
CKD.  C alcium  ssupplementation  
Calcium upplementation m ay  hhelp
may elp  aass  w ell.  
well.
(PTH)  
(PTH) Measured  
Measured a ass  iiPTH
PTH  
Secondary  
Secondary hhyperparathyroidism
yperparathyroidism   PTH  
PTH v aries  bbyy  llevel
varies evel  ooff  kkidney
idney  
(elevated  
(elevatedP TH)  iiss  aassociated
PTH) ssociated  w w ith  
ith function  
function a nd  tt yype  
and pe o off  bboneone   Additional  
Additional IInformation
nformation  
the  
the m ost  ccommon  
most o m m o n ccause ause  ooff  bbone
one   disease.  
disease. PTH  
PTH iis s  tthhe  
e h hormone  
o r m o n e tt hhat  
a t rregulates
egulates  sserum
erum  ccalcium
alcium  llevels.
evels.    LLow
ow  llevels
evels  ooff  11,25(OH)
,25(OH)22D, D,  hhypocalcemia,
ypocalcemia,  aand nd  
disease  
disease iin n  CCKD.
KD.   hyperphosphatemia  
hyperphosphatemia sstimulate timulate  PPTH
TH  ssecretion.
ecretion.    IIts
ts  m etabolic  aactions
metabolic ctions  iinclude
nclude  m obilizing  ccalcium
mobilizing alcium  aandnd  
phosphorus  
phosphorus ff rom   rom b one;  iincreasing
bone; ncreasing  iintestinal
ntestinal  aabsorption
bsorption  aand nd  rrenal
enal  tt uubular  
b u l a r rreabsorption
eabsorption  ooff  ccalcium;
alcium;  aand nd  
decreasing  
decreasing rrenal enal  tt uubular  
b u l a r rreabsorption
eabsorption  ooff  pphosphorus.
hosphorus.    PPTH TH  eenhances
nhances  cconversion
onversion  ooff  225(OH)D
5(OH)D  tto  
o
1,25(OH)
1,25(OH) 2D.  
2 D.

 
Consensus  
Consensus g uidelines  rrecommend  
guidelines ecommend h igher  PPTH
higher TH  llevels
evels  aatt  llower
ower  llevels
evels  ooff  eeGFR.
GFR.    
 

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 8 8  
IV.  
IV. P revent,  M
Prevent, onitor,  aand
Monitor, nd  TTreat
reat  CComplications
omplications  ((continued)
continued)  
Complication  
Complication a nd  IIts
and ts  
Ranges*/Goals  
Ranges*/Goals Dietary  
Dietary IIntervention
ntervention  
Relevance  
Relevance
Vitamin  
Vitamin D D   •• Supplementation  
Supplementation m ay  bbe
may e  indicated.  
indicated.  SSpecific
pecific  rrequirements
equirements  in  
inCCKDKD  hhave
ave  yyet
et  tto  
o bbe e  ddetermined.  
etermined.
Vitamin  
Vitamin D D  ≥
>  2
200  nng/mL
g/mL  
The  
The kkidneys
idneys  aactivate
ctivate  225(OH)D5(OH)D   •• Ergocalciferol  
Ergocalciferol (vitamin  
(vitamin DD22)  
)o orr  ccholecalciferol
holecalciferol  ((vitamin
vitamin  DD33)  ) m ay  bbee  uused
may sed  iin
n  eearly
arly  CCKD
KD  tt o  
o rreplete
eplete  
(calcidiol)  
(calcidiol) tt o o  11,25(OH)
,25(OH)22D D  ((calcitriol
calcitriol   Measured  
Measured a ass  225(OH)D
5(OH)D  
vvitamin  
itamin D D..  
or  
or a ctive  vv itamin  
active itamin D ).    RReduction
D). eduction  ooff   Maintain  
Maintain w w iithin  
thin n ormal  rrange
normal ange  
kidney  
kidney ff unction  
u n c t i o n rresults
esults  iin n   •• Active  
Active vvitamin  
i t a m i n DD  ((calcitriol)
calcitriol)  oor
r  its  
its aanalogs
nalogs  ((doxercalciferol,
doxercalciferol,  pparicalcitol,
aricalcitol,  oor
r  aalfacalcidol)
lfacalcidol)  mmay
ay  bbe
e  
(IOM,  
(IOM, 22011).
011).  
decreased  
decreased p roduction  aand nd   used  
used a ass  e GFR  ddeclines
eGFR eclines  ((ibid).
ibid).      
production  
conversion  
conversion o off  ccalcidiol
alcidiol  tto  
o            
calcitriol.  
calcitriol.  There
There  m ay  bbee  
may   Monitor  
M o n i t o r ffor
or  hhypercalcemia
ypercalcemia  aand/or  
nd/or h yperphosphatemia  w
hyperphosphatemia w hhen  
en u sing  ssupplements.
using upplements.    A ctive  vv itamin  
Active itamin D D  
corresponding  
corresponding iimbalances mbalances  ooff     increases  
increases ccalcium
alcium  aand
nd  pphosphorus bsorption.  
hosphorus  aabsorption.
calcium,  
calcium, p hosphorus,  aand
phosphorus, TH.  
nd  PPTH.  

Anemia  
Anemia Hemoglobin  
Hemoglobin 1 11–12  
1 - 1 2 gg/dL
/dL   Both  
Both iiron
ron  ssupplementation
upplementation  aand nd  iinjectable
njectable  eerythropoiesis-stimulating
rythropoiesis-­‐stimulating  aagents gents  ((ESAs)
ESAs)  hhave
ave  bbeen
een  uused
sed  tto  
o
correct  
correct a nemia.    TThe
anemia. he  rrisks
isks  aand
nd  bbenefits
enefits  ooff  these
these  ttrreatments  
e a t m e n t s iin
n  CCKD
KD  aare
re  nnot
ot  yyet
et  ddefined.
efined.  
Anemia  
Anemia m ay  ddevelop
may evelop  eearly
arly  dduring
uring   Without  
Without C KD:  
CKD:
tthe  
h e ccourse
ourse  ooff  CCKD
KD  ddue
ue  tto  
o Women:  
W o m e n :  1 12–16  
2 - 1 6 gg/dL
/dL    
inadequate  
inadequate ssynthesis
ynthesis  ooff   Men:  
M e n :  1
14–17  
4 - 1 7 gg/dL
/dL  
erythropoietin  
erythropoietin b y  tthhe  
by e kkidneys.
idneys.  
Transferrin  
Transferrin S aturation  ((TSAT)
Saturation TSAT)           Additional  
Additional IInformation
nformation  
Hemoglobin  
Hemoglobin iiss  u sed  ttoo  aassess
ssess  aanemia
nemia  iinn  CCKD.
KD.    U ncomplicated  aanemia
nemia  ooff  CCKD
KD  iiss  uusually
sually  nnormocytic
ormocytic  aand
nd  
  >  
> 220%0%    
normochromic.  
normochromic.
used Uncomplicated

Ferritin  
Ferritin>>  1100
00  ng/mL  
ng/mL  
Without  
Without C KD:  
CKD: TSAT  iiss  aa  m
TSAT easure  ooff  iiron
measure ron  ssaturation.
aturation.    TTransferrin
ransferrin  ttransports
ransports  iiron
ron  aabsorbed
bsorbed  bbyy  tthhe  
e iintestines.
ntestines.    FFerritin
erritin  
Women:  
W o m e n ;  1 18–160  
8 - 1 6 0 nng/mL
g/mL     levels  
levels rreflect
eflect  iiron
ron  sstores.
tores.  
Men:  
M e n :  1
18–270  
8 - 2 7 0 nng/mL
g/mL  

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 9 9  
 
IV.  
IV. P revent,  M
Prevent, onitor,  aand
Monitor, nd  TTreat
reat  CComplications
omplications  ((continued)
continued)  
 
Complication  
Complication a nd  IIts
and ts  
Ranges/Goals*  
Ranges/Goals* Dietary  
Dietary IIntervention
ntervention  
Relevance  
Relevance
Cardiovascular  
Cardiovascular D isease  
Disease Total  ccholesterol
Total holesterol  <<  2200
00  m g/dL  
mg/dL Decreasing  
Decreasing iintake ntake  ooff  ssaturated
aturated  aand
nd  ttrans
rans  ffats
ats  ((substituting
substituting  ffor
or  m onounsaturated  aand
monounsaturated nd  ppolyunsaturated
olyunsaturated  
fats),  
fats), a long  w
along w iith  
th p hysical  aactivity,
physical ctivity,  ccan
an  hhelp
elp  ccontrol
ontrol  hhyperlipidemia
yperlipidemia  aand
nd  rreduce
educe  iinflammation.
nflammation.  
(CVD)  
(CVD) LDL  
LDL ccholesterol
holesterol  <<  1100
00  m g/dL  
mg/dL

Patients  
Patients w w iith  
th C KD  aare
re  aatt  hhigh
igh  rrisk
isk    
CKD HDL  
HDL ccholesterol
holesterol  >>  4400  m g/dL  
mg/dL
for  
for d eveloping  CCVD;
developing VD;  tthhe  
e rrisk isk  
increases  
increases a as s  eeGFR
GFR  ddeclines.
eclines.   Triglycerides  <<  1150
Triglycerides 50  m g/dL  
mg/dL

   
CVD  
CVD iis s  tt hhe  
e lleading
eading  ccauseause  ooff   Additional  
Additional IInformation
nformation
mortality  
mortality iin n  CCKD. KD.   Controlling  
Controlling d yslipidemia  m
dyslipidemia ay  rreduce
may educe  tthhe  
e rrate
ate  ooff  ddecline
ecline  iinn  eeGFR.
GFR.      
To  ff urther  
To urther d ecrease  rrisk
decrease isk  ooff  ddeveloping
eveloping  CCVD,
VD,  ppharmacological
harmacological  tt hherapy  
erapy m ay  bbee  nnecessary
may ecessary  ((Fried,  
Fried,  22001).
001).

 
*Normal  
*Normal rranges
anges  m ay  vvary.
may ary.    

CKD  
CKD a nd  D
and iet  ||  A
Diet ssessment,  M
Assessment, anagement,  aand
Management, nd  TTreatment
reatment   Page  
Page 110 0  
 
 V.  
V.  P atient  EEducation
Patient ducation  M aterials    
Materials
 
NKDEP  
NKDEP o ffers  aa  ssuite
offers uite  ooff  m aterials  ttoo  ssupport
materials upport  RRDs Ds  iinn  pproviding
roviding  M NT  ttoo  ppatients
MNT atients  w ith  CCKD.
with KD.    These
These  ffreeree  m aterials—designed  ttoo  ddistill
materials—designed istill  kkey
ey  
information  
information a bout  CCKD
about KD  aand nd  ddiet
iet  for
for  RRDs
Ds  aand
nd  ppatients—are
atients—are  aavailablevailable  ttoo  ddownload
ownload  ffrom rom  tthe
he  N KDEP  w
NKDEP ebsite  aatt  w
website ww.nkdep.nih.gov/ckd_nutrition.
www.nkdep.nih.gov/ckd nutrition
 
•• Eating  
Eating R ight  ffor
Right or  KKidney
idney  H ealth:    TTips
Health: ips  ffor
or  PPeople
eople  w w iith  
th C KD—a  hhandout
CKD—a andout  oon n  tthe
he  bbasics
asics  ooff  nnutrition
utrition  aand
nd  CCKD.
KD.  
 
•• Nutrition  
Nutrition T ips  ffor
Tips or  PPeople
eople  w w iith  
th C KD—individual  nnutrient
CKD—individual utrient  hhandouts
andouts  oon: n:  
- Protein  Protein
- Phosphorus  
Phosphorus
- Potassium  
Potassium
- Sodium  Sodium
- Food-­‐label  
Food-label rreading eading (coming soon)  
 
•• Your  
Your K idney  TTest
Kidney est  RResults—a
esults—a  ttool ool  ffor
or  aassessment
ssessment  aand nd  eeducation
ducation  ooff  ttest
est  rresults
esults  w ith  ppatients.
with atients.  
 
 
 

CKD
 
CKD a nd
 D
and iet
 ||
 A
Diet ssessment,
 M
Assessment, anagement,
 aand
Management, nd
 TTreatment
reatment
  Page
 
Page 111 1
 

 
VI. References
American Dietetic Association. Chronic Kidney Disease Nutrition Therapy
for People Not On Dialysis. 2008 ADA Nutrition Care Manual. Chicago, IL:
American Dietetic Association; 2008.
Bethke PC, Jansky SH. The Effects of Boiling and Leaching on the Content
of Potassium and Other Minerals in Potatoes. Journal of Food Science.
2008;5:H80-85.
Burrowes JD, Ramer NK. Removal of potassium form tuberous root
vegetables by leaching. Journal of Renal Nutrition. 2006;2:31-38.
Byham-Gray LD, Burrowes JD, Chertow GM. (eds.) Nutrition in Kidney
Disease. Totowa, NJ: Humana Press; 2008.
Cohn F. Medicare Part B Coverage and MNT Billing Guidelines. Journal of
the American Dietetic Association. 2002;102(1):32.
de Brito-Ashurst I, Varagunam M, Raftery MJ, Yaqoob MM. Bicarbonate
Supplementation Slows Progression of CKD and Improves Nutritional
Status. Journal of the American Society of Nephrology. 2009;20(9):2075-
2084.
Diabetes Control and Complications Trial (DCCT) Research Group. The
Effect of Intensive Treatment of Diabetes on the Development and
Progression of Long-Term Complications in Insulin-Dependent Diabetes
Mellitus. New England Journal of Medicine. 1993;329:977-986.
Fried LF, Orchard TJ, Kasiske BL for the Lipids and Renal Disease
Progression Meta-Analysis Study Group. Effect of Lipid Reduction on the
Progression of Renal Disease: A Meta-Analysis. Kidney International.
2001;59:260-269.
CKD and Diet I Assessment, Management, and Treatment
Gennari FJ, Hood VL, Greene T, Wang X, Levey AS. Effect of Dietary Protein
Intake on Serum Total CO2 Concentration in Chronic Kidney Disease:
Modification of Diet in Renal Disease Study Findings. Clinical Journal of the
American Society of Nephrology. 2006;1(1):52-57.
Hemmelgarn BR, Manns BJ, Lloyd A et al. Relation Between Kidney
Function, Proteinuria, and Adverse Outcomes. Journal of the American
Medical Society. 2010;303(5):423-429.
IOM (Institute of Medicine). Dietary Reference Intakes for Calcium,
Phosphorus, Magnesium, Vitamin D and Fluoride. Washington, DC: The
National Academies Press; 1997.
IOM (Institute of Medicine). Dietary Reference Intakes for Calcium and
Vitamin D. Washington, DC: The National Academies Press; 2011.
Levey, AS, Bosch, JP, Breyer Lewis, J, Greene T, Rogers N, Roth D. A More
Accurate Method To Estimate Glomerular Filtration Rate from Serum
Creatinine: A New Prediction Equation. Annals of Internal Medicine.
1999;130(6):461-470.
Lowrie EG, Lew NL. Death Risk in Hemodialysis Patients: The Predictive
Value of Commonly Measured Variables and an Evaluation of Death Rate
Differences Between Facilities. American Journal of Kidney Diseases.
1990;15:458-482.
Maione A, Annemans L, Strippoli G. Proteinuria and Clinical Outcomes in
Hypertensive Patients. American Journal of Hypertension.
2009;22(11):1137-1147.
Martin KJ, Gonzalez EA. Metabolic Bone Disease in Chronic Kidney
Disease. Journal of American Society of Nephrology. 2007;18(3):875-885.
Page 12
Mitch WE, Ikizler TA (eds.) Handbook of Nutrition and the Kidney 6th
Edition. Philadelphia, PA. Lippincott, Williams & Wilkins: 2010.
National Kidney Disease Education Program. Quick Reference on Urine
Albumin-to-Creatinine Ratio and Estimated Glomerular Filtration Rate.
Bethesda, Md. National Institutes of Health, U.S. Department of Health
and Human Services. Revised March 2010.
Pfeffer MA, Burdmann EA, Chen C et al. A Trial of Darbepoetin Alfa in Type
2 Diabetes and Chronic Kidney Disease. New England Journal of Medicine.
2009;361(21): 2019-2032.
Snyder RW, Berns JS. Use of Insulin and Oral Hypoglycemic Medications in
Patients with Diabetes Mellitus and Advanced Kidney Disease. Seminars in
Dialysis. 2004;17(5):365-370.
CKD and Diet I Assessment, Management, and Treatment
UK Prospective Diabetes Study Group: Intensive Blood- Glucose Control
with Sulphonylureas or Insulin Compared with Conventional Treatment
and Risk of Complications in Patients with Type 2 Diabetes (UKPDS 33).
The Lancet. 1998;352:837-853.
Uribarri J. Phosphorus Homeostasis in Normal Health and in Chronic
Kidney Disease Patients with Special Emphasis on Dietary Phosphorus
Intake. Seminars in Dialysis. 2007;20(4):295-301.
U.S. Department of Agriculture and U.S. Department of Health and Human
Services. Dietary Guidelines for Americans, 2010. 7th Edition, Washington,
DC: U.S. Government Printing Office, December 2010.
Page 13

 

NKDEP
National Kidney Disease
Education Program

The  N
The ational  KKidney
National idney  D isease  EEducation
Disease ducation  PProgram
rogram  ((NKDEP)
NKDEP)  aaims
ims  ttoo  iimprove
mprove  eearly
arly  ddetection
etection  ooff  kkidney
idney  ddisease,
isease,  hhelpelp  iidentify
dentify  ppatients
atients  aatt  rrisk
isk  for
for  pprogression
rogression  tto
o      
kidney  
kidney ffailure,
ailure,  aand
nd  ppromote
romote  iinterventions
nterventions  ttoo  sslow
low  pprogression
rogression  ooff  kkidney
idney  ddisease.
isease.    N KDEP  iiss  pprogram
NKDEP rogram  ooff  the
the  N ational  IInstitutes
National nstitutes  ooff  H ealth  ((NIH).
Health NIH).  
 
For  
For m ore  iinformation,
more nformation,  vvisit
isit  N KDEP  aatt  w
NKDEP ww.nkdep.nih.gov  oorr  ccall
www.nkdep.nih.gov all  11-866-4
-­‐866-­‐4  KKIDNEY
IDNEY  ((1-866-454-3639).
1-­‐866-­‐454-­‐3639).  

    NIH  
NIH P ublication  N
Publication o.  111-7406
No. 1-­‐7406    ●
•    R evised  M
Revised M aarch  
r c h 22011  
011