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RENAL DISEASE PACKETPLEASE ANSWER ALL QUESTIONS IN YOUR OWN WORDS. KEEP A CUMULATIVE LIST OF REFERENCES AT THE END OF THE PACKET AND LIST THE APPLICABLE REFERENCES NUMBERS AT THE END OF EACH SECTION.

A.) MEDICAL TERMINOLOGY

1. Fill in the blanks in the following table:

BODY PART RELATED ROOT WORD

PRIMARY FUNTION OF BODY PART

Example: Renal Pelvis pyel Collects urine produced by the kidney

the kidney

or nephron

nephr, ren organ that filters blood and waste products, concentrates and excretes urine

urine (or uric acid) -uria, urin fluid containing dissolved substances, excreted by the kidney(uric acid is a purine solute in the urine)

ureter ureter carries urine from the kidney to the bladder for excretion

urinary bladder

Also could refer to any abnormal sac with a membranous lining; a vesical, bladder or blister.

cyst, vesic urinary bladder stores urine before it is expelled from the body

A bladder is any small sac that contains liquid or gas.

urethra ureth tube that drains urine from the bladder

2. Break the following words up into their prefix, root and suffix and then provide the meaning of the word. Not all words will have all three parts.

Medical Term Prefix & Meaning

Root & Meaning Suffix & Meaning

Meaning of Medical Term

Ex: Nephrotic - nephro - kidney tic – pertaining to Pertaining to the Kidney

Uremia ure – urine or urea

emia – blood abnormal amounts of urea in the blood

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table continuedMedical Term Prefix &

MeaningRoot & Meaning Suffix &

MeaningMeaning of Medical Term

Nephrologist nephro - kidney ology – study of a specific subject

ist – one who one who specializes in the study of the kidney and/or treats related disorders

Anuria an – not, without or before

uria - urine absence of urine formation

Nephrosis nephro - kidney osis – a condition disease of the kidney

Glomerulo-nephritis

glomerulo- glomerulus, part of the nephron, filtering structure of the kidney

nephro - kidney itis – inflammation

inflammation of the glomeruli

Nephrolithiasis nephro - kidney litho - stone iasis – a condition

formation of stones in the kidney

Cystorrhagia cysto – bladder, cyst or sac

-rrhagia – excessive bleeding or discharge

bleeding or hemorrhage from the urinary bladder

Hemodialysis hemo – blood dia - through lysis – dissolving or freeing

filtering the blood through a semipermiable membrane to separate waste products

dialys – to separate

Cystectomy cyst – bladder, cyst or sac

ectomy - excision surgical excision (removal) of the bladder

Polyuria poly – many, multiply

uria - urine excessive urine excretion

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B.) Normal Renal Anatomy and Function

1. Label the parts of the kidney.

List your answers here

a. renal medulla or pyramid e. convoluted tubules, proximal and distal

b. ureter f. collecting tubule or duct

c. renal pelvis g. nephron loop, loop of Henle

d. glomerulus or Bowman’s capsule

2. In your own words, discuss the mechanism of action for the following functions of the kidneys:

NOTE: THE 3 BASIC FUNCTIONS OF THE KIDNEYS ARE BLOOD FILTRATION, BLOOD PRESSURE CONTROL AND HORMONE PRODUCTION.

a. Blood filtration, excretion and regulation of body wastes

The kidney removes waste products and extra fluid from the bloodstream by continuous filtration of blood plasma. It separates wastes from the useful substances and eliminates the wastes in the urine while returning the rest to the bloodstream.

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a.

b.

c.

e.

f.

d.

g.

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(1.)Filtering occurs in the glomerulii and tubule system of the nephrons.

(2.)Blood enters the glomerulus, which is a mass of capillaries, where water and solutes are filtered by passive perfusion based on the pressure of the blood flow. This process filters out the larger molecules like blood cells and large proteins that need to remain in the blood stream. Some substances of low molecular weight, such as calcium, iron, and thyroid hormone in the blood, are retained in the bloodstream because they are bound to plasma proteins that cannot get through the membrane.

(3.)The glomerular filtrate that is left in the tubules after filtration contains water, electrolytes, glucose, fatty acids, small amino acids, nitrogenous wastes, and vitamins. Filtrate passes through the glomerulus to the network of tubules where about 65% of the filtrate is reabsorbed into the surrounding capillaries. Solutes that are reabsorbed back into the circulatory system include sodium, chloride, bicarbonate, potassium, magnesium, phosphate, small amounts of unbound calcium, glucose, nitrogenous compounds (about 40-60% of urea in the tubular fluid is reabsorbed), amino acids, lactate, peptide hormones, small peptides, and water.

(4.)The remaining waste products, water and electrolytes move into the collecting tubules for removal in the urine. The kidneys filter about 1600 L of blood every 24 hours.

(5.)Kidneys detoxify free radicals, blood born toxins, alcohol and other drugs. Peroxisomes use molecular oxygen to oxidize organic molecules. These reactions produce hydrogen peroxide which is then used to oxidize other molecules; excess is broken down to water and oxygen by the enzyme catalase.

NOTE: Kidney infections and trauma can damage the filtration membrane and allow albumin or blood cells to filter through. Kidney disease is sometimes marked by the presences of protein or blood in the urine.

b. Regulation of blood volume, blood pressure and electrolyte balance.

(1.)Kidneys regulate blood pressure primarily by hormonal control. They also regulate the blood volume by eliminating or conserving water as needed depending on the body’s state of hydration. This happens by a constant exchange of water, ions, and other solutes across the membranes of nephron. Maintaining blood volume in normal range helps to prevent variability of blood pressure.

(2.)When blood volume drops, the kidneys secrete the enzyme renin which activates

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hormonal mechanisms that control blood pressure and electrolyte balance. Renin acts on a plasma protein, angiotensinogen, to remove a fragment called angiotensin I. In the lungs and kidneys, angiotensin-converting enzyme (ACE) removes two amino acids, converting it to angiotensin II, a hormone with multiple effects:

It constricts both the afferent and efferent arterioles. The net effect of this is to reduce glomerular filtration rate (GFR) and water loss.

Stimulates widespread vasoconstriction that raises blood pressure

It stimulates the adrenal cortex to secrete the salt-retaining hormone aldosterone. Since water follows sodium osmotically, Na+ retention pulls fluid back into the blood, promoting a higher blood volume and pressure. As sodium is conserved under the influence of high aldosterone levels, potassium is excreted into the urine.

(3.)When blood volume is low, the pituitary secretes anti-diuretic hormone (ADH), which stimulates renal tubules to reabsorb more water back into the bloodstream.

(4.)As blood volume increases, blood pressure normalizes and the pituitary releases less ADH, renal vessels increase their filtration rate to increase the production of urine.

(5.)In overhydration the release of ADH decreases and the collecting duct becomes less permeable to water. This will produce large volumes of hypotonic urine (water diuresis)

c. Acid-base regulation of body fluids

Kidneys function with the lungs to regulate the PCO2 and acid-base balance of the body fluids. Kidneys excrete acids into the urine and return bicarbonate to the blood. This “reclaimed” bicarbonate neutralizes much of the acid in body fluids.

d. Gluconeogenesis (occurs under specific condition)

In times of starvation, the kidneys can carry out gluconeogenesis. They deaminate glucogenic amino acids (remove the –NH2 group), excrete the amino group as ammonia (NH3), and synthesize glucose from the rest of the molecule.

e. Note: Hormone production is another important function but is discussed in later sections.

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Reference numbers for this section: 2, 6, 10, 11

C.) RENAL DISEASES AND CONDITIONS

1. Define the following as they relate to renal function or disease.a. Azotemia

Excess urea and nitrogenous wastes accumulate in the bloodstream.

b. Oliguria

Urine output of <30ml/hr or less than 400 ml/day

c. Hyperparathyroid

Elevated levels of parathyroid hormone (PTH). This occurs in kidney failure as a compensating (but often inadequate) mechanism to maintain levels of free calcium in the blood. If not treated it can result in renal osteodystrophy, osteomalacia, and calcification of soft tissues.

d. Glomerular filtration rate (GFR), what does it measure and how is it used

Glomerular filtration rate measures the overall level of kidney function to determine the stage of kidney disease. It can be calculated from a blood creatinine level and is expressed as ml/min/1.73m2.

Stage 1 CKD: Kidney function is slightly diminished. There is some kidney damage, with normal or possibly even increased GFR levels (greater than 90 mL/min/1.73 m2).

Stage 2 CKD: Along with kidney damage, a mild reduction in GFR is present (60-89 mL/min/1.73 m2).

Stage 3 CKD: GFR is moderately reduced (30-59 mL/min/1.73 m2).

Stage 4 CKD: A severe reduction in GFR occurs (15-29 mL/min/1.73 m2).

Stage 5 CKD: Kidney failure is established (with GFR less than 15 mL/min/1.73 m2), possibly countered with permanent renal replacement therapy (RRT).

From: http://www.endstagekidneydisease.com/

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INTERNS CHECK THIS PART OF SECTION C

For each of the following kidney diseases and conditions:

a. I am giving you the definition of the disease or condition

b. I am giving you the causes (etiologies)

c. You describe the physical changes specific to the disease process and progression (pathogenesis).

d. You explain how the disease impacts the patient’s nutritional status (in some cases there will be no impact.)

e. You tell me - is a modified diet recommended for this condition? If so what is the diet prescription?

2. Glomerulonephritis (GN)a. Definition: Condition resulting from inflammation of the capillaries of the glomeruli.

b. Etiology: Acute GN is most commonly triggered by an infectious process, often

streptococcal, but may also result from drug/toxin exposure, immunological

abnormalities, vascular or other systemic disease. Starts as an acute syndrome but if

underlying cause isn’t treated, may persist in the form of rapidly progressing

glomerulonephritis (RPGN). Chronic GN is often an autoimmune disease

c. Pathophysiology: Inflammation in the glomerular capillary walls causes scarring and

increases the permeability of the glomerular basement membrane. This decreases its

ability to filter larger molecules such as plasma proteins, WBC and erythrocytes, which

can pass into the urine. Albumin losses in the urine, cause a decrease in plasma oncotic

pressure, allowing fluid to leak into the interstitial spaces - causing edema. Protein

losses also include anti-clotting factors putting patient at risk for blood clots. The

syndrome of GN includes hematuria, proteinuria, azotemia, edema and hypertension.

If not resolved, RPGN develops, renal function declines, and serum creatinine and

azotemia levels rise.

In chronic GN, kidneys lose the ability to concentrate urine and urine output increases

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(diuretic phase). Chronic renal failure generally results. 13% of chronic kidney failure

cases are caused by GN.

d. Nutrition status: Azotemia may cause N&V resulting in poor intake, further

complicated by protein losses in the urine which increases risk of protein depletion.

Inflammation increases energy needs.

e. MNT:

Sodium restriction, 2 g/d: depending on edema and HTN

With uremia, restrict protein to 0.6 g protein/kg, >50% HBV: to slow progression of disease

30-40 kcal/kg, high carbohydrate: to spare protein. Calculation of energy needs should be based on dry weight.

Fluid restriction: based on urine output

Monitor phosphorus and potassium levels: adjust intake or medications

Supplement calcium, iron, and multivitamin if need

3. Acute Renal Failure

a. Definition: An abrupt decline in renal function with elevation of BUN and plasma

creatinine levels. Oliguria or anuria is common in the first phase, although urine

output may be normal or increased.

b. Etiology: Chronic risk factors include diabetes, heart failure, HTN, other renal disease

or damage, chronic liver disease, advancing age.

Causes may be:

prerenal (associated with alterations in the blood supply to the kidneys – hypovolemia, decreased cardiac output, obstruction of renal blood flow);

intrarenal (damage to the kidney nephrons – inflammatory, lack of blood flow within the renal tubules, toxic effect of medications or other substances); or

postrenal (obstruction to the urinary tract beyond the kidney – stones, UTI, strictures, tumor.

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c. Pathophysiology:

Prerenal: Reduction of GFR due to decreased blood flow to the kidneys. Less filtrate

(which eventually becomes urine) is produced, and what is produced moves more

slowly through the renal tubules resulting in greater resorption of sodium and water

back into the bloodstream. Decreased perfusion also initiates the renin-angiotensin-

aldosterone system, further retaining sodium and water. Urine output drops,

nitrogenous wastes cannot be excreted and build up in the blood (a condition called

azotemia).

Intrarenal or Intrinsic: Damage to the nephron and/or glomerulus lead to acute

tubular necrosis (ATN). Epithelial debris is released into the renal tubule lumen, and

along with proteins and other cells these obstruct the lumen. Pressure in the tubules

backs up to increase pressure in Bowman’s capsule (part of the glomerulus), damaging

the glomeruli and slowing GFR. Glomerular filtrate leaks back into the tissue further

decreasing perfusion. Other inflammatory byproducts also contribute to congestion of

the kidney (cytokines, WBC, platelets). Impact of decreased GFR is then the same as in

prerenal failure.

Postrenal: Bilateral obstruction of urine flow backs up to increase pressure in the

glomerulus decreasing GFR. Generally reversed by removal of the obstruction.

Phases: In acute renal failure the production of urine rapidly diminishes with the

damage to the tubules and the inability of the kidney to filter urine. This oliguric

phase, output drops to less than 500 ml/d and generally lasts 1-2 weeks. Dialysis is

usually needed during this phase to remove fluid, potassium and nitrogenous wastes. In

the diuretic phase of ARF, the kidney loses the ability to concentrate urine and

produces large quantities of dilute urine. Generally this indicates that the kidney is

recovering, and lasts 2 days to 2 weeks. Full recovery time varies. Mortality may be

as high as 50%.

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d. Nutrition status: Early in ARF patient may not be conscious. If they are, azotemia may

cause N&V resulting in poor intake. Protein needs increase due to inflammation and

tissue damage.

e. MNT: Diet prescription depends on whether patient is being dialyzed. If not:

30-40 kcal/kg, may need nutrition support if unable to take p.o.

0.6-0.8g prot/kg, increase as kidney function returns, >50% HBV.

Fluid intake based on output plus 500 ml

Sodium and potassium intake depend on phase – monitor K+ labs closely

4. Chronic Renal Failure (Chronic Kidney Disease)

a. Definition: Progressive and irreversible loss of renal function. May take months to

years to develop. GFR is less that 60 mo/min/1.73m2 for greater than 3 months

b. Etiology: Diabetes is the leading cause, uncontrolled HTN is another common cause.

CRF often results from other renal conditions, or from unresolved ARF.

c. Pathophysiology: Pathogenisis of ARF and Glomerular nephritis described above.

Either of these can progress to CRF if not effectively treated.

When the cause is diabetes, chronic hyperglycemia damages capillary basement

membranes in the glomeruli. During early stages of diabetic nephropathy, kidney

perfusion is increased resulting in the common diabetic symptom of frequent urination

and also the albumin in the urine. Eventually this hyperfiltration damages the

gloemeruli, causing thickening and hardening of the glomeruli – this causes blockage

and decreases the GFR.

With hypertension, the heart pumps harder to circulate the blood and this can damage

the kidney vessels and damage the glomeruli.

As renal insufficiency progresses (70-90% of nephrons damaged), GFR declines and

serum creatinine and BUN levels rise. Kidneys lose their ability to excrete phosphate,

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potassium and acids, and are unable to dilute urine. Hypocalcimia and

hyperphosphatemia result from abnormalities of Ca+, PO4, Vitamin D and PTH

metabolism. Anemia and acidosis are also present.

Early symptoms may be mild and include nocturia, some fatigue and anorexia. As

uremia increases there is often a decline in mental acuity. See ESRD for late stage

symptoms.

d. Nutrition status: With early, progressive loss of renal function there is little change in

nutritional status. Patients with advanced CRF are often malnourished because of the

restricted diet prior to dialysis and their lack of energy and appetite due to uremia.

Edema may further decrease intake. Anemia occurs due to the kidney’s inability to

make erythropoietin. Vitamin D and calcium status decline because the normal

feedback loop for parathyroid hormone (PTH) is impaired.

e. MNT: Early in CRF nutrition therapy focuses on slowing the progression by

controlling associated or comorbid conditions – including following diet for control of

diabetes, hypertension, and heart disease.

As GFR decreases diet therapy is recommended to slow the progression of the disease and to decrease the symptoms of uremia:

30-35 kcal/kg

0.6-.75 g prot/kg (50% high biological value)

1-3 g sodium (varies with edema)

Fluid intake based on output

10 mg/kg/d phosphorus

Monitor potassium levels, restriction may be needed

Supplement calcium, vit D, B-complex, iron and zinc

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5. End-stage Renal Disease (will discuss MNT in Nutrition Prescription section, can leave it out here.)

a. Definition: Final stage of chronic, irreversible kidney failure. Less than 10% of renal

function remains

b. Etiology: May be last stage of chronic disease or resulting from infection or acute

disease. See previous sections for etiology.

c. Pathophysiology: In ESRD the kidneys are no longer able to excrete nitrogenous

wastes, maintain fluid and electrolyte balance or produce hormones. Hypertension and

edema increase risk of heart failure. Increasing uremia causes neuromuscular

symptoms: cramps, twitching and itching. Other symptoms include anorexia, nausea

and vomiting, unpleasant taste in mouth, skin appears yellow-gray. Treatment is

required to maintain life: dialysis or transplant.

d. Nutrition status: Individuals with ESRD following chronic kidney failure are usually

malnourished due to poor intake. Nutritional status of ARF patients may be better

depending on the progression of their disease. Ongoing nutrition status of patients

with ESRD depends on the treatment.

6. Polycystic Kidney Disease

a. Definition: Loss of kidney function due to the formation of multiple fluid-filled cysts in

the kidneys.

b. Etiology: This is most commonly a genetic disease. Autosomal recessive PCK (rare)

occurs in fetuses and infants, half of whom die within a few days of birth, 25% live to

their 10th year. Autosomal dominant PCK (90% of cases) is also genetic but generally

doesn’t manifest until adulthood; symptoms usually start between ages 30 and 50.

A third type is acquired cystic kidney disease (ACKD) most typically occurs in patients

with kidney failure from other causes who have been on long term dialysis.

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c. Pathophysiology: PCK is believed to start with hyperplasia of the nephron epithelial

cells. The collecting ducts dilate and fluid filled cysts form and enlarge – disrupting

urine formation. As the disease progresses, thousands of cysts may develop and enlarge

the kidney as they fill with fluid. The cysts replace functional tissue of kidney. (A PCK

cyst-filled kidney can weigh up to 22 pounds.) Proteinuria may occur. Signs and

symptoms include back or flank pain, vomiting, hypertension, UTIs, vomiting,

hematuria, proteinuria, headaches, and gradual loss of kidney function. Cysts may

also develop on the liver. About 50% of adults with PCK will progress to kidney

failure.

d. Nutrition status: In adults, anorexia, nausea and vomiting can cause poor intake.

Urine protein and albumin losses increase risk of protein malnutrition. Failure to

thrive is common in infants and children with PCK.

e. MNT: Lifestyle modifications to control hypertension may slow the progression of the

disease. DASH diet may be beneficial but is high in potassium and phosphorus (fruits

and veg, dairy products, nuts/seeds, and whole grains)—thus the RD needs to adapt the

diet according to the kidney function and as indicated by patient lab values.

If renal failure progresses, reduction of protein intake may slow the rate of failure.

This must be adjusted to prevent protein deficiency.

Antibiotics are used for UTIs, common with PCK. In these cases, pre/probiotics may be beneficial.

For HTN: sodium restriction, modified DASH diet and limit fat/SFA, limit caffeine, weight management.

0.6-0.8 g/kg protein to slow renal failure, adjusted for protein status

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8. Renal tubular acidosis

a. Definition: Metabolic acidosis develops because kidneys don’t excrete excess acid into

the urine and/or are unable to retain adequate bicarbonate to buffer the blood.

b. Etiology: May be caused by drug or heavy metal toxicity, by autoimmune disorders,

diabetes, or obstruction. Types 1 and 2 may also be hereditary.

c. Pathophysiology: One function of the healthy kidney is to maintain acid-base balance

in the body. In renal tubular acidosis there is a defect in the ability of the renal tubule

to perform this function. There are 3 types of renal tubular acidosis, each impacting

the control mechanism differently. The signs and symptoms include muscle weakness,

fragile bones, and kidney stones. Children with this condition have growth retardation.

Type 1 is cause when the kidneys lose their ability to excrete acid. This results in high

blood acidity, dehydration, and low blood potassium.

Type 2 results when the kidneys cannot reabsorb bicarbonate from the urine filtrate.

This results in high blood acidity, dehydration, and low blood potassium.

Type 4 is caused when the kidneys no longer respond to aldosterone. This results in

moderately high blood acidity and high potassium levels. High potassium can cause

irregular heartbeats in some cases death.

(Type 3 appears to have been discontinued??)

d. There is a risk of dehydration due to the acidosis. Metabolic acidosis also increases

protein metabolism. There is also increased risk for osteoporosis. If untreated there

will be growth retardation.

Modified diet:

High potassium diet for types 1 & 2

Low potassium diet for type 4

Calcium supplements may be needed

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Reference numbers for this section: 1, 3, 4, 6, 9, 11

D.) NUTRITION RELATED TOPICS

1. Describe the process of hemodialysis and how it works. How does CAPD differ from hemodialysis?

Hemodialysis attempts to mimic the filtration function of the body. The dialysate fluid is

designed to be similar to human plasma. Over a 3-5 hour treatment time, the patient’s

blood is pumped into a dialysis machine and through a capsule of microscopic semi-

permeable membranes. This is repeated approximately three times each week. Using the

concept of diffusion and osmosis, waste products are pulled from the blood into the

dialysate. The composition of the dialysate is determined by the patient’s individual

laboratory parameters and can be adjusted to osmolality and electrolyte content.

CAPD is continuous ambulatory peritoneal dialysis. It involves artificial filtering of the

blood by transfer across the patient’s own peritoneum (a semi-permeable membrane),

utilizing a dialysis solution which is intermittently introduced into and removed from the

peritoneal cavity. The patient infuses the dialysate themselves so they do not need to be

connected to a machine. There are higher protein and amino acid losses with peritoneal

dialysis, so protein intake recommendations are higher. In general the diet is more liberal

(sodium, potassium, fluid) since dialysis is “continuous”, however some glucose is

absorbed by the body from the dialysate and this should be considered as it can increase

weight, glucose and triglyceride levels.

2. What is “dry” weight?

Dry weight (edema free weight) is the weight at which the water content of the body is

normal; no edema or swelling; and blood pressure is not too low when standing. This is the

weight a person should weigh after dialysis treatment without extra fluid. Sometimes called

“true weight” or edema free actual weight for dialysis patients. Weight gained between

treatments is referred to as fluid weight.

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3. Why would a dialysis patient be prescribed a daily water-soluble vitamin supplement instead of a regular multivitamin?

The renal diet may be inadequate in vitamins. Water-soluble vitamins are lost during the

dialysis procedure. Fat-soluble vitamins can build to unhealthy levels, especially serum

Vitamin A levels. Risk of Vitamin A toxicity is high. Vitamin K is contraindicated with

anticoagulant meds given to many dialysis patients. The form of Vitamin D from

multivitamin supplements cannot be activated in kidney failure. Regular multi’s may

contain minerals which are harmful or not bioavailable to people with kidney failure

(phosphorus, iron, etc.)

4. Discuss the causes of anemia in chronic renal failure. Are iron supplements an effective treatment? Why or why not?

Several factors cause anemia in CRF. Primarily the kidney loses its ability to produce

erythropoietin (EPO). This hormone stimulates the production of RBCs in the bone

marrow. Additionally, as uremia increases, the nitrogenous waste products in the blood

destroy existing RBCs. Finally, the hemodialysis patient loses blood due to frequent

sampling and residuals left in the dialysis tubing, about 2-5 liters of blood per year. While

iron is needed for RBC production, supplements are not effective unless given with

synthetic EPO. Oral iron supplements have been used in the past but IV iron has been

found to be more effective in combination with EPO to maintain iron stores.

5. How would a low serum albumin impact your interpretation of calcium labs and why?

Nearly half of the calcium in the blood is bound to plasma proteins, mostly albumin. Total

serum calcium measures the amount of free ionized calcium plus bound calcium. Reduced

total serum calcium can be the result of a low albumin level, caused by protein losses or

catabolism. Ionized calcium can be measured and would be a better indication of hypo or

hypercalcemia.

6. Describe the influence of dietary oxalates on urinary oxalates. Give examples of foods

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with high bioavailability of oxalate that may increase urinary oxalate excretion.

(Not related to renal failure)

Oxalate from the diet is absorbed but cannot be metabolized so it is excreted in the urine.

When oxalate concentration is high, it combines with calcium. When the urine is

supersaturated with calcium oxalate, these complexes crystallize in the kidney to form

kidney stones. Because there is more calcium than oxalate in the urine, increases in dietary

oxalate absorption may promote increase in the formation of these complexes.

The impact of dietary oxalates on urinary oxalate excretion varies; it is proposed that

some people have enhanced gut absorption of oxalates and this may promote stone

formation – this is common in inflammatory bowel diseases. It is recommended that people

with calcium oxalate kidney stones limit their intake of oxalate containing foods with high

bioavailability: spinach, rhubarb, nuts, tea (without milk), chocolate, wheat bran, nuts, and

strawberries. They should also drink plenty of water.

Reference numbers for this section: 4, 6, 9

E.) NUTRITION PRESCRIPTIONS

1. For each of the following treatments, list the nutrient recommendations in the chart. Then answer the related questions below in your own words.

Calories Protein Fluid Sodium Potas-sium

Phos-phorous

Calcium

Pre-dialysis (un-dialyzed patient in chronic renal failure)

30-35 kcal/kg IBW35 kcal/kg if <60 yrs

0.6-1.0 gm/kg IBW

Varies Varies 2-3 g/d

Varies 800-1200 mg/d

1200 g/d +

Hemo-dialysis

35 kcal/kg

1.2 g/kg IBW

750-1000 ml/day plus urine output

2-3 g/d 2-3 g/d

Usually 2 g/d

800-1200 mg/d

Not to exceed 2000/d from sup’t (7)

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Continuous Peritoneal Dialysis (CAPD)

30-35 kcal/kg35 kcal/kg if <60 yrs

1.2-1.3 g/kg* often more

Ad lib. 2000 ml/d plus urine output

2-4 g/d 3-4 g/d

Generally not restricted

800-1200 mg/d

Not to exceed 2000/d from sup’t (7)

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2. Give the rational for the protein restriction in pre-dialyzed renal failure. What would you monitor to determine the adequacy of protein intake in these patients?

Since one of the main functions of the kidney is to excrete nitrogenous wastes generated

during protein metabolism, reducing protein intake will decrease the workload on the

failing kidneys. Additionally, once the GFR is <25, reduced protein intake of 0.6-0.8 g/kg

has been shown to delay progression of kidney disease – though there is some controversy

on this benefit in the research. High biological value (HBV) protein sources with adequate

calories (35 kcal/kg/d) to spare protein allow lower dietary protein intakes. In a best case

scenario, these are adequate levels to maintain protein status; however, most patients with

renal failure have had other nutritional problems and so must be monitored for protein

deficiency, Most individual labs will be impacted by fluid retention and other aspects of

renal failure; therefore it is important that the RD follow the full clinical picture to assess

status: albumin, prealbumin, diet history, weight changes, etc. BUN is elevated when

nitrogenous wastes increase and will generally declines with controlled protein intake. If

protein malnutrition is evident the diet should be adjusted to provide protein levels closer to

the upper end of the 0.6-0.8 g/kg range.

3. Why is it recommended for patients to have at least 50% of their protein from sources that have high biological value (HBV)?

HBV protein provides all of the essential amino acids which are needed for protein

synthesis. Theoretically, there would be less nitrogenous waste produced since all of the

amino acids are used for synthesis.

4. Why are CAPD patients allowed more sodium, potassium and fluid than HD patients?

Since dialysis is continuous with CAPD there is not the risk of fluid, K+, Na+ building up

as there is with HD treatment offered every 2 or 3 days.

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5. When might CAPD patients need more protein than HD patients? Explain why.

Protein losses are greater in CAPD so the recommended intake is greater. This is because

pores in the peritoneal membrane are larger than the membranes used in hemodialysis, so

larger protein molecules can pass through the membrane. Peritonitis is a potential side

effect of CAPD treatment. Both protein needs and losses increase with peritonitis, intake of

up to 1.5 g/kg is recommended.

6. Why is fluid restricted in most hemodialysis patients? Make 4 suggestions to help patients control their fluid intake.

Level of fluid restriction depends on edema, HTN and urine output – some ESRD patients

may still have some urine output but not enough to manage without dialysis. HD patients

should not gain more than 4-5 lb (or 3-5% dry weight) between treatments. Larger gains

mean that dialysis must be more aggressive to “pull the water” out of the tissues. This

usually causes painful cramps and may also require longer dialysis.

Measure out water for the day to help keep track of intake. Pour water out of container

to account for other beverages taken.

Remember that foods that are liquid at room temp are considered liquids: popsicles,

sherbet, jello.

Freeze lemon slices and grapes to help quench thirst, use sour candy or thirst quencher

gums

Drink only when thirsty. Choose very cold beverages and ones that are less sweet.

Swish with ice water or mouthwash when thirsty – don’t swallow. Brush teeth often.

Avoid hot environments

Use lip balm to keep lips moist

Limit salty foods to help control thirst

Take pills with mealtime liquids

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Drink from small glasses or cups

7. Why is potassium a critical restriction in kidney failure?

Potassium is found in many foods. As kidney function declines, the ability to excrete

potassium is lost and this can increase blood potassium to dangerous levels. One of

potassium’s functions is to regulate muscle contraction and so it can impact the heart

muscle. If blood potassium levels rise, they may cause an irregular heartbeat, heart attack

or death.

8. List 6 commonly consumed foods or beverages that are high in potassium and suggest alternatives that are acceptable and economical substitutions in menu planning.

HIGH POTASSIUM FOOD LOWER POTASSIUM ALTERNATIVE

yogurt, milk, esp. choc milk water, tea, or decrease portion size, add calcium supplement, rice pudding made with non-dairy creamer.

bananas, most melons, oranges, fresh peaches, fresh pears, dried fruits

apples, blueberries, grapes, canned peaches or pears, cherries, grapefruit, canned pineapple, watermelon, strawberries – keep portion sizes small (1/2 c.)

orange juice, prune juice, tomato juice apple juice, pear or peach nectar

spinach, chard, beet greens lettuce, raw cabbage

tomatoes, legumes, winter squash, beets cucumber, celery, eggplant, summer squash, carrots, onions, and frozen vegetables such as broccoli, cauliflower, green beans.

potatoes, sweet potatoes rice, some pasta

salt substitutes (KCl) lemon juice, vinegar, herbs and spices

nuts, seeds, peanut butter Pretzels, rice cakes and jam

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9. List 3 potential problems resulting from an excessive sodium intake in a patient with kidney failure. Make 4 suggestions to help patients control their sodium and salt intake.

Causes thirst making fluid restriction more difficult, HTN, edema, CHF or cardiac

overload, and more difficult dialysis. Suggestions:

Don’t add salt at the table, season foods with lemon juice, vinegar, herbs and spices

Avoid or check sodium levels on processed foods, especially soups, fast foods, and many frozen dinners

Ask for no salt to be added when eating out

Replace cured meats with fresh

Avoid gravy’s and sauces

Prepare more food from scratch

Try low sodium products but check labels for added KCl if potassium is restricted

Check sodium content of medications

10 The balance between serum levels of calcium and phosphorus is difficult to maintain in patients with kidney failure, sometimes resulting in a condition called renal osteodystrophy.

Discuss the following related to this balance: a. Give 3 reasons that serum calcium levels drop with progressive kidney disease.

Vitamin D is not activated in the kidney and this decreases gut absorption of calcium

Phosphorus cannot be excreted in the urine and serum phosphate levels rise – this causes more of the free serum calcium to be bonded with phosphate

Failing kidneys don’t respond to normal PTH stimulation to retain calcium

Renal diet recommendations limit intake of dairy products, a good source of dietary calcium

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b. How does kidney failure impact the regulation of calcium-phosphate product (also known as calcium-phosphate ratio)? How might these changes lead to osteomalcia? How might they lead to tissue calcification and why is this a critical issue?

Because other mechanisms for regulating calcium levels in the kidney are not

functioning well (see above), the body relies on PTH stimulating bone resorption to

bring calcium levels up. This releases both calcium and phosphorus into the blood.

Kidneys are not excreting phosphorus, plus patients are often non-compliant with

phosphate binding medications. High phosphorus levels cause the formation of the

calcium-phosphate product. When this product reaches a level of saturation in the

blood, it precipitates out and deposits in soft tissue causing calcification and

hardening of the tissues, including the heart. Calcification in the soft tissues impedes

their function. Higher levels of bone resorption cause bone demineralization or

osteomalacia.

c. Why are phosphate binders used? What their nutrition related side effects?

Because almost all foods contain some phosphorus, it is difficult to limit in the diet.

Phosphate binders decrease absorption of phosphorus into the blood by binding it in

the bowel. They should be taken with all meals and snacks. Phosphate binders should

be aluminum free because aluminum may cause anemia and be toxic. Some contain

calcium and should be calculated into total calcium intake. Side effects include

constipation; this can often cause patients not take these medications.

d. What are the diet modifications suggested for renal osteodystrophy?

This condition increases the need for calcium and active vitamin D. Phosphorus

should be limited.

Modified diet:

1200-1600(3), or 1500-2000(7) mg calcium/day Supplement with active vitamin D if needed – monitor calcium levels, hypercalcium

may occur with active D

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Less than 800 mg phosphorus/day, add phosphate binders with meals and snacks High fiber with fluid as tolerated. (but many high fiber foods are high phosphorus)

e. Would you suggest increasing milk intake to treat low serum calcium levels in a renal

patient? Why or why not?

No. Dairy is high in potassium and phosphorus, plus must be counted in with fluid

allowance. These are nutrients that should be limited in ESRD.

f. What is calcitriol and why is it often supplemented in kidney failure. Why must the

response to calcitriol be carefully monitored?

Calcitriol is the active form of vitamin D. It is supplemented in kidney failure because

kidneys are unable to activate vitamin D from food or regular vitamin supplements.

However when taking calcitriol, absorption of calcium can increase to the point of

hypercalcemia, therefore levels must be closely monitored.

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11

.

Your patient is starting hemodialysis and has a nutrition prescription of: 35 kcal/kg, 1.2 g protein/kg, 2 g K, 1 g phosphorus, 2 g Na, 1,000 mL fluid + urine output per day; decrease saturated fat and cholesterol intake. She has approximately 200 ml urine output per day. Use a weight of 75 kg for the calculations.

Consider her typical intake; plan a sample menu to meet her nutrition prescription. Do a nutrition analysis to show that your menu meets the recommendations.

Nutrient Analysis: Calories: 2090, Protein: 91g, Potassium: 2150mg, Sodium: 2061mg , Phosphorus: 899mg, Fluid: 820ml, Saturated fat: 14g, Cholesterol: 356mg.

Reference numbers for this section: 1, 3, 4, 5, 7, 8, 9

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Typical Intake Sample Menu RecommendationBreakfast: Cold cereal (¾ c unsweetened), 2% milk (½c)

1 egg + 2 egg whites fried, , ½ cup melon cubes, 1 cup coffee with non dairy creamer

Bread (2 slices) or fried potatoes (1 med potato)

     

1 fried egg (occasionally)      

Lunch: Bologna sandwich (2 slices white bread, 2 slices bologna, mustard)

LS tuna fish with celery, oil and mayo, 2 pc white bread, lettuce

Potato chips (1 oz) 1/2 cup canned pear halves in light syrup

1 can Coke 1/2 cup 2% milkAfternoon snack - sugar cookies and sm apple

Dinner: Chopped meat (3 oz beef) Chicken stew with soaked potatoes, carrots and

onionsFried potatoes (1½ medium) 2 rolls, 1/2 c fruit jello

HS Snack: Crackers (6 saltines) and peanut butter (2 tbsp)

air popped popcorn with olive oil and herb seasoning, 1 c herb tea

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REFERENCE LIST

1. Beto, J.A., Bansal, V.K. (2004). Medical nutrition therapy in chronic kidney failure: Integrating clinical practice guidelines. Journal of the American Dietetic Association, 104(3), 404-409.

2. Copstead, L.C., and Banasik, J.L, (2005). Pathophysiology. (pp. 710-752). St.Louis, MO: Elsvier / Sauders.

3. Escott-Stump, S. (2002). Nutrition and Diagnosis Related Care. (pp.657-682). Baltimore: Lippincott Williams and Wilkins.

4. Mahan, L.K. and Escott-Stump, S. (2004). Krause’s Food Nutrition and Diet Therapy. (pp. 961-993). Philadelphia: Elsvier / Sauders.

5. McKenry, L.M. and Salerno, E. (2003). Mosby’s pharmacology in nursing. (pp.769-773). St.Louis, MO: Mosby.

6. MedicineNet (2006). Diseases and Conditions. Retreived September 18, 2006 from http://www.medicinenet.com/diseases_and_conditions/article.htm

7. National Kidney Foundation. (n.d.). Kidney Disease Outcomes Quality Initiative. Retrieved November 20, 2006 from http://www.kidney.org/professionals/kdoqi/

8. National Kidney and Urological Disease Clearinghouse. (n.d.). Dialysis. Retrieved November 20, 2006 from http://www.kidney.niddk.nih.gov/kudiseases/topics/dialysis.asp

9. Nelms, M., Sucher, K., and Long, S. (2007). Nutrition Therapy and Pathophysiology. (pp.609-646). Belmont, CA: Thomson Brooks/Cole.

10. Pathophysiology Made Incredibly Easy! (3rd ed.). (2006). Philadelphia: Lippincott Williams and Wilkins.

11. Saladin, K.S. (2007). Anatomy & Physiology: The Unity of Form and Function (4th ed.). New York: McGraw Hill

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