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Chronic Kidney Disease Heidi Anderson Erica Bailey Anai Villalobos Katie Pearce

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Page 1: Chronic Kidney Disease - Heidi Washburn Dietetic …heidiwashburnportfolio.weebly.com/uploads/1/3/5/8/...is the best measure of kidney function. A doctor will order a blood test to

Chronic Kidney Disease

Heidi Anderson Erica Bailey

Anai Villalobos Katie Pearce

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Anatomy of the Kidney

2 major parts: Cortex Medulla

Functional Unit Nephrons

Renal Pyramid

Renal Pelvis

Ureter

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Nephrons

Presenter
Presentation Notes
Functional Unit of the Kidney ,about 1 millions nephrons in a kidney, if one segment is destroyed the entire nephron cannot function, two types: Juxtamedullary and Cortical. Cortical having the short loop of Henle and being about 80% of nephrons. Biggest difference between these two nephrons is that the juxtamedullary nephrons create a solute gradient of sodium chloride and urea in the medulla that permits the concentration of urine.
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1.) Glomerular Filtration

Fluids and solutes in the blood plasma of the glomerulus pass into the glomerular capsule (glomerular filtrate) Mechanisms to cause this fluid to be filtered is High hydrostatic pressure of the blood in the glomerulus Large number of pores

Substances present in the glomerular filtrate: water, electrolytes, glucose, AA, urea, hormones, and vitamins. -exclude large molecules that are in the blood.

Presenter
Presentation Notes
Glomerular filtrate does not include plasma proteins, RBCs, WBC, and platelets to pass through because of their large size. Presence of these things indicates the hydrostatic pressure in the capillaries is high or there is a defect in the membrane.
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GFR

The best way to measure levels of kidney function. GFR= urine volume x inulin conc. In urine inulin conc. In plasma (mg/ml)

Best estimates of GFR: Inulin clearance Creatine clearance Plasma creatinine concentration Blood urea nitrogen (BUN)

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2.) Tubular Reabsorption

Trans-epithelial transport

Most solutes reabsorped completely

Urine volume is regulated by the needs of the body

Active vs. Diffusion

Tm

Presenter
Presentation Notes
Transfer of fluid and solutes out of the lumen of the nephron into the peritubular capillaries. Aprox. 99% of the filtrate is reabsorbed from the renal tubules, primarily in the proximal convoluted portion. Tm-Transport maximum. Tm for glucose is 375 mg/min filtered. Glucose above that value will not be reabsorbed and will appear in the urine. (diabetes mellitus)
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3.) Tubular Secretion

Movement from the peritubular capillaries into the lumen of the tubule.

Main Substances secreted H+ K+ Some organic anions

Presenter
Presentation Notes
Same transepithelial transport movement Organic anions-food additives, pesticides, some drugs such as penicillin H+ secretion is important in the regulation of acid base balance. The extent of secretion depends on how acidic the body is. K is reabsorbed in the proximal tubule and secreted in the distal tubule. Aldosterone stimulates K secretion-which is coupled with Na reabsorption.
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http://ccn.aacnjournals.org/cgi/content/full/26/4/17/F1

Presenter
Presentation Notes
Potassium and Phosphorus will be very important in the diet
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Functions of the Kidney

Elimination of wastes, excess water and solutes, and conserves nutrients

Acid-base balance

Renin-angiotensin system

Erythropoietin release

Activation of Vitamin D

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Elimination of Waste

Kidney receives 20% of cardiac output, which allows the filtering of approximately 1600 L/day of blood.

This is translated into 1.5 L of urine a day to be excreted, on average

The fluid filtered from the blood plasma is modified and reabsorbed as it travels along the tubules. The remainder finds its way into the ureter, which carries the urine to the bladder from each kidney.

Presenter
Presentation Notes
http://www.dialysisindia.com/kidneyfunction.html
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Acid-Base Balance

Kidney is responsible for 2 major activities: Reabsorption of filtered bicarbonate Excretion of the fixed acids (acid anion and associated H+) Both of these processes involve secretion of H+ into the lumen

by the renal tubule cells Only the 2nd one leads to excretion of H+ from the body.

Acidosis vs. Alkalosis

Presenter
Presentation Notes
These two movements are interdependent on each other, the reabsorption of bicarbonate occurs as a result of the filtration and secretion of H+. Acidosis-ratio of CO2 to HCO3 in the extracellular fluid is increased bc of the production of CO2 or increase in H+ formation from metabolism. Renal response: increased amounts of CO2 enter the tubular cells from the extracellular fluid, increased amounts of H+ are secreted into the lumen of the nephron, some combines with HCO3 and one Na+ is reabsorbed for each H+ excreted. HCO3 in the lumen of the nephron is reabsorbed vs. Alkalosis-ratio of HCO3 increases as the pH rises. (potassium retention?) Net result is that H ions are retained and bicarbonate ions are excreted.
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Renin-

Angiotensin

System

Regulation

Of Blood

Pressure

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Erythropoietin Release

EPO is a hormone primarily produced by the kidney

Occurs when a drop in blood oxygen level is perceived.

Used to treat anemia.

Glycosylated erythropoietin comes in 3 forms:

alpha (the most commonly used type in veterinary medicine),

beta (of similar clinical efficacy to alpha)

Darbepoetin (which is particularly heavily glycosylated and lasts the longest).

Presenter
Presentation Notes
10-15% of EPO comes from the liver.
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Vitamin D Activation

Parathyroid hormone is able to drive stored calcium and phosphorus from the bones as is vitamin D so these hormones are able to work in concert here but in the kidney they have different functions. In the kidney, while vitamin D saves both calcium and phosphate, parathyroid hormone causes only calcium to be saved and phophate to be dumped. There is a third hormone called “calcitonin” that keeps the blood calcium level from indefinitely rising. When blood calcium starts to get too high, calcitonin is released to begin storing calcium and phosphate back in the bones until it is needed again.

Presenter
Presentation Notes
Pth releases calcium from the bone
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At Risk Populations

Racial Groups: African Americans Native Americans Hispanics Pacific Islanders

Risk Factors: Diabetes Hypertension Family history of kidney failure

Presenter
Presentation Notes
AA are 4x as likely to devlop kidney failure as whites Indians are 3x as likely Hispanics have twice the risk
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Looking at Geographics

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Hypertension

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CKD

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Genetics

The angiotensinogen promotor G(-6) allele lowers transcription and is inversely associated with hypertension.

the A1166C 3'-UTR variant of angiotensin II type 1 receptor (AT1R) has been associated with CKD.

The AT1R C1166 allele may increase susceptibility but only in the presence of hypertension.

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What is CKD?

CKD is the gradual loss of the kidney’s ability to filter waste and fluid from the bloodstream.

Nephrons filter waste out of the blood.

Nephrons become damaged and lose their filtering ability overtime.

As more nephrons are damaged, the healthy ones work harder.

Kidneys become scarred or may shrink in size.

Presenter
Presentation Notes
Eventually, the healthy nephrons become damaged as well.
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Etiology

• Diabetes is the number one cause of kidney disease, responsible for about 40% of all kidney failure.

• High blood pressure is the second cause, responsible for about 25%.

• About 12.2% of Native Americans over the age of 19 have type 2 diabetes.

Diabetes and high blood pressure are the leading causes of CKD.

Presenter
Presentation Notes
About one third of people with diabetes will eventually develop CKD.
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Etiology-cont.

Other causes include:

- Glomerulonephritis (kidney inflammation)

- Genetic diseases (i.e. polycystic kidney disease)

- Autoimmune diseases (i.e. lupus)

- Birth defects

- Obstructions caused by problems like kidney stones or tumors

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Pathophysiology

As the renal tissue loses function, the remaining tissue increases its performance

↓ renal function interferes with the ability to maintain fluid and electrolyte homeostasis.

↓ability to concentrate urine

↓ability to excrete phosphate, acid and K

↑creatinine and urea and ↓GFR

Heart failure can result from Na and water overload

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Pathophysiology-cont.

↓production of calcitriol leads to hypocalcemia→osteopenia or osteomalacia.

↓excretion of phosphate leads to hyperphosphatemia

Secondary hyperparathyrodism is common→renal osteodystrophy.

Normochromic-normocytic anemia (Hct of 20-30%) caused by ↓erythropoietin production due to ↓functional renal mass.

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Phosphorus Pathophysiology

Decreased renal function

Increased blood phosphorus

Decreased active vitamin D

Increase blood calcium levels

Decreased bone mass

Increased blood PTH

Cacliphylaxis

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Cacliphylaxis

Deposition of calcium phosphate in soft tissues This occurs when the phosphorus-calcium product is too high

(greater than 4.5 (mmol/l)2

Cacliphylaxis is associated with CVD Calcium phosphate is deposited on heart valves and blood

vessels

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Diagnosis

Based on laboratory testing of renal function:

- Creatinine

- GFR

- BUN

Urinalysis (check for protein, blood and WBC in urine-which should not be there).

Sometimes renal biopsy.

MRI or ultrasound to check the size.

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LABS

Glomerular filtration rate (GFR) is the best measure of kidney function.

A doctor will order a blood test to measure the serum creatinine level. As kidney function ↓, blood levels of creatinine ↑.

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Creatinine

It is a waste product that is passed through the kidneys.

A by-product formed by muscle contractions. It also comes from protein foods we eat.

↑creatinine may signal that the kidneys aren’t eliminating this waste, leaving it in the body.

Normal range: 0.8-1.4mg/dL

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Glomerular Filtration Rate (GFR)

Measures the kidney function and the stage of CKD.

As the kidneys become more damaged, the GFR will decrease.

Normal range: >90, with little or no protein or albumin in the urine.

Presenter
Presentation Notes
Image: http://ccn.aacnjournals.org/cgi/content/full/26/4/17#SEC2
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Blood Urea Nitrogen (BUN)

The BUN test measures the amount of urea in your bloodstream.

Urea is a waste product left over from the protein we eat, which is normally eliminated through the kidneys.

↑urea mean the kidneys are not getting rid of waste and it remains in the body.

Normal range: 7-20 mg/dL

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S/S CKD is a silent, but devastating disease. Azotemia

Uremia

↑↓urination (nocturia)

Fatigue/weakness

Nausea and vomiting

Bruising/bleeding

Uremic frost (crystals in and on skin)

Presenter
Presentation Notes
Chronic kidney disease is a slow process. Because CKD occurs over a long period of time (often years), you may not notice any symptoms until there is a significant loss of kidney function. Azotemia is the build up of toxins in bloodstream
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S/S – cont.

Loss of appetite

Edema in feet, ankles, hands, or face

Back pain

Itching

Shortness of breath (fluid can build up I lungs)

Ammonia breath or taste in the mouth

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5 Stages of CKD

Help doctors give the best treatment to patients

Each stage requires different tests and treatments

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Stage GFR Level Description

Stage 1 90 mL/min or more Healthy kidneys or kidney damage with normal or high GFR

Stage 2 60 to 89 mL/min Kidney damage and mild decrease in GFR

Stage 3 30 to 59 mL/min Moderate decrease in GFR

Stage 4 15 to 29 mL/min Severe decrease in GFR

Stage 5 Less than 15 mL/min or on dialysis

Kidney failure

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Stage 1

GFR > 90 ml/min

Kidney damage

Normal or increased function

No symptoms of damaged kidney

People aren’t usually diagnosed unless they are being tested for something else

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Stage 2

GFR 60-89 ml/min

Mild decrease in kidney function

This GFR is normal for some people

People with GFR >60 are still considered to have Chronic Kidney Disease if they have some kind of damage to their kidney

Presenter
Presentation Notes
A GFR of 60 ml/min is not that low, but because the kidney is damaged it is still considered Kidney Disease. The kidney can still sometimes keep the GFR high even if it is damaged, and it is classified as kidney disease because it can still lead to loss of kidney function.
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Stage 3

GFR 30-59 ml/min

Moderate decrease in kidney function

Uremia

Symptoms may start to develop

Presenter
Presentation Notes
At this point many people start to see a dietitian
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Stage 4

GFR 15-29 ml/min

Severe decrease in kidney function

Patients will start thinking about dialysis or transplant

Think about getting a fistula so it has time to mature

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Stage 5

Less than 15 ml/min

Kidney failure with treatment

End stage renal disease

Kidneys are unable to remove waste and fluid from the body

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Complications of CKD

Cardiovascular disease

Anemia

High blood pressure

Bone disease

Presenter
Presentation Notes
CKD can be caused by hyper tension but it can also cause high blood pressure
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Can CKD be Halted or Reversed?

Cannot be reversed

No known cure (other than kidney transplant)

Can be halted! Use preventative techniques to halt the progression.

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Prevention

Prevent and control high blood pressure

Prevent and control diabetes

Early diagnosis Routine physical examinations

Stop smoking

Decrease alcohol consumption

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Hypertension Prevention/Control

Most important thing to prevent of CKD

Maintain Healthy weight

Exercise to raise your heart rate

Reduce Sodium in diet

Take Medication Can slow rate of kidney damage by 50%!

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Diabetes prevention

Eat a healthy Diet Fiber, whole grains Fruits and vegetables

Maintain normal blood glucose levels

Exercise

Obtain and maintain healthy weight

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Prevention Programs

National Kidney Foundation’s KEEP Free screening Educational materials Designed to raise awareness

Need a better global effort

Require a lot of man power and funds

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Diabetes and Birth

Can lead to complications for the fetus as soon as the first 6-8 weeks of life CNS deformities Musculoskeletal deformities Congenital heart disease Spontaneous abortion

Large birth weights

Shoulder dystocia

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Diabetes and Birth

Large birth weight If diabetes is not controlled Baby gets high blood sugar Baby makes more insulin Stores the extra calories as fat “overfed”

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Compliance with Diabetes treatments and development of

CKD Study done showing that intensely treated diabetics were

21% less likely to have nephropathy.

Patients who more tightly control their blood sugar are less likely to have renal complications

The longer a patient is noncompliant with diabetes treatments, the greater risk he/she has of developing CKD.

Presenter
Presentation Notes
Add study about compliance with hypertension
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Quality of Life

Physical Function

Social Activity

Energy

Cognition

Emotion (anxiety, fear, denial, anger, depression, etc)

Sleep patterns-sleep apnea

Health Perception

General Life Satisfaction

Presenter
Presentation Notes
Frequently Overlooked Women are more at risk for the quality of life being reduced Fatigue is caused by anemia Psychological recovery is just as important-we feel our bodies have let us down. Denial can lead to noncompliance Important to learn of the disease to help handle fear and anxiety. Talk with someone. Sleep apnea causes hypertensions and hypertension causes Kidney Disease
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Life Expectancy

Mortality increases as kidney function decreases.

Leads to increased risk of CVD

Life expectancy of a 40- to 44-year-old white male in the general population in the US is more than 35 years.

Long Term Dialysis can add about 8 more years

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Organizations/Support Groups

Organizations National Kidney Foundation American Kidney Fund

Support Groups Renal Support Network American Association of Kidney Patients

Presenter
Presentation Notes
All are non-profit except NKF Patient run and provide non-medical services
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Medical Treatment

There is no cure to CKD, but there are ways to slow the progression of the disease: Control blood glucose Insulin therapy

Metformin

Other diabetes medications

Presenter
Presentation Notes
There are ways to stop CKD from progressing any more.
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Medical Treatment—cont.

Control blood pressure ACE inhibitors

ARBs

Diuretics

MNT Decrease protein intake

Decrease phosphorus intake Phosphorus binders

Decrease sodium intake

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Effect of diet on progression

For diabetic patients, management of their diabetes can prevent or decrease the progression of CKD.

Managing blood pressure can also help to control the progression of CKD.

Cochrane Database study found that lower protein diets reduced “renal death” by 32% in non diabetic adults

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MNT

Energy 30-35 kcal/kg IBW

Protein 0.6-1.0 g/kg IBW

Fluid Ad libitum

Sodium Variable, 2-3 g/day

Potassium Variable, usually ad libitum or increased to cover losses with diuretics

Phosphorus 0.8-1.2 g/day or 8-12 mg/kg IBW

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MNT--Protein Urine Output Percent HBV Protein

Recommendations

> 55 ml/min 60% 0.8 g/kg/day

25-55 ml/min 60% 0.8 g/kg/day

<25 ml/min 50% 0.6 g/kg/day *

*This can increase to 0.75 g/day if the patient cannot get 35 cal/kg IBW.

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MNT—Protein Excess protein in the diet

Excess ammonia in the blood

Increased stress on the kidney

More rapid kidney failure

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MDRD Study

Kidney Failure Death Kidney Failure or Death

Low protein diet (.58 g/kg/day) 90.7% 23.3% 96.1%

Very low protein diet (.28 g/kg/day with .28 g/kg/day EAA)

87.3% 38.9% 95.2%

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MNT—Sodium

Restriction of sodium to 2-3 grams/day. This may help decrease blood pressure . It may also decrease proteinuria.

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MNT--potassium

In stages I-IV CKD, potassium intake may need to be increased or decreased depending on the lab values for the specific patient.

Fruits and vegetables are generally high in potassium. The potassium content can be decreased by soaking

vegetables in water.

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MNT--Phosphorus

Phosphorus is normally excreted in the kidneys. In CKD, phosphorus can build up in the blood.

Depending on lab values, it may be necessary to decrease dietary intake of phosphorus.

High-Phosphorus Foods Dairy products Meat Nuts

Presenter
Presentation Notes
Excess phosphorus in the blood will pull calcium out of the bones. Ca3(PO3)2 will then deposit in soft tissues of the body.
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MNT—Vitamin D

When serum active vitamin D is low, PTH is secreted. This causes increases in calcium and phosphorus which can lead to calciphylaxis.

Vitamin D supplementation is still controversial.

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MNT--Carbohydrates

It is important for diabetic patients to manage their diabetes: Spread carbohydrates throughout the day. Eat at consistent times throughout the day.

Presenter
Presentation Notes
Impact of diet vs meds in controlling blood sugar
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Case Study--ET

24 YOF

Pima Indian

Dx with type 2 DM at 13 years old, poorly compliant

GFR decreasing over the past year

1 + pitting generalized edema

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Lab Values Parameter Normal Value Patient’s Value Rationale

Albumin 3.6-5.0 3.2 Albumin is being lost in the urine

Osmolality 275-295 400 Glucose is high

BUN 8-26 80 Indicates kidney dysfunction

Creatinine 0.6-1.3 1.5 Indicates kidney dysfunction

Cholesterol 140-199 443 High sat fat diet

HDL 40-85 37 High sat fat diet

LDL <130 132 High sat fat diet

Triglyceride 35-160 300 High sat fat diet

HbA1C 4.8-7.8 8.2 Glucose has been consistently too high

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PES Statement

Excessive fat intake relating to eating too many high fat foods as evidenced by 24 hour recall and high blood lipid levels (chol: 443 mg/dl, LDL: 132 mg/dl, TG: 300 mg/dl).

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Sample Diet

Pt weighs 63.6 kg

Recommended amounts:

.8 g protein/kg = 51 g

30-35 kcal/kg = 1908-2226 kcals

8-12 mg/kg phosphorus = 509-763 mg

3 g sodium restriction

Presenter
Presentation Notes
Patient is in stage
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Sample Diet

Breakfast Lunch Apple juice - Taco: Toast w/ butter ground beef, tortilla, Margarine onion, tomato, lettuce Peach - Grapes Rice krispies Milk

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Sample Diet

Dinner Penne pasta Marinara Green beans Caesar salad Romaine lettuce, croutons, tomato, dressing

Rolls with butter

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Sample Diet

Actual from Diet: Protein: 46 g Calories: 1954 kcals Phosphorus: 785 mg Sodium: 3111 mg