Renal Disorders MNT

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  • The Nephron

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    The Most Common Kidney DiseasesDiabetic 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.

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    The Most Common Kidney DiseasesAcute 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.

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    Kidney DiseasesGlomerular diseasesNephrotic syndromeNephritic syndrometubular or interstitialTubular defectsAcute renal failure (ARF)Other End-stage renal disease (ESRD) Kidney stones

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    Nephrotic SyndromeAlterations of the glomerular basement membrane allows persistent loss of large amounts of protein in the urineAssociated with diabetes, glomerulonephritis, amyloidosis, lupusHigh risk for cardiovascular diseaseHypercoagulabilityAbnormal bone metabolism

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    Nephrotic SyndromeAlbuminuria: more than 3 g/day urinary albumin losses, with proportionally lesser amounts for childrenHypoalbuminemiaHypertensionHyperlipidemiaEdema

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    Medical Mgt of Nephrotic SyndromeCorticosteroidsImmunosuppressantsACE inhibitors/angiotensin receptor blockers to reduce protein losses, control blood pressure and fluid balanceCoenzyme A reductase inhibitors to control hyperlipidemia

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    MNT in Nephrotic SyndromeProtein 0.8 to 1 g/kg IBW 80% HBVSodium based on fluid statusPotassium and other minerals (calcium, phosphorus) monitored and individualizedFluid unrestrictedDiet 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

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    Nephritic syndromeAcute glomerulonephritis (inflammation of the glomerulusSudden onset, often after streptococcus infectionsSymptoms include hematuria, hypertensionUsually resolve on their own or advance to nephrotic syndrome or ESRD

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    Nephritic syndrome: Nutritional ManagementDiet to treat underlying diseaseRestrict diet if necessary to control symptomsProtein restricted in uremiaSodium restriction in hypertensionPotassium restriction in hyperkalemia

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    Acute Renal FailureRapid, often reversible deterioration of renal functionGFR declines over hours to daysMost 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

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    Causes of Acute Renal FailurePre-renal: caused by intravascular volume depletion, decreased cardiac outputPost-renal: benign prostatic hypertrophy, prostate cancer, cervical cancer, colorectal cancer, neurogenic bladder, urethral stricturesIntrinsic or parenchymal ARF: vascular disease, interstitial nephritis, glomerular disease, acute tubular necrosisByham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney disease.ADA, 2004

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    Causes of Acute Renal FailureIschemic Injury (50% of all incidence) d/t loss of blood supply to the kidneys secondary to surgical complications, thrombosis, hypotension, hypovolemiaNephrotoxic injury: medications, contrast medium, chemotherapy, poisons (35%)Multiorgan system failure, particularly liver failureSepsis, especially bacterialObstructive uropathy (trauma during surgery, urolithiasis, enlarged prostate)Acute glomerular nephritis

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    Acute Tubular NecrosisMost common cause of ARFIschemia: due to major surgery, hypotension, cardiogenic, septic, or hypovolemic shockNephrotoxicity: drugs, chemotherapeutic agents, organic solvents, heavy metals, cocaine

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    Acute Tubular NecrosisInitiating phasePeriod between onset and established renal failureUsually reversible by treating the underlying disorder or removing offending agentTime frame: hours or daysByham-Gray L, Wiesen K. A clinical guide to nutrition care in kidney disease.ADA, 2004

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    Acute Tubular NecrosisMaintenance PhaseEpithelial cell injuryUrine output is at its lowest; complications associated with uremia, fluid overload, electrolyte imbalance (decreased sodium, increased potassium levels)Time frame: 10-16 days in oliguric patients; 5-8 days in nonoliguric patients

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    Acute Tubular NecrosisRecovery PhaseTubule cell regeneration and gradual return of GFRBUN and creatinine return to near normalMay be complicated by marked diuresis, dehydration and fluid and electrolyte imbalance (increased sodium, decreased potassium)Time frame: days to months

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    Renal Replacement Therapies in ARFRecommended for patients with pronounced azotemia, electrolyte imbalance, fluid overload, severe acidosisUsed in 85% of patients with oliguric ARF and 30% of nonoliguricPurpose is to correct imbalances as well as provide sufficient renal support to other organs

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    Renal Replacement Therapies in ARFHemodialysis: standard treatment if patient is hemodynamically stableHowever, risk of hypotension and wide swings in body weight in unstable patientsContinuous hemofiltration (CAVH, CVVH) provides slow, continuous filtration across a membrane, driven by arterial pressure (CAVH) or pump (CVVH)

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

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    CAVH

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    MNT for Adult ARFEnergy: BEE X 1.2-1.3 or 25-35 kcal/kgProtein: .8-1.2 g/kg noncatabolic, without dialysis; 1.2-1.5 g/kg catabolic and/or initiation of dialysisFluid: 24 hour urine output + 500 ml (750-1500 ml)Sodium: 2.0-3.0 gramsPotassium: 2.0-3.0 gramsPhosphorus: 8-15 mg/kg; may need binders; needs may increase with dialysis, return of kidney function, anabolismSource: Byham-Gray, Wiesen, eds. A Clinical Guide to Nutrition Care in Kidney Disease. ADA, 2004

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    Nitrogen Balance in ARFStandard nitrogen balance studies require a creatinine clearance of more than 50 mL/min/1.73m2In ARF, urea nitrogen appearance (UNA) is a better method of determining nitrogen balanceUNA = UUN + change in the urea nitrogen pool

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    Calculation of Urea Nitrogen Appearance (UNA)

    UNA (g) = UUN + [BUN2 BUN1) x .6 x BW1] + [(BW2-BW1) x BUN2]Net protein breakdown = UNA x 6.25UUN = 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)

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    Chronic Kidney Disease

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    Causes of Chronic Kidney Disease

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    Progression to End-Stage Renal Disease (ESRD)FirstDecline in glomerular filtration rate (GFR)SecondAdaptations in renal function, i.e., increase in GFR ThirdAdaptations improve renal function in short termFourthLong term loss of nephron units.FifthSlow, progressive decline in renal function SixthEventually this decline leads to renal insufficiency, i.e., ESRD

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    Stages of Chronic Kidney DiseaseNational Kidney Foundation K/DOQI Clinical Practice Guidelines on CKD. Am J Kidney Dis 2002;39(suppl 1):46.

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    ESRD: Medical ManagementDialysisImmunosuppressant drugsKidney transplantPsychological support

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    Uremia, a Clinical SyndromeSigns and SymptomsMalaiseWeaknessNausea and vomitingMuscle crampsItchingMetallic taste (mouth)Neurologic impairment

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    Stages of CKD Nutrient RecommendationsFedje and Karalis. Nutrition mgt in early stages of CKD. Clin Guide Nutr Care Kidney Dis, ADA, 2004

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    Treatments: CKD, HD, CAPD

    CKD Early

    Hemodialysis

    CAPD or CCPD

    Treatment

    Diet and medications

    Diet and medications

    Hemodialysis

    Diet and

    medications

    Peritoneal

    dialysis

    Modality

    Vascular access

    Peritoneal membrane

    Duration

    Indefinite

    3-5 h

    2-3 d/wk

    3-5 exchanges

    7 d/wk

    Concerns

    Glomerular hyperfiltration:

    BUN:

    bone disease:

    HTN:

    Glucose control in diabetes

    AA loss;

    interdialytic

    electrolyte and

    fluid changes:

    Bone disease:

    HTN

    Protein loss:

    glucose absorption:

    Bone disease:

    weight gain:

    hyperlipidemia:

    glucose control in diabetes

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    MNT for CKD, HD, PDCKD HemodialysisCAPD or CCPDProtein0.6-1.01.1-1.41.2-1.5g/kg/dayEnergy30-3530-3530-35(kcal/kg IBW)Phosphorus 8-12 indiv1000 mL/day or serum NL, do not need to restrict K+

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    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 bonePhos binders prevent phosphorus from being absorbed in the gut; form insoluble compound so phos is excreted in stoolPhos clearance poor in HD and CAPD phos may mean excess phos binder or poor p.o.

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    Calcium (8.4-9.5 mg/dL)Most abundant mineral in human bodyNearly half of calcium is bound to albumin; if serum calcium is low, evaluate albumin level; can correct for low albuminCalcium-Phosphorus Product: multiply serum calcium x serum phos: if >55-75, calcification can occur

  • PERITONEAL DIALYSISSAMPLE GLUCOSE ABSORPTIONg glucose per liter x volume = total g of glucoseExample: one 2 L. exchange of 1.5% solution = 30 g glucoseTotal g of glucose x absorption rate (~60%) = g glucose absorbedExample: 30 g glucose x 60% = 18 g glucose absorbedg glucose absorbed x kcal per g glucose (3.7)= calories absorbedExample: 18 x 3.7=66.6 calories/2 L. exchangePatient does 4 exchanges/d 67 x 4 = 268 calories/d from diaysate

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

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    MNT for PD: SodiumPD clears sodium very well, so sodium can be fairly liberalHowever, high salt diets increase thirst and may make adherence to fluid limits more difficultGeneral recommendation is 2-4 grams sodium

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    MNT for PDPotassium: is easily cleared by PD; some patients may need K+ supplementationCalcium: limit to 2000 mg elemental calciumGenerally pts get ~1500 mg from calcium-based phosphate bindersSerum calcium should be maintained in low normal range (8.4-9.5 mg/dl)

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    MNT for PDPhosphorus: limited to 800-1000 mg/day which is difficult with high protein dietUse phosphate bindersFluid: can be adjusted by varying the dextrose concentrations of the dialysateMay need to be restricted if pts cannot achieve fluid balance without frequent hypertonic exchanges

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    PD: weight gain, hypertriglyceridemia, hyperglycemiaIncrease exercise as allowed by MDLimit sodium and fluid to minimize hypertonic exchangesUse solutions with alternate hypertonic agents such as IcodextrinModify energy intake to facilitate wt lossModify intake of sugars and fats, especially saturated fats

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    PD: Protein Losses, MalnutritionPatient education regarding protein goals and ways to meet themSuggest pt eat protein foods first and limit fluids at mealtimeFrequent smaller portions of protein and easy to eat proteins such as egg white, cottage cheese, etcEducation on sterile technique to avoid peritonitis

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    RENAL EXCHANGES FOR MEAL PLANNING

    Food GroupsKcalCHO g.PRO g. FAT g. Na mg.K+ mg.PO4 mg.Milk ( c.)8564580185110Meat650742510065Starch801521803535Vegetable255101515020Fruit60150.50515015Fat (1TB.)100001115005Calorie Boosters60150015205Beverages:Coffee (1c.) tea (1 bag) wine (4 oz.) beer (12 oz.)000001000

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    Protein Foods (65 kcals, 7 grams protein, 25 mg Na, 100 mg K+, 65 mg phos) Meat 1 ounceEgg 1Fish 1 ounceShellfish 1 ouncePoultry 1 ounceEgg substitutes cBacon 4 slicesCheese 1 ozMilk 1 cupNut butters 2 TTofu cupCottage cheese cupLunchmeat 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 cup milk cup plain ice cream cup yogurt

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    Starch Servings80 kcal, 15 g CHO, 2 g pro, 1 g fat, 80 mg Na+, 35 mg K+, 35 mg PO4Bread, white or rye 1 sliceCake 2 in sq or cupcakePlain cake donut 1Cold cereal 1 cupDinner roll 1 small Macaroni, noodles, rice cupPopcorn, unsalted, 1 cup

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    Vegetable Servings25 kcal, 5 g CHO, 1 g pro, 15 g Na+, 150 mg K+, 20 mg PO4Asparagus cupGreen beans cupCabbage cupCarrots cupCauliflower cupCorn cup

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    Fruit Servings K+60 kcals, 15 g CHO, .5 g protein, 150 mg K+, 15 mg phosApple Apple juice cApplesauce cApricot nectar cBlackberries cBlueberries cFruit cocktail cGrapes cLemonLimePeachPearPineapplePlums (1)RaspberriesWatermelon

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    Fruit Servings (High potassium)60 kcals, 15 g CHO, .5 g protein, >250 mg K+, 15 mg phosApricotsBananasDatesHoneydew melonKiwifruitNectarineOrangeOrange JuicePrune juice

    Prunes (5)Raisins

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    Fat Choice100 kcals, 11 g fat, 150 mg Na+, 5 mg PO4Margarine/butter 1 TCream cheese 2 TMayonnaise 11/2 TNon-dairy topping cupSour cream cupVegetable oil 1 TTartar sauce 2 T

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    Calorie Boosters60 kcals, 15 g CHO, 15 mg Na+, 20 mg K+, 5 mg PO4Hard candy 4 piecesJam or jelly 2 TJelly beans 15Honey 2 TSugar brown or white 2 TMarshmallows 5 largeFruit snacks and candies 1 oz

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    Beverages100 mg K+ (also counts as fluid)Coffee 1 cupTea 1 bagWine 4 ozBeer 12 oz

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    Medicare Rules for MNT in Renal DiseaseAs of January, 2002, Medicare covers MNT for pre-dialysis renal diseaseIncludes nutritional, diagnostic, therapy and counseling servicesRestricted to patients with GFR 15 to 50 mL/min/1.73m2 (stages 3-4-5 not on dialysis)

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    Kidney Transplant1.Types: related donor or cadaver2.Posttransplant management:CorticosteroidsCyclosporine3.Diet while on high-dose steroids:1.3 to 2 g/kg BW protein30 to 35 kcal/kg BW energy80 to 100 mEq Na4.Diet after steroids:1 g/kg BW proteinKcal to achieve IBWIndividualize Na level

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

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    Kidney Stones1.Particulate matter crystallizesCa salts (Ca oxalate or Ca phosphate)Uric acidCystineStruvite (NH4, magnesium and phosphate)2.Ca salts in stonesRx: 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

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    Kidney Stonescontd4.Uric acid stonesAlter pH of urine to more alkalineUse high-alkaline-ash dietFood list in Krause text5.Cystine stones (rare)6.Struvite (infection stones) antibiotics and/or surgery

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    Acid-Ash DietIncreases acidity of urine (contains chloride, phosphorus, and sulfur)Meats, cheese, grains emphasizedFruits and vegetables limited (exceptions are corn, lentils, cranberries, plums, prunes)

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

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    SummaryRenal diseasesdelicate balance of nutrientsRegular monitoring of lab values, with altered dietary interventions accordingly

    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=30-300 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 nephropathyThen 20% by 20 years progress to ESRD. Albuminuria is a marker of high morbidity/mortality from cardiovascular disease; >300 mg./day albumin in urine 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