1. Medical Nutrition Therapy for Renal Disorders

2. Functions of the Kidney
Excretory
Acid-base balance
Endocrine
Fluid and electrolyte balance

3. Excretory Functions Removal of excess fluid and waste products
180 L of filtrate pass through the kidneys each day  producing 1-2 L of urine
Wastes excreted from the body in urine include urea (byproduct of protein metabolism); excess vitamins and minerals; metabolites of some drugs and poisons

4. Acid-Base Functions
Acid-base balance is maintained through a buffer system, which maintains blood at pH of 7.4
Bicarbonate carries hydrogen ions to the kidneys where they are removed from extracellular fluid in the tubules, returned to the bloodstream as needed
Phosphate buffers intracellular fluid
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney Disease. ADA, 2004

5. Acid-Base Balance Functions
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
When extracellular volume (ECV) decreases, the renin-angiotensin-aldosterone system is activated  excretes less sodium chloride
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney Disease. ADA, 2004

6. Endocrine Functions
1,25-dihydroxy-vitamin D3 or calcitriol is produced in the kidney; enhances calcium absorption
Activation of Vitamin D and excretion of excess phosphate maintain healthy bones
Erythropoietin: 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
Source: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney Disease. ADA, 2004

7. The Nephron

8. The Most Common Kidney Diseases
Diabetic Nephropathy damage to the nephrons in the kidneys from unused sugar in the blood, usually due to Diabetes.
High Blood Pressure can damage the small blood vessels in the kidneys.  The damaged vessels cannot filter poison from the blood as they are supposed to.
Polycystic Kidney Disease (PKD) is a hereditary kidney disease in which many cysts grow in the kidneys.  These cysts may lead to kidney failure.

9. The Most Common Kidney Diseases
Acute Renal Failure - Sudden kidney failure caused by blood loss, drugs or poisons.  If the kidneys are not seriously damaged, acute renal failure may be reversed.
Chronic Renal Failure - Gradual loss of kidney function is called Chronic Renal Failure or Chronic Renal Disease.
End-Stage Renal Disease - The condition of total or nearly total and permanent kidney failure. 

10. Kidney Diseases Glomerular diseases Tubular defects Other
Nephrotic syndrome
Nephritic syndrome—tubular or interstitial
Tubular defects
Acute renal failure (ARF)
Other
End-stage renal disease (ESRD)
Kidney stones

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

12. Nephrotic Syndrome
Albuminuria: more than 3 g/day urinary albumin losses, with proportionally lesser amounts for children
Hypoalbuminemia
Hypertension
Hyperlipidemia
Edema

13. Medical Mgt of Nephrotic Syndrome
Corticosteroids
Immunosuppressants
ACE inhibitors/angiotensin receptor blockers to reduce protein losses, control blood pressure and fluid balance
Coenzyme A reductase inhibitors to control hyperlipidemia

14. MNT in Nephrotic Syndrome
Protein 0.8 to 1 g/kg IBW 80% HBV
Sodium based on fluid status
Potassium and other minerals (calcium, phosphorus) monitored and individualized
Fluid unrestricted
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

15. Nephritic syndrome
Acute glomerulonephritis (inflammation of the glomerulus
Sudden onset, often after streptococcus infections
Symptoms include hematuria, hypertension
Usually resolve on their own or advance to nephrotic syndrome or ESRD

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

17. Acute Renal Failure
Rapid, often reversible deterioration of renal function
GFR declines over hours to days
Most commonly occurs during hospitalization (5% of hospitalized pts; 30% of ICU pts)
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

18. Causes of Acute Renal Failure
Pre-renal: caused by intravascular volume depletion, decreased cardiac output
Post-renal: benign prostatic hypertrophy, prostate cancer, cervical cancer, colorectal cancer, neurogenic bladder, urethral strictures
Intrinsic or parenchymal ARF: 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

19. Causes of Acute Renal Failure
Ischemic Injury (50% of all incidence) d/t loss of blood supply to the kidneys secondary to surgical complications, thrombosis, hypotension, hypovolemia
Nephrotoxic injury: medications, contrast medium, chemotherapy, poisons (35%)
Multiorgan system failure, particularly liver failure
Sepsis, especially bacterial
Obstructive uropathy (trauma during surgery, urolithiasis, enlarged prostate)
Acute glomerular nephritis

20. Acute Tubular Necrosis
Most common cause of ARF
Ischemia: due to major surgery, hypotension, cardiogenic, septic, or hypovolemic shock
Nephrotoxicity: drugs, chemotherapeutic agents, organic solvents, heavy metals, cocaine

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

22. Acute Tubular Necrosis
Maintenance Phase
Epithelial cell injury
Urine output is at its lowest; complications associated with uremia, fluid overload, electrolyte imbalance (decreased sodium, increased potassium levels)
Time frame: days in oliguric patients; 5-8 days in nonoliguric patients

23. Acute Tubular Necrosis
Recovery Phase
Tubule cell regeneration and gradual return of GFR
BUN and creatinine return to near normal
May be complicated by marked diuresis, dehydration and fluid and electrolyte imbalance (increased sodium, decreased potassium)
Time frame: days to months

24. Renal Replacement Therapies in ARF
Recommended for patients with pronounced azotemia, electrolyte imbalance, fluid overload, severe acidosis
Used in 85% of patients with oliguric ARF and 30% of nonoliguric
Purpose is to correct imbalances as well as provide sufficient renal support to other organs

25. Renal Replacement Therapies in ARF
Hemodialysis: standard treatment if patient is hemodynamically stable
However, risk of hypotension and wide swings in body weight in unstable patients
Continuous hemofiltration (CAVH, CVVH) provides slow, continuous filtration across a membrane, driven by arterial pressure (CAVH) or pump (CVVH)

26. Renal Replacement Therapies in ARF
Continuous hemodialysis (CAVHD, CVVHD) uses an ultrafiltrate fluid similar to plasma
Clearance occurs through diffusion from high concentration (blood) to low concentration
Peritoneal dialysis: less often used in the US; not as effective when large volume or solute clearances needed.

27. CAVH

28. MNT for Adult ARF Energy: BEE X 1.2-1.3 or 25-35 kcal/kg
Protein: g/kg noncatabolic, without dialysis; g/kg catabolic and/or initiation of dialysis
Fluid: 24 hour urine output ml ( ml)
Sodium: grams
Potassium: grams
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

29. Nitrogen Balance in ARF
Standard nitrogen balance studies require a creatinine clearance of more than 50 mL/min/1.73m2
In ARF, urea nitrogen appearance (UNA) is a better method of determining nitrogen balance
UNA = UUN + change in the urea nitrogen pool

30. Calculation of Urea Nitrogen Appearance (UNA)
UNA (g) = UUN + [BUN2 – BUN1) x .6 x BW1] + [(BW2-BW1) x BUN2]
Net protein breakdown = UNA x 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)

31. Chronic Kidney Disease

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

33. Progression to End-Stage Renal Disease (ESRD)
First Decline in glomerular filtration rate (GFR)
Second Adaptations in renal function, i.e., increase in GFR
Third Adaptations improve renal function in short term
Fourth Long term loss of nephron units.
Fifth Slow, progressive decline in renal function
Sixth Eventually this decline leads to renal insufficiency, i.e., ESRD

34. Stages of Chronic Kidney Disease
GFR
Action
At increased risk
CKD risk factors
Screening; CKD risk reduction
1. Kidney damage with normal or increased GFR
>90
Tx comorbid conditions. Slow progression. CVD risk reduction
2. Mild decrease in GFR
60-89
Estimating progression
3. Moderate decrease in GFR
30-59
Evaluating, treating complications
4. Severe decrease in GFR
15-29
Prepare for kidney replacement tx
5. Kidney failure
<15 or dialysis
Replacement, if uremia present
National Kidney Foundation K/DOQI Clinical Practice Guidelines on CKD. Am J Kidney Dis 2002;39(suppl 1):46.

35. ESRD: Medical Management
Dialysis
Immunosuppressant drugs
Kidney transplant
Psychological support

36. Uremia, a Clinical Syndrome— Signs and Symptoms
Malaise
Weakness
Nausea and vomiting
Muscle cramps
Itching
Metallic taste (mouth)
Neurologic impairment

37. Stages of CKD Nutrient Recommendations
Pro
g/kg
Kcal
Na+
g/day K+
Phos
Calcium 1
.75
Based on energy expenditure
1-4 g to NAS
No restriction
Unless high
Monitor and restrict if nec 2 3
mg/day 4 .6
30-35 kcal/kg
<2000 mg/day 5
Fedje and Karalis. Nutrition mgt in early stages of CKD. Clin Guide Nutr Care Kidney Dis, ADA, 2004

38. Treatments: CKD, HD, CAPD

39. MNT for CKD, HD, PD
CKD Hemodialysis CAPD or CCPD
Protein
g/kg/day
Energy
(kcal/kg IBW)
Phosphorus indiv <17 indiv <17 indiv
(mg/kg IBW)
Sodium
(mg/d)
Potassium Individualized ~ 40 Individualized
Fluid Unrestricted Individualized
(ml/d) urine output
(1000 if anuric)
Calcium Individualized Individualized Individualized
(mg/d) based on serum level ~1000 mg/day ~1000 mg/day
Use adjusted IBW if obese
National Renal Diet Professional Guide 2nd edition, ADA 2002

40. Nutrition Assessment and Monitoring in the CKD Pt

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

42. Body Weight Assessment in CKD
Use dry weight or edema-free body weight
In HD: post-dialysis weight
In PD: weight after drainage of dialysate with peritoneum empty
In obese or very underweight people, use adjusted edema-free body weight
Adjusted EFBW=
BWef + [SBW*-BWef x .25]
*Use NHANES II data for standard body weight (SBW)
National Kidney Foundation. K/DOQI clinical practice guidelines for nutrition in chronic renal failure. Am J Kidney Dis 2000;35(suppl);S27-S86.

43. Blood Urea Nitrogen (BUN)
Measure of the nitrogenous waste products of protein
High BUN in CKD may reflect high protein intake, GI bleeding or inadequate dialysis, increased catabolism due to infection, surgery, poor nutrition
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

44. Creatinine (nl 0.5-1.4 mg/dL)
Nitrogenous waste product of muscle metabolism
Produced proportionate to muscle mass
Unrelated to dietary protein intake (DPI)
Sensitive marker of renal function: the higher the serum creatinine, the greater the loss of renal function; may reflect inadequate dialysis or muscle catabolism
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

45. Causes of Hyperkalemia (K+) Goal 3.5-5.5 mEq/L
>6 mEq/L – abnormal, potentially dangerous
Renal failure (kidney is primary filter)
Excessive nutritional intake
Chronic constipation
Infection
GI bleeding
Insulin deficiency (high BG)
Metabolic acidosis
Drug interactions
Catabolism of malnutrition or cell damage caused by injury or surgery
Decreased urinary output
Chewing tobacco

46. Causes of Hypokalemia (↓ K+)
Vomiting, diarrhea
Diuresis
Potassium binder
K+ too low in dialysate
Urine output >1000 mL/day or serum NL, do not need to restrict K+

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

48. Calcium (8.4-9.5 mg/dL) Most abundant mineral in human body
Nearly half of calcium is bound to albumin; if serum calcium is low, evaluate albumin level; can correct for low albumin
Calcium-Phosphorus Product: multiply serum calcium x serum phos: if >55-75, calcification can occur
<2000 mg/day elemental calcium from diet + binders stage 3-4
High ca+: calcification, nausea, vomiting, muscle twitching may mean too much Ca+ from meds or diet

49. Serum Sodium (nl 133-145 mEq/L)
Not a reliable indicator of sodium intake in CKD
Fluid retention due to decreased urine production can dilute an elevated level
Serum levels must be evaluated in conjunction with fluid status

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

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

52. Hematological Indicators
Hemoglobin: ↓ due to lack of erythropoetin, produced by the kidney; pts receive synthetic EPO tx (Epogen)
May have anemia of chronic disease
Ferritin: may be indicator of iron overload; ↑ ferritin may mean EPO resistance

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

55. Cockroft-Gault Equation to Calculate GFR
MICROMOL: [(140-age) x weight x 1.23 x (0.85 if female)]/Creat[micromol/l]
MG: [(140-age) x wt/kg x .85 if female]/(72*serum creatinine mg/dL)

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

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

58. Monitoring Nutrition Status in CKD with GFR<12mL/min/1.73m2
Recommended measure
Frequency
Serum albumin levels
Every 3 months
Edema-free actual body weight, % std wt, SGA
Every 1-3 months
nPNA or dietary interviews and diaries
Every 3-4 months
Fedje and Karalis. Nutrition mgt in early stages of CKD. Clin Guide Nutr Care Kidney Dis, ADA, 2004

59. “scerosis”= scarring. Once microalbuminuia is detectable, inexorable progression of nephropathy occurs.
20-30% of TYPE 1 or 2 DM will develop evidence of nephropathy; much smaller % go on to EDRD.
Hyperglycemia increases filtration 2nd to osmotic load and toxic high B.G.; increase GFR with enlargement of kidneys. Incipitent “AT Risk; then within 5 years, 20% develop nephropathy on standard care; 50% do not progress. 10% of those with proteinuria, have nephrotic range. Good candidates for early intervention by reducing intraglomerular pressure through enhanced glycemic control, BP, normalized pro. intake.
Microalbuminuria= mg/day. TYPE 1 DM: Without specific interventions, 80% will progress to overt nephropathy or clinical albuminuria (>300mg./d) with HTN then 77% of these go on to ESRD in 20 year. TYPE 2 DM: 20-40% with microalbuminuria to on to overt nephropathy
Then 20% by 20 years progress to ESRD.
Albuminuria is a marker of high morbidity/mortality from cardiovascular disease; >300 mg./day albumin in urine

60. Pre-ESRD (DM) Primary Prevention Glycemic control (DCCT) B.P. control
Aim for Euglycemia
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)/exercise
Meds: ACE inhibitors and ARB’s
Diabetes Control and Complications Trial: Tight B.S. control with decrease risk of progression of kidney disease.
Meds: ACE (ace inhibitors) or ARB (angiotensin receptor blockers) may increase K+. Diuretics- decrease.
If wt. loss hinders glycemic control; back off.
Na+ restrict 2400 mg. with HTN, 3000 mg. without. Lipids: sat fat <7%, chol <200 mg.

61. Pre-ESRD Secondary Prevention (overt nephropathy; GFR ~ 25)
Protein normalization
0.6 g/kg - RDA 0.8 g/kg ( minimum for DM)
Delay need for dialysis, control uremic symptoms, reduce acidosis
Stage 4 CKD: monitor labs, may need to limit K+, Phos., Ca++, Mg++
Malnutrition: insulin deficiency increases gluconeogenesis a. Metabolic acidosis needs correction for + N-bal.
Low protein, will need to liberalize fats and CHO more common.
Insulin deficiency results in increased rates or protein degradation and EAA oxidation. Nephrotic syndrome; damage to glomeruli losses of large amounts of pro. in urine . Most frequent with dm, glomerulonephritis or amyloidosis.

62. MNT in Patients on Hemodialysis

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

64. AV (arteriovenous) Fistula

65. ESRD: Nutritional Management
Prevent deficiencies
Control edema and serum electrolytes
Prevent renal osteodystrophy
Provide an attractive and palatable diet

66. MNT in HD: Protein
10-12 g free amino acids lost per treatment during dialysis
Greater amino acid losses with glucose-free dialysate and high flux dialyzers
1.2 g protein/kg standard body weight (SBW) with 50% high biological value (meat, poultry, fish, eggs, soy, dairy)
Most HD patients take in less than 1 g/day
NKF K/DOQI practice guidelines. Am J Kid Dis 2000;35(suppl):S40-S41, Cited in Byham-Gray, p

67. MNT in HD: Energy Adults <60 years: 35 kcal/kg SBW
Adults > 60 or obese: kcals/kg body weight
Actual intakes of HD patients in studies are lower than that (mean 23 kcals/kg in HEMO study)
NKF K/DOQI practice guidelines. Am J Kid Dis 2000;35(suppl):S40-S41, Cited in Byham-Gray, p. 46

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

69. MNT in HD: sodium and fluid
≥ 1 L fluid output: 2-4 g Na and 2 L fluid
≤ 1 L fluid output: 2 g Na and L fluid
Anuria: 2 g Na and 1 L fluid
Restrict Na+ if ↑ interdialytic wt gain, CHF, edema, HTN, low serum sodium

70. MNT in HD: Potassium Potassium needs related to urinary output
Most patients on HD can tolerate 2.5 g of K+
Stricter diet may be indicated for pts w/ insulin deficiency, metabolic acidosis, treated with beta blockers or aldosterone antagonists, hypercatabolic
Individuals: 40 mg/kg edema-free IBW or SBW

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

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

73. 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-Mix

74. MNT in HD: Vitamins H2O soluble vitamins Dialyzable – take after H.D.
B vitamins and vitamin C in renal vitamin
↑ Vit. C → ↑ oxalate → calcification of soft tissues and stones
Individualize need for:
Fe++ (IV most common), Vitamin D, Ca++, Zinc.
Infed, Ferrelicit

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

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

77. Skeletal Effects of Chronic Renal Failure
Hyperphosphatemia
Hypocalcemia
Hyperparathyroidism
Low bone mass and density
Osteitis fibrosa cystica—hyperplastic demineralized bone

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

79. Monitor Patient Status (cont)
6. Kidney function
Creatinine clearance
Glomerular filtration rate (GFR)
7. Blood values
BUN 10 to 20 mg/dl (<100 mg/dl)
Creatinine 0.7 to 1.5 mg/dl ( mg/dl)
Potassium 3.5 to 5.5 mEq/L
Phosphorus 3.0 to 4.5 mg/dl
Albumin g/dl
Calcium 9-11 mg/dl

80. Peritoneal Dialysis

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

82. Peritoneal Dialysis (home dialysis)
Blood cleansed by passive movement from capillaries to dialysate (diffusion)
Ultra-filtration (UF): fluid removed by osmosis due to high osmolality of dextrose in dialysate
Better control of labs, fluid balance and B.P.
Advantages for those with heart failure, access problems. Diet liberal, independence.
Disadvantages:, anorexia, a.a. losses in dialysate, peritionitis→ catabolism, anorexia, long- term wasting, high B.S., wt. gain, lack of socialization
Indicate P.D. process in packet

83. PERITONEAL DIALYSIS Dialysis solutions CAPD CCPD
Pt. chooses depending on fluid status 1.5%, 2.5% or 4.25% glucose
CAPD
~4 – 2L. Exchanges/day
Dwells ~6 hours (dialysis) and drain
~60% glucose absorbed (3.7 kcal/g)
CCPD
~10 L exchanged throughout night
40% glucose absorbed 2nd to rapid exchanges

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

85. SAMPLE GLUCOSE ABSORPTION
PERITONEAL DIALYSIS
SAMPLE GLUCOSE ABSORPTION
g glucose per liter x volume = total g of glucose
Example: one – 2 L. exchange of 1.5% solution = 30 g glucose
Total g of glucose x absorption rate (~60%) = g glucose absorbed
Example: 30 g glucose x 60% = 18 g glucose absorbed
g glucose absorbed x kcal per g glucose (3.7)= calories absorbed
Example: 18 x 3.7=66.6 calories/2 L. exchange
Patient does 4 exchanges/d
67 x 4 = 268 calories/d from diaysate

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

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

88. MNT for PD
Potassium: is easily cleared by PD; some patients may need K+ supplementation
Calcium: 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 ( mg/dl)

89. MNT for PD
Phosphorus: limited to mg/day which is difficult with high protein diet
Use phosphate binders
Fluid: can be adjusted by varying the dextrose concentrations of the dialysate
May need to be restricted if pts cannot achieve fluid balance without frequent hypertonic exchanges

90. PD: weight gain, hypertriglyceridemia, hyperglycemia
Increase exercise as allowed by MD
Limit sodium and fluid to minimize hypertonic exchanges
Use solutions with alternate hypertonic agents such as Icodextrin
Modify energy intake to facilitate wt loss
Modify intake of sugars and fats, especially saturated fats

91. PD: Protein Losses, Malnutrition
Patient education regarding protein goals and ways to meet them
Suggest pt eat protein foods first and limit fluids at mealtime
Frequent smaller portions of protein and easy to eat proteins such as egg white, cottage cheese, etc
Education on sterile technique to avoid peritonitis

92. RENAL EXCHANGES FOR MEAL PLANNING
Food Groups
Kcal
CHO g.
PRO g.
FAT g.
Na mg.
K+ mg.
PO4 mg.
Milk ( ½ c.) 85 6 4 5 80
185
110
Meat 65 7 25
100
Starch 15 2 1 35
Vegetable
150 20
Fruit 60
0.5
Fat (1TB.) 11
Calorie
Boosters
Beverages:
Coffee (1c.) tea (1 bag) wine (4 oz.) beer (12 oz.)

93. Protein Foods (65 kcals, 7 grams protein, 25 mg Na, 100 mg K+, 65 mg phos)
Meat 1 ounce
Egg 1
Fish 1 ounce
Shellfish 1 ounce
Poultry 1 ounce
Egg substitutes ¼ c
Bacon 4 slices
Cheese 1 oz
Milk 1 cup
Nut butters 2 T
Tofu ¼ cup
Cottage cheese ¼ cup
Lunchmeat 1 oz

94. Milk Servings (2% milk) 85 kcals, 6 g CHO, 4 g pro, 5 g fat, 80 mg Na+, 185 mg K+, 110 mg Phos
½ cup milk
½ cup plain ice cream
½ cup yogurt

95. Starch Servings 80 kcal, 15 g CHO, 2 g pro, 1 g fat, 80 mg Na+, 35 mg K+, 35 mg PO4
Bread, white or rye 1 slice
Cake 2 in sq or cupcake
Plain cake donut 1
Cold cereal 1 cup
Dinner roll 1 small
Macaroni, noodles, rice ½ cup
Popcorn, unsalted, 1 cup

96. Vegetable Servings 25 kcal, 5 g CHO, 1 g pro, 15 g Na+, 150 mg K+, 20 mg PO4
Asparagus ½ cup
Green beans ½ cup
Cabbage ½ cup
Carrots ½ cup
Cauliflower ½ cup
Corn ½ cup

97. Fruit Servings ↓ K+ 60 kcals, 15 g CHO,
Fruit Servings ↓ K+ 60 kcals, 15 g CHO, .5 g protein, 150 mg K+, 15 mg phos
Apple
Apple juice ½ c
Applesauce ½ c
Apricot nectar ½ c
Blackberries ½ c
Blueberries ½ c
Fruit cocktail ½ c
Grapes ½ c
Lemon
Lime
Peach
Pear
Pineapple
Plums (1)
Raspberries
Watermelon

98. Fruit Servings (High potassium) 60 kcals, 15 g CHO,
Fruit Servings (High potassium) 60 kcals, 15 g CHO, .5 g protein, >250 mg K+, 15 mg phos
Apricots
Bananas
Dates
Honeydew melon
Kiwifruit
Nectarine
Orange
Orange Juice
Prune juice
Prunes (5)
Raisins

99. Fat Choice 100 kcals, 11 g fat, 150 mg Na+, 5 mg PO4
Margarine/butter 1 T
Cream cheese 2 T
Mayonnaise 11/2 T
Non-dairy topping ½ cup
Sour cream ¼ cup
Vegetable oil 1 T
Tartar sauce 2 T

100. Calorie Boosters 60 kcals, 15 g CHO, 15 mg Na+, 20 mg K+, 5 mg PO4
Hard candy 4 pieces
Jam or jelly 2 T
Jelly beans 15
Honey 2 T
Sugar brown or white 2 T
Marshmallows 5 large
Fruit snacks and candies 1 oz

101. Beverages 100 mg K+ (also counts as fluid)
Coffee 1 cup
Tea 1 bag
Wine 4 oz
Beer 12 oz

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

103. Kidney Transplant 2. Posttransplant management: Corticosteroids
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 mEq Na
4. Diet after steroids:
1 g/kg BW protein
Kcal to achieve IBW
Individualize Na level

104. Well Mr. Osborne, it may not be kidney stones after all.

105. Kidney Stones 1. Particulate matter crystallizes
Ca salts (Ca oxalate or Ca phosphate)
Uric acid
Cystine
Struvite (NH4, magnesium and phosphate)
2. Ca salts in stones—Rx: high fluid; evaluate calcium from diet; may need more!
3. Treat metabolic problem; low-oxalate diet may be needed; acid-ash diet is sometimes useful but not proven totally effective

106. Kidney Stones—cont’d 4. Uric acid stones
Alter pH of urine to more alkaline
Use high-alkaline-ash diet
Food list in Krause text
5. Cystine stones (rare)
6. Struvite (infection stones) antibiotics and/or surgery

107. Acid-Ash Diet
Increases acidity of urine (contains chloride, phosphorus, and sulfur)
Meats, cheese, grains emphasized
Fruits and vegetables limited (exceptions are corn, lentils, cranberries, plums, prunes)

108. Alkaline-Ash Diet
Increases alkalinity of urine (contains sodium, potassium, calcium, and magnesium)
Fruits and vegetables emphasized (exceptions are corn, lentils, cranberries, plums, prunes)
Meats and grains limited

109. Summary Renal diseases—delicate balance of nutrients
Regular monitoring of lab values, with altered dietary interventions accordingly