CHRONIC KIDNEY DISEASE STAGE 5

Submitted as partial fulfillment for the requirements of Nutrition and Diet therapy

[DATE] UNIVERSITY OF THE PHILIPPINES, LOS BANOS

[Company address]

I. INTRODUCTION

A. Concepts in Nutrition, Diet Therapy, and Organ System Concerned

Nutrition is the science that deals with food and how the body uses it. People,

like all living things, need food to live. Food supplies the energy for every action we

perform, from reading a book to running a race. Food also provides substances that the

body needs to build and repair its tissues and to regulate its organs and systems

(Worldbook, 2004)

Dietetics is the science of applying nutritional principles to the planning and

preparation of foods and regulation of the diet in relation to both health and disease

(Mosby, 1991). What we eat directly affects our health. A proper diet helps prevent

certain illnesses and aids in recovery from others. An improper or inadequate diet

increases the risk of various diseases. Other diseases may also result from poor

nutritional habits. For example, excessive intake of alcohol causes some forms of liver

disease. Obesity increases the risk of gallbladder disease and of diabetes in adults. The

risk of osteoporosis (loss of bone tissue) is higher for people-especially women-whose

intake of calcium and level of physical activity are low. On the other hand, good

nutritional habits can help prevent certain diseases (Worldbook, 2004).

Organs are a structural part of a system of the body that is composed of tissues

and cells that enable it to perform a particular function, such as the liver, spleen,

digestive organs, reproductive organs, or organs of special sense (Mosby, 1991).

The kidneys are a pair of bean-shaped organs that lie on either side of the spine

in the lower middle of the back. The main function of the kidneys is to remove waste

products and excess water from the blood. The waste products are generated from

normal metabolic processes including the breakdown of active tissues, ingested foods,

and other substances. The kidneys allow consumption of a variety of foods, drugs,

vitamins and supplements, additives, and excess fluids without worry that toxic by-

products will build up to harmful levels. The kidney also plays a major role in regulating

levels of various minerals such as calcium, sodium, and potassium in the blood

(eMedicinehealth.com)

Diseases affecting the kidneys disturb renal function in a limited number of

ways. A variety of renal diseases can result in a common type of damage to the kidney.

The origin of the disease and the portion of the organ it affects will determine the

symptoms and subsequently the treatment. Depending on the type, kidney diseases

may produce nephritic syndrome, decreased overall renal function or a combination of

the two (Krause and Mahan, 1979). Frequently prescription of appropriate dietetic

therapy is a logical way to help a patient compensate for the altered pattern of renal

excretion and regulation (Brod, 1994).

B. Importance/Significance of the Study

Because the kidneys perform so many functions for the body, kidney disease can

affect the body in a large number of different ways. The kidneys are remarkable in their

ability to compensate for problems in their function so kidney disease is usually

advanced by the time symptoms appear.

Prevention is the key before progression of symptoms appear. Diet Therapy is one

of the known ways of preventing the progression of diseases and symptoms. Proper

food will also lessen the burden of the affected organ and help in the process of

recovery. This case study is important in determining the role of Nutrition and Diet

Therapy with its application on Chronic Kidney disease.

C. Objectives

General Objective

The general objective of this study is to identify the role of nutrition in the

mechanism of the origin of the disease of the patient and its role in managing the

disease.

The specific objectives of this study are to:

1. Identify the specific causes of the Chronic Kidney Disease

2. To correlate the patients Nutritional status to his present condition

3. To provide a diet adapted to the patients disease condition

D. Limitations of the Study

This study only focuses on the dietary aspect of the patient. The exact medical

treatment was not included. The diet prescription was not available in the records

obtained.

II. METHODOLOGY

A signed letter from the director of the Institute of Human Nutrition and Food was given to

the Philippine General Hospital. Upon the approval of the PGH’s director, a case patient with

Chronic Kidney Disease was made available by ward 3. The medical records and progress notes

were obtained and an interview with the patient was conducted.

The medical records were then analyzed and data’s from the interview were correlated to

get a better understanding on the patient’s disease condition.

A Nutritional care plan was formulated providing short term and long term goals to help

delay of the progression of the disease and to prevent further complications to improve the

patient’s Nutritional status.

III. THEORETICAL CONSIDERATION

A. Disease Condition

Chronic Kidney disease is a progressive and irreversible damage of the functioning

unit of kidneys, the nephrons (Guyton and Hall, 1996). It is a pathophysiologic process

with multiple etiologies, resulting in the inexorable attrition of nephron number and

function (Brawnwald, 2001). The glomerular filtration rate (GFR), the rate at which the

kidneys form filtrate, gradually deteriorates and the kidney functions are irreversibly

impaired (Whitney, 2002). The GFR is inadequate to excrete nitrogenous waste and the

symptoms appear (Robinson, et al, 1986). The symptoms appear when almost 85

percent of renal function has already been lost (Mahan and Krause, 1979).

Due to the kidney damage, its functions are affected and many problems occur

including kidney’s ability to excrete waste products, reabsorb nutrients, maintains fluid

and electrolyte imbalance, produce hormones and perform other metabolic functions.

As the failure grows more severe and as more nephrons die, the kidney can no longer

compensate for their losses, and symptoms become apparent (Mahan and Krause,

1979).

As renal function deteriorates, nitrogen-containing waste products accumulate in

the blood and the uremic syndrome develops. Uremic syndrome is the cluster of clinical

findings associated with the build-up of nitrogen containing waste products in the

blood, which may include fatigue, diminished mental alertness, agitation, muscle

twitches, cramps. Anorexia, nausea, vomiting, inflammation of the membranes of the

mouth, unpleasant taste in the mouth, itchy skin, skin hemorrhages, gastritis, GI

bleeding, and diarrhea (Whitney, 2002).

Of the different complications of Chronic Kidney Disease, Anemia is most

pronounced in the case patient of the study. Anemia is a condition in which there is a

decrease in hemoglobin in the blood to levels below the normal range 0f 4.2

million/mm3 to 6.1 million/mm3 (Mosby, 1991). It develops early in the course of renal

failure, becomes a dominant feature as the disease progress, and contributes

significantly to the clinical symptoms of the patient (Jacobson, 1995). Gastrointestinal

disturbance like upper gastrointestinal bleeding is also present in the patient. This is due

to uremic gastritis. Uremic gastritis is the inflammation of the lining of the stomach

caused by uremia (Mosby, 1991). Metabolic acidosis is also present in the patient. It is a

common disturbance in advanced Chronic Kidney Disease (Brawnwald, 2001).

Hyperkalemia is also manifested in the patient. It is a condition in which there is an

excessive potassium in the blood (Whitney, 2002).

Kidney disease can also be acute, It is characterized by a sudden interruption of GFR

and impairment of the kidneys ability to excrete nitrogenous waste products (Krause

and Mahan, 1979).

There are also other diseases of the kidneys such as glomerulonephritis,

nephrosclerosis, and renal calculi. Glomerulonephritis is characterized by inflammation

of the capillary loops in the glomeruli of the kidneys. It can be acute or chronic.

Nephrosclerosis pertains to disorder involving the renal blood vessels, including

arteriosclerosis and hypertension (Mitchell, et al, 1976). Renal calculi or kidney stones

on another hand are formed when substances that normally dissolve in urine

precipitate. They vary in size, shape and number (Nutrition Incredibly made Easy, 2003).

B. Classification/ Types

Renal failure can be acute or chronic. In Acute Renal Failure, the nephrons suddenly

lose function and are unable to maintain homeostasis. On the other hand, Chronic Renal

Failure, the GFR drops suddenly and sharply. The GFR gradually deteriorates, and renal

function is irreversibly altered (Whitney, 2002).

Furthermore, Acute Renal Failure or Acute Kidney Disease can be categorized

depending on the cause. The types include pre-renal failure, intra-renal failure or

intrinsic or parenchymal renal failure and postrenal failure. Pre-renal failure results from

conditions that diminish blood flow to the kidneys. Examples include Hypovolemia,

Hypotension, Vasoconstriction, or inadequate cardiac output. Intra-renal failure results

from damage to the filtering structures of the kidneys, usually from acute tubular

necrosis (a disorder that cause cell death) or from nephrotoxic substances such as

certain antibiotics. Postrenal failure on one hand results from bilateral obstruction of

urine outflow, as in prostate hyperplasia or bladder outlet obstruction (Nutrition Made

Incredibly Easy, 2003).

Acute Renal Failure has three distinct phases; First is the Oliguric phase in which the

urine volume is reduced. Second is Diuretic phase characterized by large fluid and

electrolyte losses in the urine? Finally the recovery phase in which there is gradual

return to renal functions (Whitney, 2002).

Chronic Kidney Disease on one hand results from irreversible loss of large numbers

of functioning nephrons (Guyton and Hall, 1996). It can be categorized into five stages.

The first stage is when the kidney is damaged with GFR > 90 mL/min. Second stage is

when GFR reaches down to 60 to 89 mL/min. In the third stage, GFR falls to 30-59

mL/min. In the fourth stage, the kidney damage is severe and the GFR is already too low

reaching 15-29 mL/min. Finally in the Fifth stage, the GFR already falls below 15 mL/min.

In this stage, dialysis or kidney replacement is essential for the survival of the patient

(Braunwald, 2001).

Like Acute Kidney Disease, Chronic kidney disease can occur due to the damage in

the glomeruli; tubules, lower urinary tract, and renal blood vessels (Guyton and Hall,

1996).

C. Etiology

There are many causes of diseases of the kidneys, whether acute or chronic. The

specific etiology of the disease and the portion of the remaining nephrons that it affects

will determine the symptoms and the treatment of the kidney disease.

Chronic Kidney Disease can be caused by immunological, metabolic, renal vascular.

Primary tubular and congenital disorders. Infections and urinary tract obstruction can

also be the cause (Guyton and Hall, 1996).

Many types of vascular lesions can lead to renal ischemia and kidney tissue. The

most common of these are (1) atherosclerosis of the larger renal arteries, with

progressive sclerotic constriction of the vessels; (2) fibromuscular hyperplasia of one or

more of the arteries; and (3) nephrosclerosis, a common condition caused by sclerotic

lesions of the smaller arteries, arterioles, and glomeruli (Guyton and Hall, 1996). These

conditions can contribute to the progression of kidney damage to chronic kidney

disease.

Chronic Glomerular disease, such as glomerulonephritis, which affects the capillaries

in the glomeruli can also lead to chronic kidney disease (Nutrition Made Incredibky Easy,

2003). It is an inflammatory disease associated with Strptococcal infections. Acute

Glomerulonephritis, particularly if repeated infection occurs. The capillaries of the

glomeruli can be damaged because of the inflammation primarily due to the antibody-

antigen complexes that blocked the glomeruli (Mitchell, et al, 1976). Due to this, there

could be loss of glomerular function because of replacement by fibrous tissue, followed

by degeneration of the conjoined tubules (Williams, 1973) leading ultimately to Chronic

Kidney Disease.

Chronic infections, such as chronic pyelonephritis can cause CKD. (Nutrition Made

Incredibly Easy, 2003). Pyelonephritis is an injury to the renal interstitium caused by

bacterial infection especially Eschericha coli that originate from fecal contamination of

the urinary tract. This infection can lead to chronic renal failure especially when the

bacteria reach renal pelvis and medulla. This can be due to the urine with bacteria

propelled upward toward the kidneys. Once the site is reached, bacteria initiate

infection and inflammation associated with pyelonephritis.

With long-standing pyelonephritis, invasion of bacteria can further result to

progressive damage to renal tubules, glomeruli and other structures of the kidney. As a

result, large parts of functional renal tissue are lost and chronic renal failure can develop

(Guyton and Hall, 1996).

Metabolic disorder like diabetes mellitus can also cause CKD. The high blood sugar

levels can damage many systems and structures in the body including the blood vessels.

If the blood vessels are damaged due to the elevated blood sugar, they cannot carry

blood and waste products to the kidneys. Due to this, the kidneys can no longer do their

job and filter the waste products out of the body. Gradually, this can cause damage to

the glomeruli and nephropathy, the kidneys then becomes incapable of filtering enough

wastes from the blood. This damage to the glomeruli caused by the increased blood

sugar can eventually lead to renal failure (http: /www.hmc. psu.edu/healthinfo

/diabeticnephropathy. htm).

Another factor that can lead to CKD is when there is excessive pressure against the

blood vessel walls or hypertension. The blood supply to the kidneys has lowered

gradually due to the thickening of the wall and narrowing of the lumen of the blood

vessels (Mitchell, et,al, 1976). This causes injury to the blood vessels in the kidneys

which can consequently lead to CKD. The renal arteries can also harden because of

hypertension which is known as Nephrosclerosis which restricts blood flow to the

kidneys that can also progress to CKD (Nutrition Made Incredibly Easy, 2003).

Development of kidney disease can also be genetic and can run in the family. If one

member of the family has a kidney disease; most likely there is a risk for other members

of developing the same disease (http:/kidney:niddk.nih.gov/kudiseases/pubs

/chronickidneydiseases/index.htm).

D. Incidence

Based from the Phillipine Society of Nephrology and Philippine College Physicians

organization survey shows that 2.6% or approximately 1,212,306 of adult Filipinos have

CKD with stages 3 to 5. Figure 2 shows the prevalence of CKD stages 3-5 according to

age.

Figure 1. Prevalence of CKD stages 3-5 according to age

The figure above shows that most CKD occurs at ages 70 and above. Majority are

suffering from CKD stage 3. Distinct cases of CKD stage 5 are from ages 40-49. This age

group is also where the patient belongs (46). Etiology is not clear why stage 5 occurs

mostly in the age groups 40-49.

The figure below shows the top causes of End stage Renal Disease or CKD stage 5.

Figure 2. Causes and the distribution of top 3 causes of CKD stage 5.

The top cause of Renal failure in the Philippines is Diabetes Mellitus followed by

Glomerulonephritis. Hypertension is the third cause of Renal failure. The patient

acquired CKD because of Hypertension.

Overall Kidney disease is the top 10 cause of mortality in the Philippines.

E. Pathology

Kidneys perform vital functions that are essential to survival. These include

maintaining fluid and electrolyte balance, excretion of nitrogenous waste products,

production of hormone and enzymes and regulating blood pressure (Nutrition Made

Incredibly Easy, 2003).

At the first stage of chronic renal failure, there is gradual reduction of renal mass.

This stage involves the specific mechanisms to the underlying cause whether from

diabetes, hypertension, glomerulonephritis, pyelonephritis or others. But as these

progress, there is a consequent loss of renal function regardless of the cause

(Braunwald, et al, 2001). Nephrons are damaged and lost their functions. Once they are

damaged, they can no longer perform their activities. Due to this, the remaining healthy

nephrons compensate for the destroyed nephrons by enlarging and increasing their

clearance capacity. This is called structural and functional hyperthropy of the surviving

nephrons (Guyton and Hall, 1996). The mechanism is adaptive at first because it tries to

maintain kidney functions even there are lost nephrons. However, this short term

adaptation in turn proves to be maladaptive or harmful because it predisposes the

remaining nephrons to sclerosis (Braunwald, et al, 2001).

When there are loss of renal mass, even 20 to 30 percent of normal (Guyton and

Hall, 1996) the remaining nephrons increase the GFR, called-single nephron glomerular

filtration rate (SNGFR) up to three times its normal value. This mechanism enables the

body to increase the clearance of waste substances, which would otherwise accumulate

and cause toxicity because of lost nephrons (Jacobson, 1995).

The loss of renal function can reach up to 85 percent before person experiences

symptoms of uremia and renal failure (Krause and Mahan, 1979). Symptoms also appear

when the GFR is inadequate to eliminate nitrogenous waste products of protein and

amino acid metabolisms (Robinson, et, al, 1986). These symptoms become worse as the

renal failure progresses. These are also experienced in overlapping stages of chronic

renal failure (Jacobson, 1995).

In reduced renal reserve, the renal function is reduced to only 25 percent and the

GFR is 30 to 50 percent of the normal rate (Nutrition Made Incredibly Easy, 2003). At

this stage, azotemia is not yet present and acid-base, potassium, calcium and

phosphorous balances are maintained through the hyperthrophy or adaptation of the

remaining nephrons. But as the adaptation continues, the loss of renal function can

reach up to 75 percent. This stage is renal insufficiency (Jacobson, 1995). The GFR is 20

to 35 percent of the normal rate (Nutrition Made Incredibly Easy, 2003). Accumulation

of nitrogenous wastes or azotemia is already present and there is reduction in the

production of erythropoietin (Jacobson, 1995). The third stage is the renal failure in

which the GFR is reduced to 20-25 percent of the normal rate and renal function is

reduced to less than ten percent (Nutrition Made Incredibly Easy, 2003). At this stage,

azotemia is worsening as more nitrogenous wastes accumulate in the blood. A symptom

of uremia and renal failure is more pronounced. There is usually sodium and water

retention. Anemia, edema, hypertension, hypocalcemia, and acidosis appear.

Hyperkalemia may also appear (Jacobson, 1995). As more and more nephrons die, the

GFR falls less than 20 percent of the normal rate, or less than 25ml/min. The BUN may

also rise. At this stage of Chronic Renal Failure, dialysis or kidney transplantation is

necessary to sustain life (Braunwald et, al, 2001). The figure below shows the pathology

of the disease.

Figure 3. Pathology of CKD

F. Clinical Manifestations and Underlying Mechanisms

Because the kidneys perform so many functions for the body, kidney disease

can affect the body in a large number of different ways. Symptoms vary greatly. Several

different body systems may be affected. Notably, most patients have no decrease in

urine output even with very advanced chronic kidney disease. The following are the

common symptoms with the underlying mechanisms;

• Fatigue and weakness (from anemia or accumulation of waste products in the

body)

• Loss of appetite, nausea and vomiting (because of metabolic acidosis due to fall of

ammonium excretion retaining hydrogen ions)

• Swelling of the legs and puffiness around the eyes (fluid retention causes edema)

• Itching, easy bruising, and pale skin (from anemia)

• Headaches, numbness in the feet or hands (peripheral neuropathy), disturbed

sleep, altered mental status (encephalopathy from the accumulation of waste

products or uremic poisons), and restless legs syndrome

• High blood pressure, chest pain due to pericarditis (inflammation around the

heart)

• Bone pain and fractures (impaired calcium absorption because kidneys unable to

convert vitamin D to its active form. High phosphorous retention also antagonizes

calcium absorption)

• Decreased sexual interest (low estrogen in women caused by CKD)

Figure 4. Manifestations of CKD

Due largely to the disordered physiology and complex biochemical abnormalities, a

number of distinctive and well-documented clinical phenomena arise including:

metabolic acidosis, hyperkalaemia, disorders of electrolyte and fluid balance,

disturbances in amino acid and protein metabolism, disturbances in carbohydrate,

calcium and phosphate metabolism, hyperlipidaemia and etherosclerosis and anemia.

As glomerular filtration of water and electrolytes falls, homeostasis is compromised.

Sodium may initially be depleted through polyuria and excessive intake of fluid, causing

twitching, tetany and convulsions. Patients with advanced renal disease commonly

demonstrate negative nitrogen balance. Impaired protein synthesis together with

accelerated protein catabolism contributes to a poor protein status which results in a

reduction in lean body mass. Uraemic toxicity results in anorexia and poor exogenous

protein intake, which exacerbates the poor plane of protein nutrition. Proteinuria occurs

in most patients and some evidence suggests that the proteinuria may accelerate

glomerular unjury (Sadler, 1999).

Kidney failure provoked by glomerulosclerosis lead to fluid filtration deficits and

other disorders of kidney function. There is an increase in blood pressure (hypertension)

and fluid retention in the body (edema). When the kidneys are not functioning normally,

the wastes products of protein metabolism such as BUN, uric acid and creatinine, are

not excreted properly and nitrogen accumulates in the blood and tissues, causing

anorexia, nausea and vomiting, drowsiness and a general ill feeling of health (Goodhart,

1980).

IV. THE PATIENT-GENERAL INFORMATION

A. Personal Data

The patient is Julie G. Belo. A 46 year old. He was admitted in the Philippine General

Hospital’s Emergency Room for the first time last July 14,2008 for a chief complaint of

general weakness. He weighs 69 kg with a height of 170 cm.

B. Physician’s Diagnosis/ Impression

The patient was diagnosed to have a Chronic Kidney Disease Stage 5, secondary

to Hypertensive Nephrosclerosis, in Uremia with the following complications;

• Anemia

• Upper Gastro-Intestinal Bleeding (resolving)

• Hyperkalemia

• Metabolic Acidosis (resolving)

The complaint for the patient’s admission was “generalized weakness”. The

present physical examination shows that he has pale conjunctivae, pale nailbeds, and

blackish discoloration over posterior part of the tongue and a uremic breath. He has an

elevated blood pressure (180/100 mmHg).

The Creatinine and potassium was highly elevated with reference to normal

values. The complete blood count also showed that there are low levels of RBC,

Hemoglobin and Hematocrit. The patients’ Glomerular filtration rate is 2.9 mL/min per

1.73m2. The patient was told that one of his kidneys is malfunctioning and is confirmed

to be under stage 5 of Chronic Kidney Disease.

C. Medical History

1. Chief Complaint

The chief complaint was ‘Generalized Body weakness”. But two days prior to

admission, there were one episode of epistaxis (bleeding from the nose), one

episode of vomiting (coffee-ground material), progressive weakness, chills and

increased sleeping time.

2. History of Present Illness

One month prior to admission, the patient complained of gradual onset of

on and off epigastric, burning in character. Associated symptoms are nausea,

occasional vomiting of previously ingested food, progressive body weakness and

myalgia (diffuse muscle pain, usually accompanied by malaise). Symptoms persisted

until two weeks prior to admission, this time with episodes of low-grade fever and

worsening epigastric pain.

3. History of Other Illness in the Past

The patient is a known hypertensive for more than 20 years with poor

compliance with Metoprolol as “prn med” (abbreviation for pro re nata, a Latin

phrase meaning 'as needed.' The times of administration are determined by the

needs of the patient).

4. Family History

The patient’s mother was a known hypertensive. The patient was the first to

acquire the disease (CKD) in the family. There are no other heredofamilial diseases

known.

5. Personal and Social History

The patient is married with already 5 children and works as a security guard.

He is the current breadwinner of the family. The patient used to a smoker of 50-

pack years smoking history. He recently stopped a month upon onset of illness. The

patient also used to drink alcoholic beverages until intoxicated for 28 years (17-45

years of age) and stopped drinking a year ago. The patient denies illicit drug use. He

admits that his diet is mostly high fat and high salt.

D. Nutritional and Dietary History

Mr. Belo has no preferred food. But due to his job as a security guard, he wakes up

early in the morning eating cup noodles and fried foods because it requires less effort in

food preparation. He commonly consumes sardines as his typical lunch side dish

because it is cheap and fits in his budget. Even though he is hypertensive, he does not

restrict fat intake. He normally weighs around 68-70 kg and is not experiencing weight

loss.

V. TREATMENT/ MODIFICATION

A. Dietary Intervention

1. Diet Order

The patient was subjected to hemodialysis. Based on the interview, the

patient was eating a normal diet but with limited intake of potassium. There were

no exact amounts of carbohydrates, proteins, fat, and potassium indicated.

Based on the 24 hour food recall, the patient commonly consumes boiled

rice, pandesal and fried tilapia for breakfast, Sautéed mungbean and chicken tinola

for lunch and ginisang ampalaya for dinner. However, the actual intake did not meet

the patient’s requirement for his present condition

2. Principles and Rationale for the Diet

Hemodialysis was referred instead of peritoneal dialysis due to the

persistent clogging of the pericatheter due to formation of blood cloths even with

Heparinized (heparin is used therapeutically as an anticoagulant) infusions. The

Hemodialysis was performed daily until resolution of uremic symptoms and stable

blood pressure. Hemodialysis was performed 2-3 times a week with a period of 3-4

hours each session.

Commonly accepted criteria for initiating patients on maintenance dialysis

include the following;

1. Presence of uremic symptoms

2. Presence of hyperkalemia unresponsive to conservative measures

3. Persistent extracellular volume expansion despite diuretic therapy

4. Acidosis refractory to medical therapy

5. A Bleeding diathesis

6. And a creatinine clearance or estimated GFR below 10 mL/min per 1.73m2.

Since the patient manifested the criteria for dialysis written above, he was

ordered to undergo hemodialysis.

The patient was given more liberal diet compared to those patients with

renal failure who are not undergoing dialysis. The requirement for energy was

moderate to maintain the patient’s weight. Protein was also liberal as he would be

able to excrete the nitrogenous metabolite of protein metabolism. This is because

dialysis can remove the nitrogen containing waste products of protein metabolism.

In Hemodialysis, protein losses average about 5-8 grams per treatment. Potassium

was needed to be controlled since the dialysate in Hemodialysis also contains

potassium. Because a relatively large volume of blood is pumped through the

dialyzer, potassium levels can drop rapidly, and hypokalemia can follow and

interfere with heart function thus, there is a need to moderately restrict potassium

between dialysis treatments (Whitney, 2002).

3. Patient’s Acceptance, Tolerance, Perception of the Diet

The patient has a high compliance to the diet hence; the diet was more

liberated because of the dialysis treatment. The patient was also allowed to eat

other foods other than hospital foods, which were commonly delivered to the

hospital by his family members in-charge of looking over him. However, the patient

was still not able to consume the needed amount to meet his nutritional

requirement due to his present condition.

4. Nutritional support

The patient was not receiving any other nutritional support. The glucose

present in the dialysate was the only added calories to the patient’s nutrient intake.

Yet, glucose absorption in hemodialysis is only minimal (Whitney, 2002).

The patient was given with ferrous sulfate and folic acid to alleviate anemia.

Vitamin K supplementation was also given for hepatic synthesis of blood coagulation

factors against hypokalemia which is induced by hemodialysis.

B. Medical Intervention

1. Drugs Prescribed/ Given

The patient was given Erythropoetin 4000 u’ SC (subcutaneous) to stimulate

erythropoesis or RBC production (against anemia). Ferrous sulfate and folic acid (for

iron supplementation) were also given to ensure an adequate response to EPO in

patients with CKD because the demand for iron by the bone marrow frequently

exceeds the amount of iron that is immediately available for erythropoesis.

The patient was also given Clonidine (BP> 160/90) against hypertension.

There are two overall goals of therapy for hypertension in these case; to slow the

progression of the kidney disease itself, and to prevent the extrarenal complications

of high blood pressure, such as cardiovascular disease and stroke. Clonidine acts by

stimulating the alpha-adrenergic receptors in the CNS; which results in decreased

symphatetic outflow inhibiting cardioacceleration and vasoconstriction centers. It

also prevents pain transmission to the CNS by stimulating the receptors in the spinal

cord.

Sodium Polyesterene Sulfonate or Kalimate was given for treatment of

Hyperkalemia. It exchanges sodium ions in the intestine for potassium.

Amlodipine was given to inhibit the transport of calcium into myocardial

and vascular smooth muscles, resulting in inhibition of excitation-contraction

coupling and subsequent contraction.

Other medications are given such as Furosemide for increase renal

excretion of water, sodium chloride and magnesium. Vitamin K tablet for hepatic

synthesis of blood coagulation factors against hypokalemia which is induced by

hemodialysis. NaHCO3 grX for metabolic acidosis which acts as an alkalinizing agent

by releasing bicarbonate ions and Lactulose Q8 which inhibits the diffusion of

ammonia from the colon into the blood, thereby reducing blood ammonia levels.

The table below shows the drug, amount and timing of medication.

Table 1. The Amount and Timing of Drugs used for Medical Treatment. Drug Amount Timing Erythropoetin (subcutaneous)

4000 u’ Twice a week

FeSO4 + FA 1 tablet Three times a day (TID)

Amlodipine 10 mg/ 1 tab OD Once daily Clonidine SL (soda lime) 75 mg/ 1 tab Prn (depends on

patients need) NaHCO3 gr (grain) 2 tablets Thrice a day (6AM,

1PM, 8PM) Lactulose Q8 30cc Prn Furosemide 20 mg BID (twice a day) Vitamin k tab 10 mg/ 1 tab Prn Kalimate( Sodium polysterene sulfonate)

1 sachet Prn

2. Medical Treatment and Procedures

Since the patient’s kidney disease was already at the fifth stage of CKD,

dialysis was prescribed. But because the patient was not capable of peritoneal

dialysis due to persistent clogging of the pericatheter due to formation of blood

clots, Hemodialysis was prescribed. The patient was undergoing hemodialysis two to

three times a week with a session of three to four hours each. Figure 4 shows the

hemodialysis machine that will be used by the patient.

In Hemodialysis, the patient's blood is shunted from the body through a

machine for diffusion and ultrafiltration and then returned to the patient's

circulation. Hemodialysis requires access to the patient's bloodstream, a mechanism

for the transport of the blood to and from the dialyzer, and a dialyzer

(Wikipedia.org).

Dialysis works on the principles of the diffusion and osmosis of solutes and

fluid across a semi-permeable membrane. Blood flows by one side of a semi-

permeable membrane, and a dialysate or fluid flows by the opposite side. Smaller

solutes and fluid pass through the membrane. The blood flows in one direction and

the dialysate flows in the opposite. The concentrations of undesired solutes (for

example potassium, calcium, and urea) are high in the blood, but low or absent in

the dialysis solution and constant replacement of the dialysate ensures that the

concentration of undesired solutes is kept low on this side of the membrane. The

dialysis solution has levels of minerals like potassium and calcium that are similar to

their natural concentration in healthy blood. For another solute, bicarbonate,

dialysis solution level is set at a slightly higher level than in normal blood, to

encourage diffusion of bicarbonate into the blood, to neutralise the metabolic

acidosis that is often present in these patients. Figure 5 shows the illustration of

how dialysis works.

Figure 6. Hemodialysis Machine

VI. RESULTS AND EVALUATION

A. The Disease Condition

Upon admission, the patient was assessed to have a high blood pressure and

fast heart rate and respiratory rate with acidotic breathing pattern. The patient was

known to have Hypertension.

The patient experienced general weakness which progressed for a month before

admission to the hospital. He also has an unnatural paleness or absence of color in the

skin (pallor).

Figure 5. Illustration on how dialysis works

The patient was encephalopathic, drowsy, had a uremic breath and experienced

an increase in sleeping time which was all suggested as signs of uremia.

One month prior to admission, the patient experiences passage of black tarry

stools. Tarry black stools indicate a bleeding source in the upper GI tract. Episodes of

vomiting of coffee-ground material were also manifested two days prior to admission.

These were dark brown vomitus, the color and consistency of coffee grounds composed

of gastric juices and old blood and indicative of slow upper GI bleeding. The Upper

Gastrointestinal Bleeding was probably due to uremic gastritis which is the inflammation

of the lining of the stomach caused by uremia.

Pale conjunctivae and pale nail beds were also observed in the patient

associated by low hemoglobin and RBC counts. All were manifestations of an anemic

person.

The dizziness and weakness the patient felt might be the results of anemia.

Furthermore, it was rooted from the diminished production of erythropoitein by the

diseased kidneys. Blood loss in the UGIB may also have contributed to the progression

of anemia.

The causative factor for the patient’s Chronic Kidney Disease may be due to his

dietary habits and behavior. He admitted to always have a high salt and high fat diet.

This diet was also a causative factor for the patient’s hypertension. Hypertension might

also be genetic since the patient’s mother also experienced the same. Drinking alcohol

and smoking may also have contributed to Hypertension because these acts as

vasoconstrictors (constricts the blood vessels). This condition, hypertension, can be the

main contributing factor that lead to the patient’s development kidney disease. Due to

hypertension there is an excessive pressure against the blood vessel walls. The blood

supply to the kidneys has lowered gradually due to the thickening of the wall and

narrowing of the lumen of the blood vessels (Mitchell, et al, 1976). This can cause injury

to the blood vessels in the kidneys. Consequently, this can further lead to chronic kidney

disease (http:www.hmc.psu.edu). The patient’s condition, chronic kidney disease stage

5 can be secondary to hypertensive nephrosclerosis.

B. Anthropometric Results

Using Tannhausers’ Method, Desirable Body Weight (DBW) is 63 kg (see

appendix for computation). The patient’s Actual Body Weight is 69 kg which is 6 kg

excessive of his DBW. His Nutritional Status is at the high normal classification using the

Asia Pacific Classification with a Body Mass Index of 23.88.

The patient’s percent standard weight is 109.5%. The patient doesn’t have a

habit of skipping meals and makes sure that he eats regularly because of his work as a

security guard.

C. Laboratory Test Results/Biochemical Findings

Laboratory examination revealed that his Blood Urea Nitrogen (BUN) creatinine,

and potassium levels were elevated. These were the result of CKD as the kidneys no

longer able to excrete efficiently the nitrogenous waste in the blood. The RBC,

hemoglobin and hematocrit values fall below the normal values. These were probably

due to reduced erythropoesis because of deficient erythropoietin produced by the

diseased kidneys. Other laboratory examination results are within the normal range.

The BUN was 94.13 mmol/L and creatinine was 3202 umol/L which are both high

compared to the normal values of 2.60-6.48 mmol/L for BUN and 53.00-115.00 umol/L

for creatinine indicative of CKD which is accompanied by the patient’s inability to

excrete waste products.

The low levels of RBC (2.25 x 106/mm3), hemoglobin (6 g/L), and hematocrit (19%)

were indications that the patient is suffering from anemia which is a complication of

CKD. The primary cause of anemia in patients with CKD is insufficient production of

erythropoietin (EPO) by the diseased kidneys.

The potassium levels (6.9 mmol/L) also exceed the normal values (3.8- 5 mmol/L).

Potassium retention commonly occurs in people with impaired renal function.

The GFR also reflects the incapability of the patient’s kidneys with a result of 2.9

mL/min per 1.73m2 which is considered to be in a stage of kidney failure (stage 5) due to

a GFR less than 15 mL/min per 1.73m2 ( Harrison’s Principle of Internal Medicine).

The total results of the laboratory experiments confirmed that the patient is

suffering from Chronic Kidney Disease Stage 5.

Regular monitoring of the biochemical test, on a daily basis was recommended by

the doctor to evaluate the patient’s condition.

The table below shows the results of the laboratory tests with the normal values,

variance and rationale for the variance. These tests helped to confirm the patient’s

condition.

Table 3. Laboratory Examination with Elevated and Lowered Value Results. Laboratory Results

Normal Values Actual Values Variance Rationale for Variance

BUN 2.60-6.48 mmol/L

94.13 mmol/L 87.65 mmol/L or higher

Failure in kidney functions

Creatinine 53.00-115.00 umol/L

3202 umol/L 3087 umol/L or higher

Failure in kidney functions

RBC 4.3-5.9 x 106/mm3

2.25 x 106/mm3 3.65 x 106/mm3 or less

Anemia (reduced EPO roduction)

Hemoglobin 13.6-17 g/L 6 g/L 11 g/L or lower Anemia (reduced EPO roduction)

Hematocrit 39-49% 19% 30% or lower Anemia (reduced EPO roduction)

GFR <grater than 130 mL/min per 1.73m2

2.9 mL/min per 1.73m2

127.1 L/min per 1.73m2

Renal Failure (CKD stage 5)

Potassium 3.8- 5 mmol/L 6.9 mmol/L 1.9 mmol/L or higher

Hyperkalemia

Table 4. Other Laboratory Examination Results with Normal Values Laboratory Examination Normal Values Actual Values Triglyceride 10-150 mg/dL 116 mg/dL Cholesterol 150-250 mg/dL 182 mg/dL HDL Cholesterol 35-85 mg/dL 45 mg/dL LDL Cholesterol 80-210 mg/dl 114 mg/dL Calcium 8.5-10.5 mg/dL 8.7 mg/dL

These laboratory examinations were prescribed by the doctor to observe the

patient’s status and his disease condition. Blood Urea Nitrogen (BUN) creatinine, and

potassium tests were needed to check the status of the kidneys functioning. RBC,

hemoglobin and hematocrit examinations were done to monitor the patient’s condition,

the anemia as it was one of the primary manifestations of CKD.

D. Clinical Assessment

Table 5 shows the clinical signs experienced by the patient. These clinical signs

were manifested as consequences of CKD. Iron deficiency was affected by the deficient

production of erythropoietin. Because of this, erythropoiesis is affected producing less

RBC.

Table 5. Clinical Signs Present in the Patient Body parts Clinical sign Possible Nutrient

Deficiency Others

Conjunctivae pale Iron, Vitamin A Low hemoglobin/RBC Nailbeds pale Vita Iron in A Low hemoglobin/RBC Tongue (posterior)

Blackish discoloration

- Presence of infection

Mouth Uremic Breathe Riboflavin/Niacin Caused by uremia Vascular system

High blood pressure

- Caused by alcohol and smoking

Muscular system

Weakness Iron Low hemoglobin/RBC

E. Qualitative and Quantitative Analysis of the Diet

1. Typical Food Intake PTA at Home

Table 6. 24 hour Food Recall PTA at Home Time and Place Food Items Description Amount

BREAKFAST 5:30 AM (House) Instant noodles Cooked with

seasonings 1 pack or 80 gm

Rice Boiled 1 cup 12:00 PM (work place)

Sardines in tomato sauce

1 can, 3pcs sardine 3 (10x4x1/2 cm)

Rice Boiled Boiled 3 cups coke 1 bottle, 237 mL SNACK 3:00 PM (work place)

Turon 1 pc (9.5x3.5x1cm)

DINNER 8:00 PM (house) Fried liempo

Fried 2 matchbox size

oil Cooking oil 2 tsp Rice Boiled 2 cups Fried Hotdog 2 pcs oil Cooking oil 2 tsp

2. Food Intake while in the Hospital

Table 7. 24-Hour Food Recall during Confinement Time and Place Food Items Description Amount BREAKFAST 7:00 AM Rice Boiled 1 cup Pandesal 3 pcs Fried Tilapia 2 small pc oil Cooking oil 1 t LUNCH 12:00 nn Chicken Tinola Lean meat 3 slices Sautéed mungbean ½ cup cooked oil Cooking oil 1 t Rice Boiled 1 cup DINNER 6:00 PM Rice Boiled 1 cup Ginisang Ampalaya ½ cup Egg (included in

ginisang ampalaya) Boiled 1 pc

oil Cooking oil 2t

3. Quantitative Evaluation of C, P, F, Adequacy

a. Food Intake PTA

Table 8. Evaluation of Food Intake PTA Food Intake HH measure Exchange CHO PRO FAT Calories BREAKFAST Instant Noodles

1 pack 2 ex Rice 3 ex Fat 46 4 15 336

Rice 1/2 cup 1 ex 23 2 - 100 LUNCH Sardines in tomato sauce

1 can, 3pcs sardine 3 ex MF meat - 24 18 258

Rice 3 cups 6 ex Rice 138 12 - 600 Soft drink 237mL ( 1 bottle) 5 ex sugar 15 60 SNACK Banana cue 1 pc (9.5x3.5x1cm) 2 ex fruit 20 - - 80 DINNER Fried Liempo

2 matchbox size 2 ex LF meat - 16 2 82

Cooking oil 2 t 2 ex Fat - - 10 90 Rice 2 cups 4 ex rice 92 8 - 400 Hotdog 2 pcs (10x4 cm) 1 HF meat

½ Fat - -

8 -

10 2.5 144

Cooking oil 2 t 2 ex Fat - - 10 90 Total 334 74 67.5 2240

DBW= 63 kg

Height= 5’5”

PA= light

TER= 63 x 35 (method II)*

= 2205 kcal or 2200 kcal

CPF distribution (60-15-25)*

CHO= 2200 x 0.6=1323/4= 330.75 g or 330 g

PRO= 2200 x 0.15= 330/4= 82.5 or 85g

FAT= 2200 x 0.25= 550/9= 61.1 or 60 g

Diet Rx: 2200 kcal CHO330 PRO85 FAT55

CHO % Adequacy= 334/330 x 100

= 101.21%

PRO % Adequacy= 74/85 x 100

= 87.1%

FAT % Adequacy= 67.5/60 x 100

=112.5%

Energy % Adequacy= 2240/2200 x 100

= 101.18

*Method II and normal CPF distribution were used because it was assumed that the patient does not have the disease prior to admission.

b. Food Intake during Confinement

Table 9. Evaluation of Food Intake During Confinement Food Intake HH measure Exchange CHO PRO FAT CALORIES BREAKFAST Rice 1 cup 2 Ex Rice 46 4 - 200 Pandesal 3 pcs 1 Ex Rice 23 2 - 100 Fried Tilapia 2 small pc 1 Ex LF

meat - 8 1 41

oil 1 t 1 Ex Fat - - 5 45 LUNCH Chicken Tinola 3 slices 3 Ex LF

meat - 24 3 123

Sautéed mungbean ½ cup cooked 1 Ex Veg B 3 2 - 16 oil 1 t 1 Ex Fat - - 5 45 Rice 1 cup 2 Ex Rice 46 4 - 200 DINNER Rice 1 cup 2 Ex Rice 46 4 - 200 Ginisang Ampalaya ½ cup 1 Ex Veg A - - - - Egg 1 pc 1 Ex MF

meat - 8 6 86

oil 2t 2 Ex Fat - - 10 90 Total 164 56 30 946

TER= 1900 kcal

CPF (see appendix for the computation)

Diet Rx: 1900 Kcal CHO435 PRO45 FAT50

CHO % adequacy= 164/245 x 100

=66.94%

PRO % adequacy= 56/70 x 100

= 80%

FAT % adequacy= 30/55 x 100

= 54.5%

Calorie % adequacy= 946/1900 x 100

= 49.8%

4. Qualitative Evaluation of Food Intake (using NGF)

a. PTA

Table 10. Evaluation of Food Intake PTA using NGF NGF Actual Intake Variance

Rice and alternatives 5 ½- 8 cup

7.5 cups 0

Meat and alternatives 2 ¾-3 servings

3 servings 0

Egg 1 pc

0 1 deficient

Milk 1 cup

0 1 deficient

Vegetables Green and Leafy ¾ cup Others ¾ cup

0 0

¾ cup deficient ¾ cup deficient

Fruits Vitamin C rich 1 med size Others 1 med size

0 0

1 deficient 1 deficient

Fats and oil 6-8 tsp 7 tsp 0 Sugar 5-8 tsp 5 tsp 0 Water and Beverages (6-8 glasses)

7 glasses 0

The qualitative evaluation of the patient’s food intake PTA using Nutritional

Guidelines for Filipinos shows that the patient has deficient intake of milk, egg,

vegetables and fruits. The other food groups were met.

The qualitative evaluation of food intake using NGF during confinement was

not appropriate since NGF is used only to evaluate the nutritional requirements of a

healthy individual. It is not recommended to use for the evaluation of the food

intake for patients with Chronic Kidney Failure because the requirements differ.

5. Qualitative evaluation is not a practical way of evaluating the patients’ nutrient

requirement since it is not precise and accurate. Qualitative evaluation only gives

the estimate of the nutrient needs and not the actual amount of carbohydrate,

proteins and fat. On the other hand, the quantitative evaluation gives a more

precise estimation since it represents the actual excess and deficient nutrients in

figures or numbers.

6. a.) The Doctor’s prescribed diet was more of a regular diet since restriction in

nutrients and micronutrients were liberated due to dialysis treatment. The exact

amount of CHO, PRO and Fat was not inscribed in the records given by the hospital.

b.) The distribution was not known but the liberation of diet was appropriate to

meet the patient’s DBW and TER. Dialysis therapies involve the exchange of high

levels of circulating products that the kidney no longer excretes ( urea,

phosphorous, potassium, fluid, sodium, etc.)The dialysis treatment enabled the

increase in protein intake with respect to proteins with HBV and LBV and food

choices. However, the patient’s serum BUN and serum creatinine levels, uremic

symptoms and weight should be monitored.

c.) Modification of the diet was not of significance anymore since the patient is able

to eat and tolerate foods of regular consistency since the UGIB was not severe and

was resolved on the first few days of confinement.

d.) There are limitations in mineral contents which should be considered like

phosporous (< 17mEq), sodium (< 3000 mg/dL), potassium (< 2000mg /dL). Special

attention should be given to potassium since the patient suffers from hyperkalemia

and potassium levels can affect by the hemodialysis treatment. The exact level of

the minerals was not indicated in the records.

F. Nutrient-Drug Interaction

Drug therapy plays an important role in the management of many acute and

chronic diseases. In recent years, clinicians have developed a greater awareness of the

potential effects of drug therapy on nutritional status and, conversely, of the influence

of nutrition on drug effectiveness. Drug therapy may influence nutrient intake,

absorption, metabolism, or excretion; likewise, foods or their components may affect

the absorption, metabolism, and excretion of drugs.

The table below shows the drugs taken of the patient with its nutrient

interaction or its effect with respect to nutrient absorption.

Table 11. Nutrient-Drug interaction DRUG INTERACTION NaHCO3 Acts as an alkalinizing agent by releasing bicarbonate ions. Following

oral administrations, releases bicarbonate, which is capable of neutralizing gastric acid. Side effect is metabolic alkalosis

Amlodipine Inhibit the transport of calcium into myocardial and vascular smooth muscles, resulting in inhibition of excitation-contraction coupling and subsequent contraction. Side effect is headache and peripheral edema.

Clonidine Inhibits cadioacceleration and vasoconstriction. It also prevents pain transmission. Side effect is drowsiness, dry mouth and withdrawal phenomenon.

Kalimate Exchanges sodium ions for potassium. Each 1 gram is exchanged for 1 mEq potassium. Side effects are constipations and fecal impaction.

Lactulose Q8 Increases water content and softens stool. It lowers the pH of the colon, which inhibits diffusion of ammonia from the colon to the blood. Side effects are belching, cramps, abdominal distention and flatulence.

Furosemide Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tube. Side effects includes; dehydration, hychloremia, hypokalemia, hypomagnesia, myponatremia, hypovolemia and metabolic alkalosis.

Vitamin K tablets Required for hepatic synthesis of blood coagulation factors (prothrombin, VII, IX and X). Side effects rarely occur; gastric upset, rash, hemolytic anemia, allergic reaction.

Erythropoetin 4000 ‘u

Stimulates erythropoesis.

The patient was given NaHCO3 to alleviate the gastritis and metabolic acidosis he

was experiencing. Amlodipine was also given in order to prevent the development of

osteodystrophy in the patient. Clonidine was prescribed to relieve the hypertension of

the patient. Kalimate was also given to lessen the hyperkalemia. Lactulose Q8 and

furosemide were given to correct uremia. Vitamin K tablets were also given for hepatic

synthesis of blood coagulation factors against hypokalemia which is induced by

hemodialysis. Erythropoietin was also given to stimulates erythropoesis and alleviate

anemia.

VII. Nutritional Implications

Due to the disease condition of the patient, nutritional requirements of the patient

is altered. Protein allowance needs to be restricted to prevent the accumulation of

nitrogenous waste produced as by-product of protein metabolism. Energy requirement is

liberal in order to maintain the ideal body weight of the patient. Electrolytes like sodium,

potassium and phosphorus should be controlled in order to prevent its accumulation and

development of further complications.

VIII. Summary and Recommendations

A. The patient was diagnosed to have a Chronic Kidney Failure secondary to Hypertensive

Nephrosclerosis with Anemia, Hyperkalemia, Upper Gastrointestinal Bleeding and

Metabolic Acidosis.

The CKD was not genetic since it was the first case in the family history. The only

disease existing in their family was Hypertension. The patient being hypertensive gave

rise to the necrosis of the renal arterioles (hypertensive nephrosclerosis). Uncontrolled

systemic hypertension causes permanent damage to the kidneys which leads to its

failure.

Because of renal failure, there is more retention of potassium, thus

hyperkalemia is developed. Because of the high levels of potassium, it depresses the

ammonia production. Less ammonia tends to increase the acidity thus metabolic

acidosis follows. Metabolic acidosis is a common disturbance in advanced CKD wherein

the patient can still acidify the urine, but they produce less ammonia making the

environment more acidic. Generalized metabolic acidosis and uremia causes the Upper

Gastro-Intestinal Bleeding. The blood loss due to the bleeding can be a causative factor

to anemia other than the insufficient production of EPO for RBC production.

The laboratory examination results reflected the patient’s condition. CKD was

manifested by high BUN and Creatinine and the classification of Stage 5 was determined

by the very low GFR. Annemia was manifested by low RBC, Hemoglobin and Hematocrit

levels. Hyperkalemia was manifested by high potassium levels in blood.

Signs of the complications also appear. The black tarry stool and the coffee

ground vomit was an indication of UGIB while nausea and vomiting (1 month PTA)

suggested that the patient has metabolic acidosis.

Medications were given in form of drugs. Erythropoitein was given against

anemia, NaHCO against metabolic acidosis, Vitamin K tablets against hypokalemia

(induced by dialysis), kalimate against Hyperkalemia, Amlodipine for Hypertension

The patient maintains the normal BMI because he has a habit of not missing or

skipping any meal. Eating the right amount of food is essential as a security guard. Even

though the patient eats the right amount, he doesn’t eat the right type of food. The

patient (PTA) was always in a high fat and high salt diet. The patient commonly

consumes canned goods and fried foods because it requires less preparation.

The patient is now on hemodialysis and can tolerate a variety of foods provided

that BUN, creatinine, phosphorous, sodium and potassium levels are monitored. The

patient will be on hemodialysis until kidney transplant.

B. The short term recommendation of the diet. It should have enough energy and protein

to maintain the patients DBW. The diet should contain 1900 Calories, 70 g of protein,

285 g of carbohydrate and 55 g of fat. It is also advisable to avoid foods high in

cholesterol.

Two thirds of the protein must come from sources of High Biological Value

(HBV) to assure the essential amino acid requirements. The body uses the extra

Nitrogen to synthesize the essential amino acid and thus reduces the amount of urea

that must be removed. Examples of foods with HBV protein are eggs, milk, meat, fish

and poultry. The other one-third will come from proteins of Low Biological Value (LBV)

such as vegetables and rice.

There should also be restriction for phosphorous (< 1200mg) since it lowers the

calcium levels. The calcium levels should reach the required amount (1800 mg) prevent

bone diseases. If calcium cannot be supplied by foods, supplementation is allowed.

Potassium should also be monitored since hemodialysis can lower potassium

levels (causes hypokalemia).

The long term diet prescription is also the same for the short term.

C. Other Recommendations

Kidney transplant is recommended for the patient to prolong his life. However,

while on hemodialysis, regular monitoring of lab results is essential to evaluate the

patient’s condition. Liberal energy and protein should be given to the patient to

maintain his ideal body weight. Potassium and sodium should be controlled in order to

prevent its accumulation and prevent further complications. Supplementation with iron,

calcium, and vitamin K and EPO is also recommended. The amount of supplement given

(like EPO and calcium) can be adjusted to fit the required levels.

Diet counseling is also advised to instruct the patient on food choices and

behaviors appropriate for the patient’s condition. Alcohol drinking and smoking should

also be avoided in order to prevent further complications and progression of

hypertension.

IX. GLOSSARY OF MEDICAL TERMS AND ABBREIATIONS

Acidosis- an abnormal increase in hydrogen ion concentration in the body resulting from an

accumulation of an acid or the loss of a base

Acute renal failure- the sudden loss of the kidney’s ability to function

Anemia- deficiency in circulating hemoglobin, RBC, or packed cell volume

Anuria- Lack of urinary excretion

Azotemia- accumulation of nitrogenous waste substances in the body

Creatinine- a nitrogen containing substance derived from the catabolism of creatine.

CKD- Chronic Kidney Disease, inability of the kidneys to excrete wastes.

Dialysis- removal of waste from the blood through a semipermeable membrane using

principles of simple diffusion and osmosis.

Edema- Presence of abnormal amounts of fluid in the intracellular space.

End-stage renal disease- the severe stage of chronic renal failure in which dialysis or kidney

transplantation is necessary to sustain life

Erythropoietein- hormone produced by the kidneys to stimulate the bone marrow to

produce Red Blood Cells.

GFR- Glomerular Filtration Rate, the rate at which the kidneys form filtrate

Hypertension- a common, often asymptomatic disorder characterized by elevated blood

pressure persistently exceeding 140/90 mm Hg

Nephron- functional unit of the kidney consisting of a tuft of capillaries known as the

glomerulus attached to the renal tubule

Nephrotic Syndrome- a distinct cluster of symptoms caused by damage to the glomerular

capillaries.

Oliguria- scanty secretion of urine, less than 500 ml.

Sclerotic- pertaining to induration or hardening.

Renal Insufficiency- partial kidney function failure characterized by less than normal urine

excretion.

Urea- chief nitrogenous consistent of the urine; formed by liver when amino acids are

deaminized.

Uremia- the presence of excessive amounts of urea and other nitrogenous waste products

in the blood, as occurs in renal failure

X. REFERENCES/ LITERATURE CITED

Braunwald, E., et al. 2001. Harrisons principles of internal medicine. 15th ed. Vol 2

McGrawhill. USA

Brod, T. 1994. Nutritional Biochemistry. Academic Press, Inc. USA

Guyton, A.C. and J.E. Hall 1996. Textbook of Medical Physiology. 9th ed WB Saunders

company. Philadelpia

Jacobson, H.R., et al. 1995. The Principles and Practice of Nephrology. 2nd year ed. Mosby-

Year Book, Inc. USA

Krause M.V., and L.K. Mahan. 1979. Food and Nutrition Therapy. 6th ed. Web Saunders

Company. Philadelphia

Mitchell, HAS., et al,. 1976. Nutrition Health and Disease. 16th ed JB Lippincott Company.

USA

MIMS Manual

Mosby Medical Encyclopedia. 1991., Time-Warner Company

Nutrition Made Incredibly Easy. 2003. Lippincott Williams and Wilkins. USA

Whitney, et al. 2002. Understanding normal and clinical nutrition. 6th ed. MN: West

Publishing Company. USA

World Book Encyclopedia, 2003, 233 N. Michigan Avenue Chicago, World book Inc.

Internet Resources

http:/www.hmc.psu.edu/healthinfo/diabeticnephropathy.htm

http:/www.wikipedia.org

APPENDICES

APPENDIX A

NUTRITIONAL CARE PLAN

PERSONAL INFORMATION

Patients Name: Belo, Julie G.

Age: 46 years old

Sex: Male

Weight: 69 kg

Height: 170 cm

Type of activity: Light

SUBJECTIVE

The patient is 46 years old

He works as a security guard

He complains of general weakness upon admission

Has black tarry stools and coffee ground vomitus

Felt epigastric pain, nausea and vomiting one month PTA

He often eats foods high in salt and fat.

24 hour food recall shows that there is no intake of fruits and vegetables

Hypertensive for more than 20 years

Stopped smoking 1 month PTA

Drinks alcohol for 28 years (17-45 y/o), quitted last year

Peritoneal Dialysis is deferred due to persistent clogging of blood cloths in the catheter site

OBJECTIVE

Weight: 69 kg

Height: 170 cm

DBW: 63 kg

BMI: 23.88

% standard weight: 109.5%

Increased BUN: 94.13 mmol/L

Increased Creatinine: 3202 umol/L

Increased Potassium: 6.9 mmol/L

Lowered RBC, Hemoglobin, and Hematocrit: 2.25 x 106/mm3, 6 g/L and 19%

Low GFR: 2.9 mL/min per 1.73m2 (Indicative of stage 5 CKD)

Adequate 24 Hr food recall PTA; CHO % Adequacy= 101.21%, PRO % Adequacy=87.1% FAT % Adequacy=112.5%, Energy % Adequacy= 101.18%

Blood Pressure: 160/100

ASSESSMENT

Nutritional Status: Normal (Asia Pacific)

Adequate Food Intake PTA as defined by the 24-hour food recall; inadequate food intake during

confinement

Failure in kidney functions to eliminate nitrogenous waste products indicated by increased BUN

and Creatinine

Anemia might be due to poor production of EPO by the kidneys and blood loss from UGIB which

is indicated by the low RBC, Hemoglobin, and Hematocrit.

Hyperkalemia due to increased potassium retention because of the diseased kidney as shown by

the increased level in lab tests.

Metabolic acidosis due to uremia and hyperkalemia as manifested by nausea and vomiting

UGIB, might be caused by acidosis and uremia as manifested by black tarry stool and coffee

ground vomitus

Chronic Kidney Disease Stage 5 as confirmed by lab tests and low GFR.

PROBLEM LIST

Medical Nutritional • Accumulation of BUN and

Creatinine • Anemia • Hyperkalemia • Metabolic acidosis • Upper Gastro-Intestinal

Bleeding • Hypertensive

• High fat and salt diet • Long history of drinking alcohol

and smoking

PLAN

Short-term (one to two months)

Problem: Chronic Kidney Disease secondary to Hypertensive Nephrosclerosis

With: Anemia, Hyperkalemia, Upper Gastro-Intestinal Bleeding, Metabolic acidosis

Objectives: To alleviate anemia

To control potassium levels

To provide the patient a diet while in hemodialysis. (while waiting for kidney

transplantation)

To stop UGIB and metabolic acidosis

Interventions: Patient will be provided a suitable diet for his disease condition.

Diet Rx: 1900 Calories, CHO245, PRO70, FAT55 148 kcal from dialysate 1200 mg P 3000 mg Na 2000 mg K 1800 mg Ca 1500 ml Fluid

The patient will be given iron supplements and EPO to correct anemia

The patient will also be given medications to control potassium levels and lessen

UGIB and metabolic acidosis

Hemodialysis

Nutrition Education and Dietary Counseling for the patient to accept the diet

suitable for his condition; as well as ways on how to prepare more appealing

meals

Long-term (after two months)

Problem: Chronic Kidney Disease Stage 5

Objectives: To still continue on Hemodialysis while waiting for kidney transplant

To prevent development of other complications

Interventions: Patient will be provided the same diet

Diet Rx: 1900 Calories, CHO245, PRO70, FAT55 148 kcal from dialysate

Hemodialysis

Nutrition Education

MONITORING

Record Food intake

Laboratory examinations of Cretinine, BUN, Potassium, RBC, Hemoglobin and Hematocrit

Weekly Anthropometric measurement to monitor weight changes and nutritional status

Measuring Blood Pressure daily

EVALUATION

If patient has increase RBC, Hemoglobin and Hematocrit

If patient reached the required BUN and Creatinine values

If patient has controlled potassium levels

If patient has normal Blood pressure

COMPUTATIONS

Rationale for computation are taken from the REL (CRF on Hemodialysis page 26)

DBW= 170-100 -10% % std wt= (69 kg/ 63 kg) x 100= 109.5% NS= Normal

= 70- 7 BMI= 69/ 1.702= 23.88 NS= Normal

=63 kg

TER= 63 x 30= 1900 kcal

PRO= 63 x 1.1= 70 g

Non Protein Calories

PRO kcal= 70 x 4= 280 kcal

Non PRO kcal= 1900-280= 1620 kcal

CHO: 1620 x 0.7= 1134 - 148 (dialysate)= 986/ 4=246.5 or 245 g

FAT: 1620 x 0.3= 486/9= 55 g

Dialysate computation: 2L of 2.5% solution

2L x 25 g glucose= 50 g total glucose

50 g glucose x 0.80= 40 glucose absorbed

40 g x 3.7 kcal/g= 148 kcal from dialysate solution

Diet Rx: 1900 Calorie CHO245 PRO70 FAT55 148 kcal from dialysate

1200 mg P 3000 mg Na 2000 mg K 1800 mg Ca 1500 ml Fluid

Meal Planning

1. PRO: HBV = 2/3 (70)= 45 g

Food group Ex Pro Na K Ca P Fluid CHO Fat Kcal

Milk A powd 1 8 160 400 360 250 0.6 12 10 170

Meat Grp A 3 24 90 600 45 210 93 - 1 105

Lean Meat

Fish B.1 1/2 4 15 100 17.5 45 17.5 - 0.5 20.5

Egg 1 8 110 95 50 115 45 - 6 86

Total 44 375 1195 472.5 620 156.1 12 17.5 381.5

2. LBV= 1/3 (70)= 25 g

Food grp Ex Pro Na K Ca P Fluid CHO Fat Kcal

Veg grp A 2 1.2 4 120 30 30 60 3 - 16.8

Rice -

A -

B 6 24 920 240 80 140 40 138 - 648

Total 25.2 924 360 110 170 100 141 - 664.8

Total 1+2 69.2 1299 1555 582.5 790 256.1 153 17.5 1046.3

3. Fruit and sugar exchange

Food grp Ex Pro Na K Ca P Fluid CHO Fat Kcal

Fruits

A 2 0.8 6 240 20 20 96 20 - 83.2

B 3 0.6 6 180 15 15 126 30 - 122.4

Sugar 8.5 - - - - - - 42.5 - 170

Total 1.4 12 420 35 35 222 92.5 - 375.6

Total 1+2+3 70.6 1311 1975 617.5 825 478.1 245.5 17.5 1421.9

4. Fat exchange

Food grp Ex Pro Na K Ca P Fluid CHO Fat Kcal

Fat 3 0 120 6 3 3 3 - 15 135

A

B

Free foods 5 - - - - - - - 25 225

Total - 120 6 3 3 3 - 35 360

Total

1+2+3+4

70.6 1431 1981 620.5 828 481.1 245.5 57.5 1781.9*

*Add 148 kcal from dialysate (1781.9+148= 1929 kcal)

4. Salt Solution= 3000- 1431= 1569

=1569/500

=3.138 or 3T

5. Additional calcium= 1800-620.5=1179.5 mg 1 tablet

Distribution into Meals

Food Group Exchange Breakfast Snack Lunch Snack Dinner Milk A powd 1 1 Meat Grp A 3 1 1 1 Fish B1 ½ ½ Egg 1 1 Veg grp A 2 2 Rice B 6 2 2 2 Fruit A 2 1 1 Fruit B 3 2 1 Sugar( free) 8 ½ 4 4 ½ Fat A 3 1 1 1 Fat (free) 5 3 2

Diet Rx: 1900 Calorie CHO245 PRO70 FAT55 148 kcal from dialysate

1200 mg P 3000 mg Na 2000 mg K

1800 mg Ca 1500 ml Fluid

One-Day Sample Menu

FOOD EX SAMPLE MENU HOUSEHOLD MEASUREMENT

Breakfast Rice Fruit, A Milk A, powdered Egg Meat, Group A

2 1 1 1 1

Boiled Rice Ripe papaya Powdered Milk Boiled Chicken egg Grilled Chicken leg

1 cup ½ slice 4T 1pc ½ small piece

AM Snack Fruit, B Sugar

1 5

Peach Coca cola - diet

1 medium 15 T

Lunch Meat, A Veg. Group A Rice B. Fruit, A Fish B.1 Fat, A Fat, free

1 2 2 1 ½ 1 3

Fried Tenderloin sautéed togue Boiled rice Saging, Latundan Braised Tilapia Butter added as rice topping Cooking oil

1 pc 3 cm cube ½ cup cooked 1 cup 1 small 10x4 cm 1 small 12 ¾ x 4 ½ 1 t 3T

PM Snack Fruit, B

1

Crushed pineapple

3 T

Sugar, free

2 2 ½

Nara de coco Ubedol

4 T ¾ bar

Dinner Meat, a Rice B Fat A Fat, free

1 2 1 2

Grilled Pigi, ham Sinangag na kanin Margarine added to fried rice Cooking oil

1 pc 3 cm cube 1 cup 1 t 2 t

Foods to be Avoided or Restricted

Vegetables: Legumes, pickled vegetables, salt fermented vegetables like burong

mustasa, sauerkraut kimchi; canned and frozen vegetables if sodium is restricted.

Fruit: Maraschino cherries, candies fruits, dried fruits

Milk: in excess of allowance; commercial foods with milk, condensed milk, malted milk,

milk mixes, sherbet, chocolate, cocoa.

Rice: Commercially prepared desserts, mixes, and pastries; potato chips, pretzels,

instant noodles, cookies and sweets made with nuts.

Meat or substitute: in excess of allowance; nuts, seeds and beans

Fat: coconuts, other nuts in allowed amounts

Sugar and sweets: except those with chocolates and nuts

Dessert: those with milk, eggs and cereals in allowed amounts, such as ice cream,

custard pudding; cakes, cookies, bibingka, etc: cocoa, chocolates, nuts