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Medical Nutrition Therapy for Renal Disorders

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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.


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

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)

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

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

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