Medical Nutrition Therapy for Renal

Disorders

c
áunctions of the Kidney
d { cretory
d Acid-base balance
d {ndocrine
d áluid and electrolyte balance

c
{ cretory áunctions
d Removal of e cess fluid and waste products
d 180 L of filtrate pass through the kidneys
each day producing 1-2 L of urine
d Wastes e creted from the body in urine
include urea (byproduct of protein
metabolism); e cess vitamins and minerals;
metabolites of some drugs and poisons

c
Acid-Base áunctions
d Acid-base balance is maintained through a
buffer system, which maintains blood at pH
of 7.4
d Bicarbonate carries hydrogen ions to the
kidneys where they are removed from
e tracellular fluid in the tubules, returned to
the bloodstream as needed
d Phosphate buffers intracellular fluid
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney
Disease. ADA, 2004
c
Acid-Base Balance áunctions
d When fluid volume is low, anti-diuretic
hormone (ADH) or vasopressin is released
from the anterior pituitary; increases
absorption of water in the collecting duct
d When e tracellular volume ({CV)
decreases, the renin-angiotensin-aldosterone
system is activated e cretes less sodium
chloride
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in
Kidney Disease. ADA, 2004
c
{ndocrine áunctions
d 1,25-dihydro y-vitamin D3 or calcitriol is
produced in the kidney; enhances calcium
absorption
d Activation of Vitamin D and e cretion of
e cess phosphate maintain healthy bones
d {rythropoietin: acts on the bone marrow to
increase production of red blood cells

Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in

Kidney Disease. ADA, 2004
c
The Nephron
 The Most Common Kidney Diseases
d `
 

  damage to the nephrons in
the kidneys from unused sugar in the blood,
usually due to Diabetes.

d H 

 can damage the small blood
vessels in the kidneys. The damaged vessels
cannot filter poison from the blood as they are
supposed to.

d   ` 
` is a hereditary

kidney disease in which many cysts grow in the
kidneys. These cysts may lead to kidney failure.
c
The Most Common Kidney Diseases
d A


 - Sudden kidney failure
caused by blood loss, drugs or poisons. If the
kidneys are not seriously damaged, acute renal
failure may be reversed.

d ÿ
 


 - Gradual loss of kidney
function is called Chronic Renal áailure or
Chronic Renal Disease.

d {

` 
 - The condition of total

or nearly total and permanent kidney failure.

c
 Kidney Diseases
d Glomerular diseases
± Nephrotic syndrome
± Nephritic syndrome²tubular or
interstitial
d Tubular defects
± Acute renal failure (ARá)
d Other
± {nd-stage renal disease ({SRD)
± Kidney stones

c
Nephrotic Syndrome
d Alterations of the glomerular basement
membrane allows persistent loss of large
amounts of protein in the urine
d Associated with diabetes,
glomerulonephritis, amyloidosis, lupus
d High risk for cardiovascular disease
d Hypercoagulability
d Abnormal bone metabolism

c
Nephrotic Syndrome
d Albuminuria: more than 3 g/day urinary
albumin losses, with proportionally lesser
amounts for children
d Hypoalbuminemia
d Hypertension
d Hyperlipidemia
d {dema

c
 Medical Mgt of Nephrotic Syndrome
d Corticosteroids
d Immunosuppressants
d AC{ inhibitors/angiotensin receptor blockers
to reduce protein losses, control blood
pressure and fluid balance
d Coenzyme A reductase inhibitors to control
hyperlipidemia

c
 MNT in Nephrotic Syndrome
d Protein 0.8 to 1 g/kg IBW 80% HBV
d Sodium based on fluid status
d Potassium and other minerals (calcium,
phosphorus) monitored and
individualized
d áluid unrestricted
d Diet therapy probably not effective for
hyperlipidemia; may require medication
Byham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney
disease.ADA, 2004
c
 Nephritic syndrome
d Acute glomerulonephritis (inflammation of
the glomerulus
d Sudden onset, often after streptococcus
infections
d Symptoms include hematuria, hypertension
d Usually resolve on their own or advance to
nephrotic syndrome or {SRD

c
 Nephritic syndrome: Nutritional
Management
d Diet to treat underlying disease
d Restrict diet if necessary to control
symptoms
d Protein restricted in uremia
d Sodium restriction in hypertension
d Potassium restriction in hyperkalemia

c
Acute Renal áailure
d Rapid, often reversible deterioration of
renal function
d GáR declines over hours to days
d Most commonly occurs during
hospitalization (5% of hospitalized pts; 30%
of ICU pts)
d Associated with major in-hospital morbidity
and mortality (7 to 80%)
Byham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney
disease.ADA, 2004
c
Causes of Acute Renal áailure
d Pre-renal: caused by intravascular volume
depletion, decreased cardiac output
d Post-renal: benign prostatic hypertrophy,
prostate cancer, cervical cancer, colorectal
cancer, neurogenic bladder, urethral
strictures
d Intrinsic or parenchymal ARá: vascular
disease, interstitial nephritis, glomerular
disease, acute tubular necrosis
Byham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney
disease.ADA, 2004
c
Causes of Acute Renal áailure
d Ischemic Injury (50% of all incidence) d/t loss of
blood supply to the kidneys secondary to surgical
complications, thrombosis, hypotension,
hypovolemia
d Nephroto ic injury: medications, contrast
medium, chemotherapy, poisons (35%)
d Multiorgan system failure, particularly liver
failure
d Sepsis, especially bacterial
d Obstructive uropathy (trauma during surgery,
urolithiasis, enlarged prostate)
d Acute glomerular nephritis

c
Acute Tubular Necrosis
Most common cause of ARá
d Ischemia: due to major surgery,
hypotension, cardiogenic, septic, or
hypovolemic shock
d Nephroto icity: drugs, chemotherapeutic
agents, organic solvents, heavy metals,
cocaine

c
Acute Tubular Necrosis
 
  

d Period between onset and established renal
failure
d Usually reversible by treating the
underlying disorder or removing offending
agent
d Time frame: hours or days
Byham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney
disease.ADA, 2004

c
Acute Tubular Necrosis




d {pithelial cell injury
d Urine output is at its lowest; complications
associated with uremia, fluid overload,
electrolyte imbalance (decreased sodium,
increased potassium levels)
d Time frame: 10-16 days in oliguric patients;
5-8 days in nonoliguric patients

c
Acute Tubular Necrosis



d Tubule cell regeneration and gradual return
of GáR
d BUN and creatinine return to near normal
d May be complicated by marked diuresis,
dehydration and fluid and electrolyte
imbalance (increased sodium, decreased
potassium)
d Time frame: days to months

c
Renal Replacement Therapies in ARá

d Recommended for patients with pronounced

azotemia, electrolyte imbalance, fluid
overload, severe acidosis
d Used in 85% of patients with oliguric ARá
and 30% of nonoliguric
d Purpose is to correct imbalances as well as
provide sufficient renal support to other
organs

c
Renal Replacement Therapies in ARá

d Hemodialysis: standard treatment if patient

is hemodynamically stable
± However, risk of hypotension and wide swings
in body weight in unstable patients
d Continuous hemofiltration (CAVH, CVVH)
provides slow, continuous filtration across a
membrane, driven by arterial pressure
(CAVH) or pump (CVVH)

c
Renal Replacement Therapies in ARá

d Continuous hemodialysis (CAVHD,

CVVHD) uses an ultrafiltrate fluid similar
to plasma
± Clearance occurs through diffusion from high
concentration (blood) to low concentration
d Peritoneal dialysis: less often used in the
US; not as effective when large volume or
solute clearances needed.

c
CAVH

c
MNT for Adult ARá
d {nergy: B{{ X 1.2-1.3 or 25-35 kcal/kg
d Protein: .8-1.2 g/kg noncatabolic, without dialysis;
1.2-1.5 g/kg catabolic and/or initiation of dialysis
d áluid: 24 hour urine output + 500 ml (750-1500
ml)
d Sodium: 2.0-3.0 grams
d Potassium: 2.0-3.0 grams
d Phosphorus: 8-15 mg/kg; may need binders; needs
may increase with dialysis, return of kidney
function, anabolism
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney Disease.
ADA, 2004
c
Nitrogen Balance in ARá
d Standard nitrogen balance studies require a
creatinine clearance of more than 50
mL/min/1.73m2
d In ARá, urea nitrogen appearance (UNA) is
a better method of determining nitrogen
balance
d UNA = UUN + change in the urea nitrogen
pool

c
Calculation of Urea Nitrogen
Appearance (UNA)
UNA (g) = UUN + [BUN2 ± BUN1) .6 BW1] +
[(BW2-BW1) BUN2]
Net protein breakdown = UNA 6.25
UUN = urinary urea nitrogen (g/24hr)
BUN1 = initial collection of blood urea nitrogen,
postdialysis (g/L)
BUN2 = final collection of blood urea nitrogen,
predialysis (g/L)
BW1 = postdialysis wt (kg)
BW2 = predialysis wt (kg)

c
Chronic Kidney Disease

c
Causes of Chronic Kidney Disease
Cause Incidence (%)
Diabetes 40
Hypertension 27
Glomerulonephritis 13
Interstitial disease 4
Renal cystic disease 3
Tumors 2
Other 10

c
Progression to {nd-Stage Renal
Disease ({SRD)

 Decline in glomerular filtration rate (GáR)
 Adaptations in renal function, i.e.,
increase in GáR

 Adaptations improve renal function in short
term

 Long term loss of nephron units.
  Slow, progressive decline in renal
function
  {ventually this decline leads to renal
insufficiency, i.e., {SRD
c
 Stages of Chronic Kidney Disease
Stage GáR Action

At increased risk CKD risk Screening; CKD risk reduction

factors
1. Kidney damage with >90 T comorbid conditions. Slow
normal or increased GáR progression. CVD risk reduction
2. Mild decrease in GáR 60-89 {stimating progression

3. Moderate decrease in 30-59 {valuating, treating

GáR complications
4. Severe decrease in 15-29 Prepare for kidney replacement
GáR t
5. Kidney failure <15 or Replacement, if uremia present
dialysis

National Kidney áoundation K/DOQI Clinical Practice Guidelines on CKD.

Am J Kidney Dis 2002;39(suppl 1):46.
c
{SRD: Medical Management
d Dialysis
d Immunosuppressant drugs
d Kidney transplant
d Psychological support

c
Uremia, a Clinical Syndrome²
Signs and Symptoms
d Malaise

d Weakness

d Nausea and vomiting

d Muscle cramps

d Itching

d Metallic taste (mouth)

d Neurologic impairment

c
 Stages of CKD Nutrient Recommendations
Pro Kcal Na+ K+ Phos Calcium
g/kg g/day g/day
1 .75 Based on 1-4 g to No restriction Monitor and 1.2-1.5
energy NAS Unless high restrict if nec
e penditure
2 .75 Based on 1-4 g to No restriction Monitor and 1.2-1.5
energy NAS Unless high restrict if nec
e penditure

3 .75 Based on 1-4 g to No restriction 800-1000 1.2-1.5

energy NAS Unless high mg/day
e penditure
4 .6 30-35 1-4 g to No restriction 800-1000 <2000
kcal/kg NAS Unless high mg/day mg/day
5 0.6- 30-35 1-4 g to No restriction 800-1000 <2000
0.75 kcal/kg NAS Unless high mg/day mg/day
áedje and Karalis.
c Nutrition mgt in early stages of CKD. Clin Guide Nutr Care Kidney Dis, ADA, 2004
 Treatments: CKD, HD, CAPD
ÿ`{

 !
  ÿ `
ÿÿ`

Treatment Diet and Diet and medications Diet and

medications Hemodialysis medications
Peritoneal
dialysis
Modality Vascular access Peritoneal membrane

Duration Indefinite 3-5 h 3-5 e changes

2-3 d/wk 7 d/wk

Concerns Glomerular AA loss; Protein loss:

hyperfiltration: interdialytic glucose absorption:
BUN: electrolyte and Bone disease:
bone disease: fluid changes: weight gain:
HTN: Bone disease: hyperlipidemia:
Glucose control in HTN glucose control in diabetes
diabetes

c
 MNT for CKD, HD, PD
ÿ` !
  ÿ `
ÿÿ`

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)* )

{
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)* ,
  
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 !   
 0 1&"   
 0
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Use adjusted IBW if obese

National Renal Diet Professional Guide 2nd edition, ADA 2002

c
Nutrition Assessment and
Monitoring in the CKD Pt

c
Anthropometric Measurements
d % usual body weight (%UBW)
d % standard body weight (%SBW)
d Height
d Skeletal frame size
d BMI
d Skinfold thickness
d Mid-arm muscle area, circumference, or
diameter

c
Body Weight Assessment in CKD
d Use dry weight or edema-free body weight
± In HD: post-dialysis weight
± In PD: weight after drainage of dialysate with
peritoneum empty
d In obese or very underweight people, use
adjusted edema-free body weight
Adjusted {áBW=
BWef + [SBW*-BWef .25]
*Use NHAN{S II data for standard body weight (SBW)

National Kidney áoundation. K/DOQI clinical practice guidelines for nutrition in chronic
renal failure. Am J Kidney Dis 2000;35(suppl);S27-S86.
c
Blood Urea Nitrogen (BUN)
d Measure of the nitrogenous waste products
of protein
d High BUN in CKD may reflect high protein
intake, GI bleeding or inadequate dialysis,
increased catabolism due to infection,
surgery, poor nutrition
d Decreased BUN may mean protein
anabolism, overhydration, protein loss, low
dietary protein
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney Disease.
ADA, 2004
c
Creatinine (nl 0.5-1.4 mg/dL)
d Nitrogenous waste product of muscle metabolism
d Produced proportionate to muscle mass
d Unrelated to dietary protein intake (DPI)
d Sensitive marker of renal function: the higher the
serum creatinine, the greater the loss of renal
function; may reflect inadequate dialysis or
muscle catabolism
d A decrease in creatinine over time may reflect loss
of lean body mass
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney
Disease. ADA, 2004
c
 Causes of Hyperkalemia (÷K+)
Goal 3.5-5.5 m{q/L
d >6 m{q/L ± abnormal, d Metabolic acidosis
potentially dangerous d Drug interactions
d Renal failure (kidney is
d Catabolism of
primary filter)
malnutrition or cell
d { cessive nutritional
intake damage caused by injury
or surgery
d Chronic constipation
d Decreased urinary output
d Infection
d GI bleeding d Chewing tobacco
d Insulin deficiency (high BG)

c
Causes of Hypokalemia (Ļ K+)
d Vomiting, diarrhea
d Diuresis
d Potassium binder
d K+ too low in dialysate

d Urine output >1000 mL/day or serum NL,

do not need to restrict K+

c
Phosphorus (normal 3.5-5.5 mg/dL)
d As renal function decreases, phos accumulates in
the blood
d ÷ phos triggers release of PTH that releases
calcium from bone
d Phos binders prevent phosphorus from being
absorbed in the gut; form insoluble compound so
phos is e creted in stool
d Phos clearance poor in HD and CAPD
d Ļ phos may mean e cess phos binder or poor p.o.

c
Calcium (8.4-9.5 mg/dL)
d Most abundant mineral in human body
d Nearly half of calcium is bound to albumin; if
serum calcium is low, evaluate albumin level; can
correct for low albumin
d Calcium-Phosphorus Product: multiply serum
calcium serum phos: if >55-75, calcification can
occur
d <2000 mg/day elemental calcium from diet +
binders stage 3-4
d High ca+: calcification, nausea, vomiting, muscle
twitching may mean too much Ca+ from meds or
diet
c
Serum Sodium (nl 133-145 m{q/L)
d Not a reliable indicator of sodium intake in
CKD
d áluid retention due to decreased urine
production can dilute an elevated level
d Serum levels must be evaluated in
conjunction with fluid status

c
Lipids
d Cardiovascular disease is the most common
cause of death in people with CKD
d Kidney disease is considered the equivalent
of a risk factor, like diabetes
d HD: often have normal LDL, TC, Ĺ
triglycerides, Ļ HDL
d PD: have Ĺ LDL/TC + Ĺ TG
d Renal T : Ĺ LDL/TC/TG, normal HDL,
often due to medications

c
Cholesterol in CKD
d High
‡ High risk TC 200-300 mg/dl (non-fasting)
‡ LDL goal < 100 mg/dl
d Low
‡ <150 -180, evaluate for pro-energy malnutrition
‡ Increased mortality

c
Hematological Indicators
d Hemoglobin: Ļ due to lack of erythropoetin,
produced by the kidney; pts receive
synthetic {PO t ({pogen)
d May have anemia of chronic disease
d áerritin: may be indicator of iron overload;
Ĺ ferritin may mean {PO resistance

c
Glomerular áiltration Rate (GáR)
d Best inde of kidney function
d Used to establish stage of CKD
d GáR is the amount of filtrate formed per minute
based on total surface area available for filtration
(number of functioning glomeruli)
d Can be determined using injected isotope (inulin)
measurement in urine
d Can be calculated from serum creatinine using
standard equations

c
c
Cockroft-Gault {quation to
Calculate GáR
d MICROMOL: [%&"
4 %#'+
"#-( !
5)ÿ

6! 
!)5
d 
6%&"
4)* #-( 
!
5)/'7
!

  ! )8

http://renu .dmed.ed.ac.uk/{dR{N/Handbookbits/
HDBKgfrest.html

c
Interdialytic Weight Gain
d Pts on dialysis gain several kg of fluid
between HD treatments
d If pts gain >5%, may reflect e cessive fluid
intake, leading to hypertension, edema,
ascites, pleural effusion
d áluid gains of <2% reflect minimal fluid
and food intake, may be losing body mass

c
Measures of Dialysis Adequacy
Urea Reduction Rate (URR)
d Refers to change in urea concentration between
pre and post-dialysis blood tests
d Statistically significant predictor of mortality
d CMS goal is >65%
Kt/V
d The fractional clearance of urea as a function of its
distribution volume
d Goal is 1.2 or more

c
Monitoring Nutrition Status in CKD
with GáR<12mL/min/1.73m2
Recommended measure árequency

Serum albumin levels {very 3 months

{dema-free actual body {very 1-3 months

weight, % std wt, SGA
nPNA or dietary {very 3-4 months
interviews and diaries

áedje and Karalis. Nutrition mgt in early stages of CKD. Clin Guide Nutr Care Kidney Dis,
ADA,
c 2004
     






 




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c
Pre-{SRD (DM)
d Primary Prevention
± Glycemic control (DCCT)
‡ Aim for {uglycemia
‡ Watch for low B.S.
± B.P. control
‡ 130/80
‡ Na+ restrict
± Base on comorbidities (~2-3 g.)
± Medications may increase or decrease K+; monitor
‡ Wt. loss (gradual)/e ercise
± Meds: AC{ inhibitors and ARB¶s

c
Pre-{SRD
d Secondary Prevention (overt nephropathy;
GáR ~ 25)
± Protein normalization
± 0.6 g/kg À RDA "#- g/kg ( minimum for DM)
± Delay need for dialysis, control uremic
symptoms, reduce acidosis
d Stage 4 CKD: monitor labs, may need to
limit K+, Phos., Ca++, Mg++

c
MNT in Patients on Hemodialysis

c
Hemodialysis
d Removes concentrated molecules and
e cess fluid from pts blood through
diffusion and ultrafiltration
d Three parts of the system are the dialyzer
(artificial kidney), the dialysis machine, and
the dialysate
d Requires vascular access, usually through
an AV (arteriovenous) fistula

c
AV (arteriovenous) áistula

c
{SRD: Nutritional Management
d Prevent deficiencies
d Control edema and serum electrolytes
d Prevent renal osteodystrophy
d Provide an attractive and palatable diet

c
MNT in HD: Protein
d 10-12 g free amino acids lost per treatment
during dialysis
d Greater amino acid losses with glucose-free
dialysate and high flu dialyzers
d 1.2 g protein/kg standard body weight
(SBW) with 50% high biological value
(meat, poultry, fish, eggs, soy, dairy)
d Most HD patients take in less than 1 g/day
NKá K/DOQI practice guidelines. Am J Kid Dis 2000;35(suppl):S40-S41, Cited in Byham-
Gray, p. 45-46
c
MNT in HD: {nergy
d Adults <60 years: 35 kcal/kg SBW
d Adults > 60 or obese: 30-35 kcals/kg body
weight
d Actual intakes of HD patients in studies are
lower than that (mean 23 kcals/kg in H{MO
study)

NKá K/DOQI practice guidelines. Am J Kid Dis 2000;35(suppl):S40-S41, Cited in

Byham-Gray, p. 46

c
MNT in HD: Lipids
d HD patients at risk for lipid disorders
d Recommended fat intake<30% of calories
and saturated fat<10%; cholesterol <300
mg/day
d Optimum fiber intake 20-25 g/day
d These restrictions are difficult to achieve
along with other restrictions of HD diet

c
MNT in HD: sodium and fluid
d ƒ 1 L fluid output: 2-4 g
Na and 2 L fluid
d ” 1 L fluid output: 2 g Na
and 1-1.5 L fluid
d Anuria: 2 g Na and 1 L
fluid
d Restrict Na+ if Ĺ
interdialytic wt gain, CHá,
edema, HTN, low serum
sodium
c
MNT in HD: Potassium
d Potassium needs related to urinary output
d Most patients on HD can tolerate 2.5 g of
K+
d Stricter diet may be indicated for pts w/
insulin deficiency, metabolic acidosis,
treated with beta blockers or aldosterone
antagonists, hypercatabolic
d Individuals: 40 mg/kg edema-free IBW or
SBW

c
MNT in HD: Phosphorus
d Maintain s. phos 3.5-5.5 mg/dL
d Usually ok until GáR Ļ to 20-30 mL/min
d Dialysis removes 500-1000 mg/treatment
d Use phosphorus binders with meals: absorb
50% of dietary phosphorus
d Dietary intake: 800 to 1000 mg/day or <17
mg/kg IBW or SBW
d Identify high protein, low phos food sources

c
MNT in HD: Calcium
d High from e cess Ca++ type binders,
vitamin D analogs, Ca++ fortification
d Goal 8.4-9.5 mg/dl
d Always use corrected Ca++ (adjusted
Ca++)
[ (4-alb.) 0.8] + Ca++]
d CaXPhos product: goal <55

c
Phosphate Binders
(Taken with meals to prevent phos absorption)
Calcium acetate PhosLo

Mg/Ca++ carbonate MagneBind

Sevelamer hydrochloride Renagel

Aluminum carbonate

Aluminum hydrozide Alucap, Amphogel

Calcium carbonate TUMS, Os-Cal, calci-

Chew, Calci-Mi
c
MNT in HD: Vitamins
d H2O soluble vitamins
d Dialyzable ± take after H.D.
d B vitamins and vitamin C in renal vitamin
Ĺ Vit. C ĺ Ĺ o alate ĺ calcification of soft tissues
and stones

d Individualize need for:

± áe++ (IV most common), Vitamin D, Ca++, Zinc.

c
MNT in HD: Vitamin D
d Vitamin D is activated in the kidney to
calcitriol, or vitamin D3
d As D3 levels fall, calcium absorption Ļ and
phos e cretion Ļ
d Vitamin D3 therapy helps prevent renal
bone disease but may cause hypercalcemia
d Renal pts should use calcitriol supplements
under the supervision of a physician

c
Hemodialysis
d Typical diet order
± 2000 calorie, 80 g protein, 2 g Na+, 3 g K+,
low phosphorus, 1500 cc fluid restriction

c
Skeletal {ffects of Chronic
Renal áailure
d Hyperphosphatemia
d Hypocalcemia
d Hyperparathyroidism
d Low bone mass and density
d Osteitis fibrosa cystica²hyperplastic
demineralized bone

c
Monitor Patient Status
1. BP >140/90
2. {dema
3. Weight changes
4. Urine output
5. Urine analysis:
²Albumin
²Protein

c
 Monitor Patient Status (cont)
6. Kidney function
Creatinine clearance
Glomerular filtration rate (GáR)
7. Blood values
BUN 10 to 20 mg/dl (<100 mg/dl)
Creatinine 0.7 to 1.5 mg/dl (10-15
mg/dl)
Potassium 3.5 to 5.5 m{q/L
Phosphorus 3.0 to 4.5 mg/dl
Albumin 3.5-5.5 g/dl
Calcium 9-11 mg/dl
c
Peritoneal Dialysis

c
CAPD (continuous ambulatory
peritoneal dialysis)
d Most patients do 4-5 e changes per day
d A specific volume of dialysate (1500-3000 ml) is
infused into the peritoneal cavity via a catheter
d The dialysate dwells for 4 hours as e cess fluid
and to ins diffuse through peritoneal membrane
d Dialysate and wastes are drained from the body
and the process repeated.
d Dialysate is present in the body 24 hours per day
d APD (automated peritoneal dialysis therapy)
speeds the process

c
Peritoneal Dialysis (home dialysis)
d Blood cleansed by passive movement from
capillaries to dialysate (diffusion)
d Ultra-filtration (Uá): fluid removed by
osmosis due to high osmolality of de trose in
dialysate
d Better control of labs, fluid balance and B.P.
d Advantages for those with heart failure, access
problems. Diet liberal, independence.
d Disadvantages:, anore ia, a.a. losses in dialysate,
peritionitisù

 
long- term
wasting,  c c
c 

  

c
P{RITON{AL DIALYSIS
d Dialysis solutions
± Pt. chooses depending on fluid status
1.5%, 2.5% or 4.25% glucose
d CAPD
± ~4 ± 2L. { changes/day
± Dwells ~6 hours (dialysis) and drain
± ~60% glucose absorbed (3.7 kcal/g)

d CCPD
± ~10 L e changed throughout night
± 40% glucose absorbed 2nd to rapid e changes

c
MNT for PD: {nergy
d {nergy: 35 kcals/kg/day SBW or adjusted
body weight for pts<60 years; 30 kcals/kg
for those >60
d Calories provided in the dialysate should be
included in total intake (may absorb as
much as 1/3 of daily energy needs)

c
P{RITON{AL DIALYSIS
SAMPL{ GLUCOS{ ABSORPTION

 
           


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MNT for PD: Protein
d PD patients lose 5-15 grams of protein a
day, primarily as albumin
d Goal 1.2-1.3 g/kg SBW or ABW/day

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MNT for PD: Sodium
d PD clears sodium very well, so sodium can
be fairly liberal
d However, high salt diets increase thirst and
may make adherence to fluid limits more
difficult
d General recommendation is 2-4 grams
sodium

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MNT for PD
d 
 !: is easily cleared by PD; some
patients may need K+ supplementation
d ÿ
 !: limit to 2000 mg elemental
calcium
± Generally pts get ~1500 mg from calcium-
based phosphate binders
± Serum calcium should be maintained in low
normal range (8.4-9.5 mg/dl)

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MNT for PD
d Phosphorus: limited to 800-1000 mg/day
which is difficult with high protein diet
± Use phosphate binders
d áluid: can be adjusted by varying the
de trose concentrations of the dialysate
± May need to be restricted if pts cannot achieve
fluid balance without frequent hypertonic
e changes

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PD: weight gain,
hypertriglyceridemia, hyperglycemia
d Increase e ercise as allowed by MD
d Limit sodium and fluid to minimize
hypertonic e changes
d Use solutions with alternate hypertonic
agents such as Icode trin
d Modify energy intake to facilitate wt loss
d Modify intake of sugars and fats, especially
saturated fats
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PD: Protein Losses, Malnutrition
d Patient education regarding protein goals
and ways to meet them
d Suggest pt eat protein foods first and limit
fluids at mealtime
d árequent smaller portions of protein and
easy to eat proteins such as egg white,
cottage cheese, etc
d {ducation on sterile technique to avoid
peritonitis

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 2
 
 
2  





 
 ÿ 9 # 9 #   # 
! # 3! # 9&! #

Milk ( ½ c.) 85 6 4 5 80 185 110

Meat 65 0 7 4 25 100 65

Starch 80 15 2 1 80 35 35

Vegetable 25 5 1 0 15 150 20

áruit 60 15 0.5 0 5 150 15

áat (1TB.) 100 0 0 11 150 0 5

Calorie 60 15 0 0 15 20 5
Boosters

Beverages: 0 0 0 0 0 100 0
Coffee (1c.)
tea (1 bag)
wine (4 oz.)
beer (12 oz.)

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Protein áoods
(65 kcals, 7 grams protein, 25 mg Na, 100 mg K+, 65 mg
phos)
d Meat 1 ounce d Bacon 4 slices
d {gg 1 d Cheese 1 oz
d áish 1 ounce d Milk 1 cup
d Shellfish 1 ounce d Nut butters 2 T
d Poultry 1 ounce d Tofu ¼ cup
d {gg substitutes ¼ c d Cottage cheese ¼ cup
d Lunchmeat 1 oz

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Milk Servings (2% milk)
85 kcals, 6 g CHO, 4 g pro, 5 g fat, 80 mg Na+, 185 mg K+, 110 mg Phos

d ½ cup milk
d ½ cup plain ice cream
d ½ cup yogurt

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Starch Servings
80 kcal, 15 g CHO, 2 g pro, 1 g fat, 80 mg Na+, 35 mg K+, 35 mg PO4

d Bread, white or rye 1 slice

d Cake 2 in sq or cupcake
d Plain cake donut 1
d Cold cereal 1 cup
d Dinner roll 1 small
d Macaroni, noodles, rice ½ cup
d Popcorn, unsalted, 1 cup

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Vegetable Servings
25 kcal, 5 g CHO, 1 g pro, 15 g Na+, 150 mg K+, 20 mg PO4

d Asparagus ½ cup
d Green beans ½ cup
d Cabbage ½ cup
d Carrots ½ cup
d Cauliflower ½ cup
d Corn ½ cup

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áruit Servings Ļ K+
60 kcals, 15 g CHO, .5 g protein, 150 mg K+, 15 mg phos

d Apple d Peach
d Apple juice ½ c d Pear
d Applesauce ½ c d Pineapple
d Apricot nectar ½ c d Plums (1)
d Blackberries ½ c d Raspberries
d Blueberries ½ c d Watermelon
d áruit cocktail ½ c
d Grapes ½ c
d Lemon
d Lime

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áruit Servings (High potassium)
60 kcals, 15 g CHO, .5 g protein, >250 mg K+, 15 mg phos

d Apricots d Prunes (5)

d Bananas d Raisins
d Dates
d Honeydew melon
d Kiwifruit
d Nectarine
d Orange
d Orange Juice
d Prune juice

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áat Choice
100 kcals, 11 g fat, 150 mg Na+, 5 mg PO4

d Margarine/butter 1 T
d Cream cheese 2 T
d Mayonnaise 11/2 T
d Non-dairy topping ½ cup
d Sour cream ¼ cup
d Vegetable oil 1 T
d Tartar sauce 2 T

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Calorie Boosters
60 kcals, 15 g CHO, 15 mg Na+, 20 mg K+, 5 mg PO4

d Hard candy 4 pieces

d Jam or jelly 2 T
d Jelly beans 15
d Honey 2 T
d Sugar brown or white 2 T
d Marshmallows 5 large
d áruit snacks and candies 1 oz

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Beverages
100 mg K+ (also counts as fluid)

d Coffee 1 cup
d Tea 1 bag
d Wine 4 oz
d Beer 12 oz

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Medicare Rules for MNT in
Renal Disease
d As of January, 2002, Medicare covers MNT
for pre-dialysis renal disease
d Includes nutritional, diagnostic, therapy and
counseling services
d Restricted to patients with GáR 15 to 50
mL/min/1.73m2 (stages 3-4-5 not on
dialysis)

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 Kidney Transplant
1. Types: related donor or cadaver
2. Posttransplant management:
Corticosteroids
Cyclosporine
3. Diet while on high-dose steroids:
1.3 to 2 g/kg BW protein
30 to 35 kcal/kg BW energy
80 to 100 m{q Na
4. Diet after steroids:
1 g/kg BW protein
Kcal to achieve IBW
Individualize Na level

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 Well Mr. Osborne, it may not be kidney stones after all.
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 Kidney Stones
1. Particulate matter crystallizes
Ca salts (Ca o alate or Ca phosphate)
Uric acid
Cystine
Struvite (NH4, magnesium and phosphate)
2. Ca salts in stones²R : high fluid; evaluate
calcium from diet; may need more!
3. Treat metabolic problem; low-o alate diet
may be needed; acid-ash diet is sometimes
useful but not proven totally effective

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 Kidney Stones²cont¶d
4. Uric acid stones
Alter pH of urine to more alkaline
Use high-alkaline-ash diet
áood list in Krause te t
5. Cystine stones (rare)
6. Struvite (infection stones) antibiotics and/or
surgery

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Acid-Ash Diet
d Increases acidity of urine (contains chloride,
phosphorus, and sulfur)
d Meats, cheese, grains emphasized
d áruits and vegetables limited (e ceptions
are corn, lentils, cranberries, plums, prunes)

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Alkaline-Ash Diet
d Increases alkalinity of urine (contains
sodium, potassium, calcium, and
magnesium)
d áruits and vegetables emphasized
(e ceptions are corn, lentils, cranberries,
plums, prunes)
d Meats and grains limited

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Summary
d Renal diseases²delicate balance of
nutrients
d Regular monitoring of lab values, with
altered dietary interventions accordingly