Chronic Kidney Disease Class Presentation

Objectives
• Epidemiology & etiology of CKD and nephrotic
syndrome
• Kidney functions
• Impaired kidneys, related to CKD and nephrotic
syndrome, and the nutritional implications
• Understanding of treatments for CKD and
nephrotic syndrome
• MNT for both
• Current nutrition-related research

1/4/2012 Lauren Richardson, RD Eligible 2

Epidemiology & Etiology1
• Over 20 million in US
• Women : Men
• White : Black : Mexican
• DM & HTN
– CVD, Obesity, Cholesterol, Genetics, Age
– Kidney Damage
• Infections, Drugs, Toxins


Renal Function, Homeostasis2
• pH/Fluid/Electrolytes/Bp
• Excretion of waste via urine
• Enzyme production
• Hormone production


Homeostasis2
• HOW IS IT REGULATED?
–BP
• ADH: urine output, fluid balance
• Renin Angiotensin System
• Na2+: Exchanged for K+

–pH
• Reabsorption of HCO3-
• Secretion of H+


Waste Excretion2
• Uric acid
• Creatinine
• Urea
• Drugs/Toxins


Enzymes & Hormones2
• RENIN
• 1,25-dihydroxycholecalciferol
• Erythropoietin


Checking for Functional Status2
• Microalbuminuria
• GFR
• Creatinine Clearance
• Tubular Function Tests


GFR2
• Not influenced by hydration status
• Characterizes stage of CKD


Q: What are the sx of poor
kidney function?
Q: When will they begin to appear?

Impaired Kidney Function Results In…2
• Edema, Hyperkalemia, Metabolic Acidosis,
HTN
• Uremia, Azotemia, Oliguria
• Bone & Mineral Disorders,
Hyperphosphatemia
• Anemia


Impaired Kidney Function Results In…2
• Fluid/Electrolytes/pH/BP
– Edema, Hyperkalemia, Metabolic Acidosis (PEW),
HTN
• Waste Excretion
– Uremia (PEW), Azotemia, Oliguria
• Hormone Production
– (Active Vit. D) Bone & Mineral Disorders,
Hyperphosphatemia
– (Erythropoietin) Anemia

SHPT: Secondary Hyperparathyroidism2
• NORMAL
– PTH:
• Reabsorb Ca2+
• Excrete P
• Activate D3
• DAMAGED
– High P
• PTH released, cannot excrete P
• PTH constantly triggered
• Parathyroid cells undergo hyperplasia


CKD: Chronic Kidney Disease2
• “…syndrome of progressive and
loss of the , , and
functions of the kidney,
secondary to kidney damage; progresses
slowly over time…”


Measuring Disease Progression2
• Slow, progressive degeneration of kidney
function
• How do we measure kidney function??
– GFR!


Measuring Disease Progression2

1 Normal or increased GFR w/ kidney damage

2 Mildly decreased GFR w/ kidney damage

3 30-59 GFR

4 15-29 GFR

5 (ESRD) Inadequate GF; Dialysis or replacement req’d.


Disease Treatment2
• DELAY PROGRESSION
– Treat causes; co-existing conditions
• Dialysis
– Hemodialysis (HD)
– Peritoneal Dialysis (PD)
– Continuous renal replacement therapy (CRRT)
• Transplant


Dialysis2
• Dialyzer
• Dialysate
• Filtration
– Osmosis, Ultrafiltration, Diffusion

• Does not replace endocrine or metabolic
functions


HD: Hemodialysis2
• Permanent Access Site
• Radial artery and cephalic vein
• Dialysate
• 3x wk; 4 h each


PD: Peritoneal Dialysis2
• CCPD
• CAPD
• Catheter access
• Dextrose dialysates

Prince,ES. Uremic Frost.
http://www.uremicfrost.com/2009_03_01_archive.html.
Accessed February 20, 2011.


CRRT2,3
• [Continuous Renal Replacement Therapy]
• For acute care
– Hemodynamically unstable
– Volume is gradually exchanged
• Intolerant of HD or PD
• Temporary

1/4/2012 Lauren Richardson, RD EligibleInfo. http://crrtinfo.blogspot.com/. Accessed
CRRT 23
February 20, 2011.

Transplant2,4,5
• Major histocompatibility complex
– Human leukocyte antigens (HLA)
• Immunosupressants
Drug Interactions
Cyclosporine GI effects; “oral candida, gum hyperplasia, pancreatitis,
hepatotoxicity, nephrotoxicity, hyperkalemia”

Corticosteroids GI upset; Hemorrhage; “pancreatitis; osteoporosis;
poor wound healing; fluid retention”
Imuran GI upset; “pancreatitis; muscle wasting”
Prograf GI upset; “Albuminuria, proteinuria, hematuria,
hypomagnesemia, hyperglycemia, nephrotoxicity,
appetite loss”; distorted K levels

NUTRITION THERAPY: NCP


A: Assessment2
• Dietary: Patterns, Fears, Intolerances,
Restrictions, Appetite (changes?)
• Physical Exam: Muscle wasting, edema
• Anthro’s: Baseline weight
• Changes in bowel movements/urine output
• Social circumstances; Accessibility; Food
Insecurity; Barriers to learning
• Labs, Medications, Comorbid Conditions

A: (LABS)2
LOWERED INCREASED
• Albumin* • BUN*
• BUN* • Calcium*
• Calcium
• Cl*
• C-rp
• Glucose* • Glucose
• H&H • H&H*
• K • K*
• PAB • Phos
• Phos
• Protein*
• Protein
• Na* • Na*


A: (Medications)5
PURPOSE DRUG CLASS INTERACTION
Control BP ACE Inhibitors Na subs; K; some GI effects
Angiotensin II Receptor Licorice; (*Losartan: gf-related
Blockers citrus); some GI effects; K; H&H
Diuretics K; Mg; Cl; glucose; some GI
effects (diarrhea esp.)
Beta-blockers Licorice; some GI effects (diarrhea
esp.); Reduction in insulin

Calcium channel blockers Licorice; Contains sorbitol; May
need to calcium intake
Direct renin inhibitors Avoid HF meals; some GI effects
(esp. GERD); K
Treat anemia rhEPO May need fol, B12, Fe suppl.; BP
Iron suppl. Ferrous salts (IV or Oral) Food abs; Take w/ C or MFP; Take
antacids separately; Anorexia;
severe GI effects
Electrolyte Imbalances Binders (phosphate) Some GI effects; PO4; PTH
Fluid Buildup Diuretics ““

D: Diagnosis2
NI NB
• Inadequate energy intake OR oral • Food and nutrition-related
food/beverage knowledge deficit
• Malnutrition
• Disordered Eating Pattern
• Excessive […] intake
– Fluid • Limited Adherence to nutrition-
– Protein related recommendations
– Mineral • Undesirable food choices
NC • Impaired ability to prepare
• Altered GI function food/meals
• Altered nutrition-related lab • Poor nutrition quality of life
values
• Limited access to food
• Food-RX interaction
• Involuntary weight (loss or gain)


I: Intervention2
1&2 3&4
• Meet Needs • Meet Needs
• Focus: Comorbidities • Focus: Prevent malnutrition
– Adequate energy
– Diabetes
– Balance protein needs/intake
– HTN w/ renal decline and LBM
– Hyperlipidemia preservation
– Deficiencies
• Drug Interactions?
• Drug Interactions?
• Assess @ 1-3 mo. Intervals • Manage comorbidities
• Food Record • Food Record
• Diet education (sources, • Diet education (sources,
handouts) handouts)

I: Intervention2
5 (ESRD)
• Meet needs
• Prevent malnutrition
• Manage complications and comorbidities
• Bp and fluid status
• Diet Education (sources, handouts)
• Drug-Nutrient Interactions


I: Stages 1-4 MNT2
CKD (non-dialysis) requirements
Energy 35 (<60y) 30-35 (>60 y)
Protein 0.6-0.75g/kg

Fluid Not typically restricted
Na Varies. (0-3g)
K Not typically restricted
P 800-1000mg/d OR 10-12mg/g PRO
Ca Maintenance, otherwise WNL
Vit/Min B-complex + Vit C; Maintain Vit D;
Individualize Fe, Zn


I: 5 MNT2
Hemodialysis Requirements
Energy 35 (<60y) 30-35 (>60 y)
Protein > 1.2

Fluid Output + 1000ml (*wt. gain)
Na 2g
K 2-3g (adjust to lab values)
P 800-1000mg/d OR 10-12mg/g PRO
Ca <2.0 g + binder load
Vit/Min C (60-100mg); B6 (2mg); Folate (1-5mg);
B12 (3µg/d); Vit E (15IU/d); Zn (15mg/d);
Individualize vit D and Fe


I: 5 MNT2
Peritoneal Dialysis Requirements
Energy 35 (<60y) 30-35 (>60 y)
Protein > 1.2-1.3
Fluid Maintain fluid balance
Na 2g; Monitor fluids
K 3-4g (adjust to lab values)
P 800-1000mg/d OR 10-12mg/g PRO
Ca <2.0 g + binder load
Vit/Min C (60-100mg); B6 (2mg); Folate (1-5mg);
B12 (3µg/d); B1 (1.5-2mg/d); Vit E
(15IU/d); Zn (15mg/d); Individualize vit D
and Fe


I: MNT2
Transplant Requirements
Acute Chronic
Energy 30-35 Weight
maintenance
Protein 1.3-1.5 1.0
Fluid Unrestricted Unrestricted
Na 2-4g/d 2-4mg/d
K 2-4g/d Unrestricted
P 1200-1500mg/d 1200-1500mg/d
Ca 1200-1500mg/d 1200-1500mg/d


I: Intervention
• Enteral Nutrition
– Non-dialysis
• Low-protein formula (Suplena, 45g/L)
– Dialysis
• High-protein formula (Nepro, 81g/L)
– Dialysis with less energy
• Glucerna 1.5 (82.5g/L)


I: Intervention6
• Enteral/Parenteral Recommendations (ESPEN)
– NON-DIALYSIS
– Uremic syndrome, GI Upset  PEW
– Metabolic Acidosis  Protein catabolism
• PN not usually needed
– If so, low protein


I: Intervention6
– HD
• PEW
– Typically low oral intake at beginning of HD
• Increases energy expenditure
• Nitrogen balance is negative on HD days
• 25 g loss of glucose into dialysate
• Loss of water-solubles
– Thiamin esp.
– Vit E for those at high risk of CVD
• PN indicated for severely malnourished
– BMI <20, 10% wt. loss in 6 mo., Albumin <35, PAB <300
– Consider intradialytic parenteral nutrition (IDPN)
1/4/2012 – Central accessLauren Richardson, RD Eligible
(concentration) 38

I: Intervention6
– PD (CAPD)
• Usually less severe uremia in PD than HD
• Glucose uptake of 100-200g/d
– Gaining weight?
• Intraperitoneal parenteral nutrition (IPPN)
– Reserved for severely malnourished
• Central route if acute, IPPN if non-acute


M,E: Monitor & Evaluate
• Labs
– Protein, Hydration, GFR
• Intake
– Spec. restricted nutrient intake
– Quantity
• Status
– Treatments, GI problems
• Medications
– Changes
• Weight
– Body Composition
– Input/Output
–
1/4/2012 PEW Lauren Richardson, RD Eligible 40

Specific MNT Guidelines2
• At risk for increased risk of CVD
• Secondary Hyperparathyroidism (SHPT)
• Anemia, Microcytic


Research Topics
• Vitamin D Supplementation7
• Bicarbonate Supplementation8
• Gastric Bypass Surgery in the pt requiring
transplant9


Nephrotic Syndrome: “Glomerular
Disease”2
• Membrane changes
– Problematic filtration
• Epidemiology & Etiology
– 2 in 10,000
– Children : Adults
– Males : Females
– DM, Membranous Nephropathy, Genetics, FSGS


Nephrotic Syndrome: How?2


Nephrotic Syndrome: S & S2
• Proteinuria
– Kwashiorkor or PEM


Nephrotic Syndrome: S & S2
• Hyperlipidemia
• Hypoalbuminemia
• Extravascular  Vascular Shift
• Edema
– Anasarca
– Mobile
• Frothy urine
• Oliguria

• Losses2
– ALBUMIN
– Zn, Cu, D, Fe
• Risks2
– Atherosclerosis
• Low LPL (requires protein)
• Overall increase hepatic synthesis: VLDL, IDL, LDL, and
HDL
• Chicken or the egg?
• Future damage2
– Workload is passed off, more nephrons die


Treatment2
• Etiological
• Medications
– Antihypertensives
• Decrease proteinuria
• Watch K levels
• Salt substitutes, HF meals
– HMG CoA Reductase Inhibitors
• Atherosclerotic risk
• G/f related citrus; SJW


Outcomes of Tx2

• Resolved/managed

• Retained

• Resolved/improved

• Postponed


A: Assessment2
• Physical Exam
– Edema, Recent wt. loss, clothes fitting differently
– Obvious sign of muscle wasting
• Social circumstances; Education level; Barriers to
learning; Access and Insecurity
• Anthro’s
• Labs
– BUN, Creatinine, GFR
– pH
– Lipids
– Protein status (albumin, PAB, adj. Ca, Ca/Phos product)
• [Calcium + .0704] [34-Serum albumin] = adjusted
• Calcium x Phos

A: Assessment2
• Needs
– Edema??
– Usual or IBW
• 24 Hr Recall/Dietary Record
– Protein
– Phos
– Calcium
–K
– Na


D: Diagnosis2
• Increased nutrient needs

• Excessive Na intake


I: Intervention2
Nutrient Recommendations
Energy 35 for normal or overweight; less if
obese (include complex
carbohydrates and fat composition of
<30%, limit cholesterol)
Protein .8-1.0 (urine losses??)

Fluid Maintenance

Na 1-2g/day

Phos Maintenance (bolus?)

Calcium Maintenance


M,E: Monitor & Evaluate
• Labs
– Protein, Hydration
• Intake
– Spec. restricted nutrient intake
– Quantity
• Status
– GI problems
• Medications
– Changes
• Weight
– Body Composition
– Input/Output
–
1/4/2012 PEW Lauren Richardson, RD Eligible 55

Research10
• Protein
– Changing the distribution?
– (Fuel sources)
– When increasing protein, overall energy increases!


References
1. National Chronic Kidney Disease Fact Sheet 2010. Center for Disease Control and
Prevention. http://www.cdc.gov/diabetes/pubs/factsheets/kidney.htm. Updated May 26,
2010. Accessed February 20, 2011.
2. Nelms MN, Sucher K, Lacey K, et al. Nutrition Therapy and Pathophysiology. 2nd ed.
Belmont, CA: Wadsworth; 2011.
3. National Institutes of Health.
www.cc.nih.gov/researchers/training/principles/ppt/susla_2002_crrt.ppt. Accessed
February 20, 2011.
4. Chronic Kidney Disease. WebMD. http://www.webmd.com/a-to-z-guides/chronic-kidney-
disease-medications. Updated September 17, 2009. Accessed February 20, 2011.
5. Pronsky, ZM. Food Medication Interactions. 15th ed. Birchrunville, PA: Food-Medication
Interactions; 2008.
6. Cano NJM, Aparico M, Brunori G, et al. ESPEN guidelines on parenteral nutrition: Adult
renal failure. Clin Nutr. 2009;28:401-414.
7. Williams S, Malatesta K, Norris K. Vitamin D and chronic kidney disease. Ethn Dis.
2009;19(4 suppl 5):S5-8-11.
8. Brito-Ashurst I, Varagunam M, Raftery MJ, Yaqoob MM. Bicarbonate supplementation
slows progression of CKD and improves nutritional status. J Am Soc Nephrol.
2009;20:2075-2084.
9. Majorowicz, RR. Nutrition management of gastric bypass in patients with chronic kidney
disease. Nephrol Nurs J. 2010;37(2):171-175.
10. Squire JR. Nutrition and the nephrotic syndrome in adults. Am J Clin Nutr. 1956;4:509-
1/4/2012 522. Lauren Richardson, RD Eligible 57

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