This document provides information about chronic kidney disease stage 5. It discusses concepts in nutrition, diet therapy, and the kidneys as an organ system. Chronic kidney disease results from damage to the nephrons in the kidneys, reducing their ability to filter waste from the blood. This patient has chronic kidney disease stage 5 caused by hypertension, resulting in several complications including anemia, gastrointestinal issues, metabolic acidosis, and hyperkalemia. The document outlines the pathology and progression of chronic kidney disease.

1. 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]

2. 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)

3. 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

4. 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).

5. 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

6. 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

7. 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

8. 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).

9. 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.

10. 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

11. 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

12. 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

13. 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)

14. 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)

15. 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

16. 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.

17. 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

18. 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).

19. 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

20. 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

21. 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.

22. 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

23. 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.

24. 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.

25. 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

26. 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

27. 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

28. 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

29. 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

30. 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

31. 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.

32. 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

33. 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

34. 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

35. 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.

36. 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.

37. 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

38. 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

39. 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

40. 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.

41.  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.

42.  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

43.  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

44. 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

45. 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

46. 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

47. 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