PRELIMINARY REPORT

CHRONIC KIDNEY DISEASE (CKD) CASE

IN THE ASTER ROOM OF THE BLUD HOSPITAL OF BANJAR CITY
Compiled to Fulfill One of the Clinical Practice Assignments for Basic Nursing Courses

by :
Azizah Rahmah
P20620523011
2A

BACHELOR OF APPLIED NURSING AND NURSING PROFESSIONAL

EDUCATION
MINISTRY OF HEALTH POLICE OF HEALTH, TASIKMALAYA
2024
 CHAPTER I
LITERATURE REVIEW
A. Anatomy and Physiology of the Urinary System
The urinary system or urinary system, is a system where the blood filtration process occurs
so that the blood is free from substances that are not used by the body and absorbs
substances that are still used by the body. Substances that are not used by the body dissolve
in water and are excreted in the form of urine.
The urinary system consists of:
1. Kidney
The kidney is an organ located in the retroperitoneal on the abdominal wall on the right
and left of the vertebral column at the level of the T12 vertebra to L3. The right kidney
is located lower than the left because of the large liver lobe. The kidney is wrapped by
three layers of tissue. The deepest tissue is the renal capsule, the tissue in the second
layer is adipose and the outermost tissue is the renal fascia. These three layers of tissue
function as protection from trauma and fix the kidney.

Source :(Francisco, 2013)

The kidneys are located in the back of the abdominal cavity behind the peritoneum on
both sides of the third lumbar vertebra, and are attached directly to the abdominal wall.
Its shape is like a red bean seed (kara/ercis), there are 2 left and right, the left kidney
is larger than the right kidney. In adults, the weight of the kidney is ± 200 grams. And
in general, male kidneys are longer than female kidneys. The smallest structural and
functional unit of the kidney is called a nephron. Each nephron consists of vascular
and tubular components. The vascular component consists of blood vessels, namely
the glomerulus and peritubular capillaries that surround the tubules. In the tubular
component there is a Bowman's capsule, as well as tubules, namely the proximal
convoluted tubule, distal convoluted tubule, collecting tubule and Henle's loop found
in the medulla.

a. Parts of the Kidney

 1) Renal Cortex
In the kidney skin there is a part that is responsible for carrying out blood
filtration called the nephron. In this blood filtration place, there are many blood
capillaries that are arranged in clumps called glomeruli. Each glomerulus is
surrounded by a Bowman's capsule, and the combination of the glomerulus
and the Bowman's capsule is called the Malpighian corpuscle. Blood filtration
occurs in the Malpighian corpuscle, which is between the glomerulus and the
Bowman's capsule. Substances dissolved in the blood will enter the Bowman's
capsule. From here, these substances will go to the vessels which are a
continuation of the Bowman's capsule found in the renal marrow.
2) Renal Marrow (Medulla)
The renal medulla consists of several cone-shaped bodies called renal
pyramids. With their bases facing the cortex and their peaks called the apex or
renal papilla, pointing towards the inside of the kidney. One pyramid with
cortical tissue inside is called a renal lobe. Pyramids between 8 and 18 appear
striped because they consist of parallel channel bundles (tubules and collecting
ducts). Between the pyramids there is cortical tissue called the renal column.
In this section, thousands of fine vessels are gathered which are a continuation
of the Bowman's capsule. In these fine vessels, urine is transported which is
the result of blood filtration in the Malpighian corpuscle, after undergoing
various processes.
3) Renal Cavity (Renal Pelvis)
The renal pelvis is the end of the ureter that originates in the kidney, shaped
like a wide funnel. Before it borders the renal tissue, the renal pelvis branches
into two or three branches called major calyces, each of which branches into
several minor calyces that directly cover the renal papilla of the pyramid.
These minor calyces collect urine that continues to flow out of the papilla.
From the minor calyces, urine enters the major calyces, to the renal pelvis to
the ureter, until it is collected in the urinary bladder (vesicle urinaria).

b. Kidney Function
1) Excreting metabolic waste substances containing nitrogen, for example
ammonia.
2) Excreting substances that are excessive (e.g. sugar and vitamins) and harmful
(e.g. drugs, bacteria and dyes).
3) Regulates water and salt balance by osmoregulation.
4) Regulates blood pressure in the arteries by removing excess acid or base.

c. Kidney Circulation and Nerves

1) Blood circulation
The kidneys receive blood from the abdominal aorta which has branches of the
renal arteries, which are paired left and right and branch into interlobar arteries
then into aqueous arteries, the interlobular arteries which are on the edge of
the kidneys branch into capillaries forming a lump called the glomerulus and
are surrounded by a tool called the Bowman's capsule, in which the first spasm
 occurs and the blood capillaries that leave the Bowman's capsule then become
the renal veins entering the inferior vena cava.

2) Kidney Innervation
The kidneys are innervated by the renal plexus (vasomotor). This nerve
functions to regulate the amount of blood entering the kidneys. This nerve runs
along with the blood vessels entering the kidneys. The adrenal glands are
located above the kidneys, which are blind glands that produce 2 (two) types
of hormones, namely adrenaline and cortisone.

2. Ureter
Consisting of 2 tubes, each connected from the kidney to the bladder (vesica urinaria)
with a length of ± 25 - 30 cm with a cross section of ± 0.5 cm. The ureter is partly
located in the abdominal cavity and partly in the pelvic cavity. The layers of the ureter
wall consist of:
a. Outer wall of connective tissue (fibrous tissue)
b. Middle layer of smooth muscle
c. The inner layer of the mucous layer
The layers of the ureter wall produce peristaltic movements every 5 minutes which will
push urine into the bladder (vesica urinaria).
Peristaltic movements propel urine through the ureters which is excreted by the
kidneys and sprayed in the form of a jet, through the urethral ostium into the bladder.
The ureter runs almost vertically downward along the fascia of the psoas muscle and
is covered by the pedtodinium. Narrowing of the ureter occurs where the ureter leaves
the renal pelvis, the surrounding blood vessels, nerves and vessels have sensory nerves.

3. Vesica Urinaria (Urinary Bladder)

The bladder can expand and contract like a rubber balloon, located behind the pubic
symphysis in the pelvic cavity. The bladder is cone-shaped and surrounded by strong
muscles, connected to the middle umbilical ligament. The urinary bladder consists of:
a. Fundus, which is the part facing backwards and downwards, this part is separated
from the rectum by the rectosivic space which is filled with connective tissue of
the ductus deferent, seminal vesicles and prostate.
b. Corpus, which is the part between the vertex and fundus.
c. Vertex, the part that advances towards the front and is connected to the umbilical
vesicle ligament.
The bladder wall consists of several layers, namely, the peritoneum (outer layer), tunica
muscularis, tunica submucosa, and mucosa (inner layer).

4. Urethra
The urethra is a narrow tube that originates from the bladder and functions to channel
urine out.
 In men, the urethra winds through the middle of the prostate and then penetrates the
fibrous layer that penetrates the pubic bone to the penis, its length is ± 20 cm. The
urethra in men consists of:
a. Prostrate Urethra
b. Membranous urethra
c. Cavernous urethra
The layers of the male urethra consist of the mucosal layer (the innermost layer), and
the submucosal layer. The urethra in women is located behind the pubic symphysis,
running slightly upwards, its length is ± 3 - 4 cm. The layers of the urethra in women
consist of the Tunica muscularis (outer), the spongeous layer is a plexus of veins, and
the mucosal layer (inner layer). The opening of the urethra in women is located above
the vagina (between the clitoris and vagina) and the urethra here is only an excretory
channel.

B. Definition of CKD
Chronic Kidney Disease (CKD) is a progressive and irreversible decline in kidney function
where there is a failure of the body's ability to maintain metabolic balance, electrolyte
fluids resulting in uremia or azotemia. CKD is a clinical syndrome caused by a decline in
kidney function that is chronic, progressive and quite advanced. (Suparyanto and Rosad
(2015, 2020b).
Chronic kidney disease (CKD) is defined as kidney damage for at least 3 months with or
without decreased glomerular filtration rate (GFR) (Nahas & Levin, 2010). Chronic kidney
failure is a process of progressive decline in kidney function and generally at some level
requires permanent kidney replacement therapy in the form of dialysis and kidney
transplantation (Aru A. Sudoyo, 2006).
CKD or chronic kidney failure (CKD) is defined as a condition in which the kidneys
experience a slow, progressive, irreversible and insidious decline in function, where the
body's ability to maintain metabolism, fluid and electrolyte balance fails, resulting in
uremia or azotemia (Smeltzer, 2009).
Based on the above understanding, it can be concluded that CKD is a kidney disease that
can no longer be cured or completely healed as before. CKD is an end-stage kidney disease
that can be caused by various things. Where the body's ability fails to maintain metabolism
and electrolyte fluid balance, which causes uremia.

C. Classification
Chronic kidney failure is divided into 3 stages:
a. Stage 1: decreased renal reserve, at this stage serum creatinine levels are normal and
the patient is asymptomatic.
b. Stage 2: renal insufficiency, where more than 75% of the tissue has been damaged,
Blood Urea Nitrogen (BUN) is increased, and serum creatinine is increased.
c. Stage 3: end-stage renal failure or uremia.
 K/DOQI recommends dividing CKD based on the stage of LFG decline:
a. Stage 1: kidney disorder characterized by persistent albuminuria and normal LFG (>
90 ml / minute / 1.73 m2)
b. Stage 2: Kidney disorder with persistent albuminuria and LFG between 60-89
mL/minute/1.73 m2
c. Stage 3: kidney disorder with LFG between 30-59 mL/minute/1.73m2
d. Stage 4: kidney disorder with LFG between 15-29mL/minute/1.73m2
e. Stage 5: kidney disorder with LFG < 15mL/minute/1.73m2 or terminal renal failure.
D. Etiology
Chronic kidney failure can arise from almost any disease. Whatever the cause, it can cause
progressive deterioration of kidney function. Below are some causes of chronic kidney
failure.
a. High blood pressure
Long-term hypertension can cause structural changes in arterioles throughout the
body, characterized by fibrosis and hyalinization (sclerosis) in the walls of blood
vessels. The main target organs of this organ are the heart, brain, kidneys and eyes. In
the kidneys, it is due to renal atherosclerosis due to long-term hypertension causing
nephrosclerosis beginning. This disorder is a direct result of renal ischemia. The
kidneys shrink, usually symmetrical and have holes and granular surfaces.
Histologically, the essential lesion is sclerosis of small arteries and arterioles, most
evident in the efferent arterioles. Blockage of arteries and arterioles will cause
glomerular damage and tubular atrophy, so that all nephrons are damaged (Price,
2005:933).
b. Glomerulonephritis
Glomerulonephritis occurs due to inflammation of the glomerulus caused by the
deposition of antigen antibody complexes. The inflammatory reaction in the
glomerulus causes complement activation, resulting in increased blood flow and
increased glomerular capillary permeability and glomerular filtration. Plasma proteins
and red blood cells leak through the glomerulus. Glomerulonephritis is divided into
two, namely:
1) Acute glomerulonephritis
Acute glomerulonephritis is a sudden inflammation of the glomeruli.
2) Chronic Glomerulonephritis
Chronic glomerulonephritis is a long-term inflammation of the glomerular
cells.(Price, 2005. 924).

c. Systemic Lupus Erythematosus (SLE)

Lupus nephritis is caused by circulating immune complexes that become trapped in
the glomerular basement membrane and cause damage. The earliest changes often
involve only part of the glomerular tuft or only a few scattered glomeruli. (Price,
2005:925)
d. Polycystic Kidney Disease
Polycystic kidney disease (PKD) is characterized by multiple, bilateral, and expanding
cysts that gradually disrupt and destroy normal kidney parenchyma due to pressure.
 Over time, the kidneys are unable to maintain kidney function, so that the kidneys will
become damaged (GGK) (Price, 2005:937)
e. Pyelonephritis
Pyelonephritis is an infection that occurs in the kidney itself. Pyelonephritis itself can
be acute or chronic. Acute pyelonephritis can also occur through hematogenous
infection. Chronic pyelonephritis can occur due to repeated infections and is usually
found in individuals who have stones, other obstructions, or vesicoureteral reflux.
(Price, 2005: 938)
f. Diabetes mellitus
Diabetes mellitus is the single most common cause of ESRD, accounting for 30% to
40% of all cases. Diabetes mellitus attacks the structure and function of the kidneys
in the form of. Diabetic nephropathy is a term that includes all lesions that occur in
the kidneys in diabetes mellitus (Price, 2005:941). The history of diabetic nephropathy
from onset to ESRD can be divided into five phases or stages:
1) Stage 1 (early functional change phase) is characterized by renal hypertrophy and
hyperventilation, at this stage there is often an increase in GFR caused by many
factors, namely, high blood sugar levels, abnormal glucagon, growth hormone,
the effects of renin, angiotensin II and prostaglandins.
2) Stage 2 (early structural change phase) is characterized by thickening of the
glomerular capillary basement membrane and gradual accumulation of mesangial
matrix.
3) Stage 3 (Incipient nephropathy)
4) Stage 4 (clinical or persistent nephropathy)
5) Stage 5 (Progressive renal insufficiency or failure)

E. Pathophysiology
When kidney failure occurs, some nephrons (including glomeruli and tubules) are thought
to be intact while others are damaged (intact nephron hypothesis). Intact nephrons
hypertrophy and produce increased filtration volume accompanied by reabsorption even
in a state of decreased GFR / filtering capacity. This adaptive method allows the kidneys
to function until ¾ of the nephrons are damaged. The burden of material that must be
dissolved becomes greater than that which can be reabsorbed resulting in osmotic diuresis
accompanied by polyuria and thirst. Furthermore, because the number of damaged
nephrons increases, oliguria occurs accompanied by retention of waste products. The point
at which symptoms in patients become more obvious and typical symptoms of kidney
failure appear when approximately 80% - 90% of kidney function has been lost. At this
level of renal function, the creatinine clearance value drops to 15 ml / minute or lower.
Renal function decreases, the end products of protein metabolism (which are normally
excreted in the urine) accumulate in the blood. Uremia occurs and affects every system of
the body. The more waste products accumulate, the heavier it will be. (Brunner and
Suddarth. 2002. Medical-Surgical Nursing Vol 2: 1448)
1. Renal Clearance Disorders
 Many problems arise in kidney failure as a result of a decrease in the number of
functioning glomeruli, which causes decreased clearance of blood substances that are
actually cleared by the kidneys.
Decreased glomerular filtration rate (GFR)can be detected by obtaining a 24-hour
urine for creatinine clearance. According to glomerular filtration (due to glomerular
dysfunction) creatinine clearance will decrease and creatinine levels will increase. In
addition, blood urea nitrogen (BUN) levels are usually increased. Serum creatinine is
the most sensitive indicator of function because this substance is constantly produced
by the body. BUN is affected not only by renal disease, but also by dietary protein
intake, catabolism (tissue and RBC injury), and medications such as steroids.
2. Fluid and Urea Retention
The kidneys are also unable to concentrate or dilute urine normally in end-stage renal
disease; appropriate renal responses to changes in daily fluid and electrolyte intake are
absent. Patients often retain sodium and fluid, increasing the risk of edema, congestive
heart failure, and hypertension. Hypertension may also occur as a result of activation
of the renin-angiotensin axis and their combined effects on aldosterone secretion.
Other patients have a tendency to lose salt, leading to the risk of hypotension and
hypovolemia. Episodes of vomiting and diarrhea cause water and sodium depletion,
further worsening the uremic state.
3. Acidosis
As renal disease progresses, metabolic acidosis occurs as the kidneys are unable to
excrete excess acid load (H+). The decrease in acid secretion is mainly due to the
inability of the renal tubules to secrete ammonia (NH3‾) and absorb sodium
bicarbonate (HCO3). Decreased excretion of phosphate and other organic acids also
occurs.
4. Anemia
As a result of inadequate erythropoietin production, shortened red blood cell lifespan,
nutritional deficiencies and a tendency to bleed due to the patient's uremic status,
especially from the gastrointestinal tract. In renal failure, erythropoietin production
decreases and severe anemia occurs, accompanied by fatigue, angina and shortness of
breath.
5. Calcium and Phosphate Imbalance
The main abnormality in chronic renal failure is the disturbance of calcium and
phosphate metabolism. Serum calcium and phosphate levels in the body have a
reciprocal relationship, if one increases, the other decreases. With decreased filtration
through the renal glomerulus, there is an increase in serum phosphate levels and
conversely a decrease in serum calcium levels. Decreased serum calcium levels cause
parathormone secretion from the parathyroid glands. However, in renal failure the
body does not respond normally to increased parathormone secretion and results in
changes in bone and bone disease. In addition, the active metabolite of vitamin D (1,25-
dehydrocholecalciferol) which is normally made in the kidneys decreases.
6. Uremic Bone Disease
Often called Renal osteodystrophy, it results from complex changes in calcium,
phosphate, and parathormone balance. The rate of decline in renal function and the
development of chronic renal failure are related to the underlying disorder, urinary
protein excretion, and the presence of hypertension. Patients who excrete significant
 amounts of protein or have elevated blood pressure tend to deteriorate more rapidly
than those without these conditions.

F. Clinical Manifestations
According to (Fabiana Meijon Fadul, 2019) clinical manifestations of CKD patients
include: hypertension, (due to fluid and sodium retention from the activity of the renin-
angiotensin aldosterone system), congestive heart failure and pulmonary edema (due to
excessive fluid) and pericarditis (due to irritation of the pericardial lining by toxins,
pruritis, anorexia, nausea, vomiting, and hiccups, changes in level of consciousness,
inability to concentrate). According to (Wijayanti, 2021) clinical manifestations of CKD
(Chronic kidney disease) are as follows:
1. Cardiovascular disorders. Hypertension, chest pain, and shortness of breath due to
pericarditis, pericardial effusion and heart failure due to fluid retention, heart rhythm
disturbances and edema.
2. Pulmonary disorders. Shallow breathing, Kussmaul, cough with thick sputum and
ripples. Anemia caused by reduced production of erythropoietin, so that the
stimulation of erythropoiesis in the bone marrow is reduced, hemolysis due to reduced
life span of erythrocytes in toxic uremia, thrombosis and thrombocytopenia can also
occur.
3. Gastrointestinal disorders. Anorexia, nausea, and vomiting related to intestinal protein
metabolism, gastrointestinal bleeding, oral ulceration and bleeding, ammonia odor in
the breath.
4. Musculoskeletal disorders. Resilient leg syndrome (sore legs so they always have to
be moved), Burning feet syndrome (tingling and burning sensation, especially in the
soles of the feet), tremors, myopathy (weakness and hypertrophy of the muscles of the
extremities)
5. Integumentary disorders. Pale skin due to anemia and yellowish due to urochrome
accumulation, itching due to toxicity, thin and brittle nails.
6. Endocrine disorders. Sexual disorders: decreased libido, fertility and erection,
menstrual disorders and amenorrhea. Glucose metabolic disorders, fat and vitamin D
metabolic disorders.
7. Electrolyte fluid and acid-base balance disorders. Usually there is salt and water
retention, but there can also be sodium and water loss.
8. Hematology system. Anemia caused by reduced erythropoietin production, so that
erythropoietin stimulation in the bone marrow is reduced, thrombosis and
thrombocytopenia can also occur. Pathway
 G. Pathway

CKD

Glomerular damage Tubular damage Decreased

erythropoietin
production
Increased capillary Disorders of
permeability absorption, secretion, Decreased spinal cord
excretion function function

Protein Loss
Accumulation of toxic
Decreased red blood
metabolites
Hypoalbumine cell production
(phosphate, hydrogen,
mia urea, creatinine)
Oncotic pressure
Anemia
Uremia
hypovolemia

On GI On neuromuscular
Na & air retention
v
Acid imbalance Irritation of the pain-
disorders sensing nerves
Excess fluid volume

Muscle pain
Gastric irritation

Stomach acid rises Acute pain

Nausea Nausea, vomiting

Nutritional deficiencies less than body

requirements
H. Supporting investigation
1. Laboratory :
Erythrocyte Sedimentation Rate: Elevated, exacerbated by anemia and
hypoalbuminemia. Normocytic normochromic anemia, and low reticulocyte count.
Urea and creatinine: Increased, usually the ratio between urea and creatinine is
approximately 20:1. The ratio increases due to gastrointestinal bleeding, fever,
extensive burns, steroid treatment, and urinary tract obstruction. This ratio
decreases when urea is smaller than creatinine, on a low protein diet, and a
decreased Creatinine Clearance test.
Hyponatremia: Usually due to excess fluid. Hyperkalemia: Usually occurs in
advanced renal failure along with decreased diuresis.
Hypokalemia and hyperphosphatemia: occur due to reduced synthesis of vitamin
D3 in CKD.
Alkaline phosphate: increased due to bone metabolism disorders, especially bone
leachate phosphatase isoenzymes.
Hypoalbuminemia and hypocholesterolemia: generally caused by metabolic
disorders and low protein diets.
Elevated blood sugar, due to impaired carbohydrate metabolism in kidney failure
(resistance to the effects of insulin on peripheral tissues).
Hypertriglyceridemia, due to disorders of fat metabolism, is caused by increased
insulin hormone and decreased lipoprotein lipase.
Metabolic acidosis with respiratory compensation shows decreased pH, decreased
BE, decreased CO3, decreased PCO2, all caused by retention of organic acids in
renal failure.
2. Radiology
Plain abdominal X-ray to assess the shape and size of the kidneys (presence of
stones or obstruction). Dehydration due to the diagnostic process will worsen the
condition of the kidneys, therefore the patient is expected not to fast.
3. Intravenous Pyelography (IVP)
To assess the pelvicalysis system and ureters.
4. USG
To assess the size and shape of the kidneys, thickness of the renal parenchyma,
density of the renal parenchyma, anatomy of the pelvicalyceal system, proximal
ureter, bladder and prostate.
5. ECG
To check for possible left ventricular hypertrophy, signs of pericarditis,
arrhythmias, electrolyte disturbances (hyperkalemia)

I. Management
To support recovery and healing in clients with CKD, management of CKD clients
consists of medical/pharmacological management, nursing management and dietary
management. Where the goal of management is to maintain kidney function and
homeostasis for as long as possible.
1. Medical Management
a. The permitted fluid intake is 500 to 600 ml for 24 hours or by adding up the
urine output in 24 hours plus the IWL of 500 ml, then the water intake must be
in accordance with this addition.
b. Providing vitamins to clients is important because a low-protein diet does not
provide the necessary complement of vitamins.
c. Hyperphosphatemia and hypokalemia are treated with antacids containing
aluminum or calcium carbonate, both of which should be taken with food.
d. Hypertension is managed with various antihypertensive medications and
intravascular volume control.
e. Metabolic acidosis in chronic renal failure is usually asymptomatic and does
not require treatment, however dietary carbonate supplements or dialysis may
be needed to correct metabolic acidosis if the condition is symptomatic.
f. Hyperkalemia is usually prevented by adequate dialysis management with
potassium resorption and careful monitoring of potassium levels in all oral and
intravenous medications. Patients should be placed on a low-potassium diet
with occasional kayexelate as needed.
g. Anemia in chronic renal failure is treated with epogen (recombinant human
erythropoietin). Epogen is given intravenously or subcutaneously three times
a week.
h. Kidney transplant.
i. Hemodialysis
Hemodialysis is a process of cleaning the blood by accumulating waste.
Hemodialysis is used for patients with end-stage kidney failure or patients with
acute illnesses who require short-term dialysis (DR. Nursalam M. Nurs, 2006).
Hemodialysis is performed in cases of kidney failure and some forms of
poisoning (Christin Brooker, 2001). Hemodialysis is a procedure in which
blood is removed from the patient's body and circulated in a machine outside
the body called a dialyzer. This procedure requires access to the bloodstream.
To meet this need, an artificial connection is created between the arteries and
veins (arteriovenous fistula) through surgery.

2. Nursing Management
a. Calculate intake and output, namely fluids: 500 cc plus urine and fluid loss by
other means (visible) in the previous 24 hours.
b. Electrolytes that need attention are sodium and potassium. Sodium can be
given up to 500 mg within 24 hours.
c. Patient education and home care considerations. Nurses play a critical role in
educating patients with end-stage renal disease. There is a number of pieces of
information that patients and families need to understand about kidney failure
in order to maintain their health and avoid complications associated with
kidney failure. Patients and families need to know the issues that should be
reported to healthcare providers:
 (1) worsening signs of kidney failure (nausea, vomiting, decreased urine
output, ammonia-like breath), and
(2) signs of hyperkalemia (muscle weakness, diarrhea, abdominal cramps).
(Brunner and Suddarth, 2002, Medical Surgical Nursing Vol 2: 1451).

3. Diet Management
a. Calories must be sufficient: 2000 – 3000 calories in 24 hours.
b. Carbohydrates at least 200 grams/day to prevent protein catabolism
c. Fat is given freely.
d. Uremia diet by providing vitamins: thiamine, riboflavin, niacin and folic acid.
e. Low protein diet because urea, uric acid and organic acids, the results of food
breakdown and tissue protein will accumulate rapidly in the blood if there is a
disturbance in renal clearance. The protein given must be of high biological
value such as eggs, meat as much as 0.3 - 0.5 mg / kg / day.

J. Complications
1. Hyperkalemia
High potassium content in the blood. And high potassium content in the blood can
cause sudden death, if not treated seriously.
2. Pericarditis,pericardial effusion
Due to retention of uremic waste products and inadequate dialysis.
3. Hypertension
4. Anemia
5. Bone disease
As a result of low serum calcium levels, vitamin D metabolism is abnormal
6. Dehydration
7. Skin: itching
8. Endocrine
• Men: loss of libido, impotence, and decreased sperm count and motility.
• Women: loss of libido, reduced ovulation, and infertility
• Children: growth retardation
• Adults: loss of muscle mass
9. Neurological and Psychiatric: fatigue, loss of consciousness, coma, neurological
irritation (tremor, atherosclerosis, agitation, meningismus, increased muscle tone,
seizures)
 CHAPTER II
NURSING CARE CONCEPT
A. Nursing Assessment
Assessment of patients with chronic kidney failure includes:
1. Identity
The client's identity that must be known includes: name, age, religion, education,
occupation, ethnicity/nation, address, gender, marital status, and person responsible
for the costs.
2. Main complaint
When did the complaint start to develop, how did it happen, whether suddenly or
gradually, what actions were taken to reduce the complaint, what medication was used.
The main complaints that are obtained usually vary, starting from little urine output to
not being able to urinate, restlessness to decreased consciousness, loss of appetite
(anorexia), nausea, vomiting, dry mouth, feeling tired, bad breath (ureum), and itchy
skin.
3. Current medical history
Assess the health complaints felt by the patient during anamnesis including palliative,
provocative, quality, quantity, region, radiation, severity scale and time. For cases of
chronic kidney failure, assess onet decreased urine output, decreased consciousness,
changes in breathing patterns, physical weakness, changes in skin, presence of
ammonia-smelling breath, and changes in nutritional fulfillment. Also assess where
the client has asked for help to overcome his problems and what treatment he received.
4. Past Medical History
Assess for acute renal failure, urinary tract infection, heart failure, use of nephrotoxic
drugs, Benign prostatic hyperplasia, and prostatectomy. Assess for history of urinary
tract stone disease, recurrent urinary tract infection, diabetes mellitus, and
hypertension in the past that predispose to the cause. It is important to assess the
history of past drug use and history of allergies to types of drugs and then document
it.
5. Family Medical History
Assess whether or not one of the family members has the same disease. What is the
usual lifestyle applied in the family, whether or not there is a history of repeated
urinary tract infections and a history of allergies, hereditary diseases and infectious
diseases in the family.

6. Physical examination
a) General Condition and Vital Signs
• General condition: The client is weak and looks seriously ill.
• Level of Consciousness: Decreases according to the level of uremia which
can affect the central nervous system.
• TTV: Often there is an increase in RR, blood pressure changes from mild to
severe hypertension.
b) Physical examination :
1) Head
Clients' hair is usually found to be thin, coarse, and clients often complain of
headaches.
2) Face
The face usually looks pale and tired.
3) Eye
In patients with CKD, anemic conjunctiva, blurred vision, and non-icteric
sclera are usually found.
4) Nose
Usually in patients a rapid and deep breathing pattern is found as a form of
body compensation to maintain ventilation, usually no polyps are found.
5) Lips, teeth and mouth
Usually the breath smells like ammonia, there is bleeding of the gums and
inflammation of the oral mucosa.
6) Neck
Usually there is swelling of the lymph nodes and no enlargement of the
jugular veins.
7) Lungs
Usually the breathing pattern is deep and fast, there is chest wall retraction,
increased breathing frequency, productive cough and pulmonary edema
(Haryono, 2013)
8) Heart
Usually found increased blood pressure, chest pain, dysrhythmia or heart
rhythm disturbances.
9) Abdomen
Usually there is distension, shiny, and the skin looks tight indicating urinary
retention, ascites due to accumulation of fluid in the peritoneum (LeMone,
2016)
10) Extremities
Usually edema is often found in the extremities (generally in the lower
extremities), dry and scaly skin, burning sensation in the soles of the feet,
cold acral feel, CRT > 2 seconds (Haryono, 2013).

7. Diagnostic Examination
a. Urinalysis
Urinalysis is performed to measure the specific gravity of urine and detect
abnormal urine components. In CKD, the specific gravity can remain at
around 1.010 due to impaired tubular secretion, reabsorption and the ability
to concentrate urine. Abnormal proteins, blood cells and cell clots may also
be found in the urine.
 b. Urine culture
Instructed to identify urinary tract infections that accelerate the progression
of CKD
c. BUN and Serum Creatinine
Taken to evaluate kidney function and assess the development of kidney
failure. BUN 20-50 mg/dL identifies mild azotemia, levels greater than 100
mg/dL Indicates severe kidney damage. Symptoms of uremia are found when
BUN is around 200 mg/dL or higher. Serum creatinine levels greater than 4
mg/dL. indicate serious kidney damage.
d. GFR
Used to evaluate GFR and the stage of chronic kidney disease. GFR is a
calculated value determined using a formula that includes serum creatinine,
age, sex and race of the patient.
e. Serum electrolytes
Monitored throughout the course of CKD. Serum sodium may be within
normal limits or low due to water retention. Potassium levels are elevated but
usually remain below 6.5 mEq/L. Serum phosphate is elevated and calcium
levels are decreased. Metabolic acidosis is identified by low pH, low CO2
and low bicarbonate levels.

B. Nursing Diagnosis
1. Hypervolemia is associated with impaired regulatory mechanisms.
2. Ineffective breathing pattern related to hypoventilation syndrome
3. Ineffective peripheral perfusion related to decreased hemoglobin concentration.
4. Nutritional deficits related to anorexia, nausea, vomiting, dietary restrictions and
changes in the oral mucous membranes.
5. Activity intolerance related to an imbalance between oxygen supply and demand.
C. Nursing Interventions

Planning
No Nursing Diagnosis Objectives and Outcome Intervention
Criteria
1. Hypervolemia After nursing care was Hypervolemia
carried out, the following Management (I.03114)
Definition:increased criteria were obtained: Observation
isotonic fluid retention • Check for signs and
1. Increased fluid intake
2. Increased urine output symptoms of
Characteristic limitations: 3. Moist mucous hypervolemia (eg,
• Additional breath membranes increase orthopnea,
sounds 4. Edema decreased dyspnea, edema,
• Anasarca: general 5. Dehydration decreases increased
swelling/severe 6. Blood pressure improves JVP/CVP, positive
edema 7. Pulse rate improves hepatojugular
• Anxiety. 8. Pulse strength improves reflex, adventitious
• Azotemia 9. Mean arterial pressure breath sounds)
• Blood pressure • Identify the causes
improved
changes 10. Sunken eyes improve of hypervolemia
• Monitor
• Changes in breathing 11. Skin turgor improves
patterns hemodynamic
status (eg, heart
• Decrease in Ht, Hb
rate, blood
• Edema
pressure, MAP,
• Electrolyte imbalance
CVP, PAP, PCWP,
• Increased central
CO, CI) if
venous pressure
available.
• Intake exceeds output
• Monitor fluid
• Jugular venous intake and output
distension. • Monitor for signs
• Oliguria of
• Pleural effusion hemoconcentration
• Pulmonary artery (eg, sodium levels,
pressure changes BUN, hematocrit,
• Weight gain in a short urine specific
period gravity)
• Monitor for signs
Related factors of increased
• Disturbance of plasma oncotic
regulatory mechanisms pressure (eg,
• Increase fluid intake increased protein
and albumin levels)
 • Monitor the
infusion rate
closely
• Monitor for
diuretic side effects
(eg, orthostatic
hypotension,
hypovolemia,
hypokalemia,
hyponatremia)
Therapeutic
• Weigh yourself
every day at the
same time
• Limit fluid and salt
intake
• Elevate the head of
the bed 30 – 40
degrees
Education
• Advise to report if
urine output < 0.5
mL/kg/hr in 6
hours
• Advise to report if
weight increases >
1 kg in a day
• Teach how to limit
fluids
Collaboration
• Collaboration of
diuretic
administration
• Collaboration to
replace potassium
loss due to diuretics
• Collaboration in
providing
continuous renal
replacement
therapy (CRRT) if
necessary
2. Ineffective breathing After nursing care was Airway Management
pattern carried out, the following (I.01011)
criteria were obtained:
Definition: Inadequate Observation
1. Dyspnea decreases
exchange of inspiratory 2. Decreased use of
and/or expiratory air. 1. Monitor breathing
accessory muscles of
patterns
respiration
Characteristic limitations: (frequency, depth,
3. Decreased expiratory
respiratory effort)
phase prolongation
• Decreased 4. Breathing rate
2. Monitor for
inspiratory/expiratory additional breath
improves
pressure sounds (eg,
5. Deep breathing
• Decreased air exchange improves
gurgling,
per minute wheezing, dry
• Uses additional respiratory rhonchi)
muscles 3. Monitor sputum
• Dyspnea (amount, color,
odor)
• Orthopnea
• Chest deviation changes
Therapeutic
• Shortness of breath
1. Maintain airway
Related factors:
patency with head-
tilt and chin-lift
• Hyperventilation
(jaw thrust if
• Bone deformity
cervical fracture
• Chest wall deformity
trauma is
• Decreased energy/fatigue
suspected)
• Musculo-skeletal 2. Position semi
destruction/weakening fowler or fowler
• Obesity 3. Give warm water to
• Respiratory muscle fatigue drink
• Hypoventilation syndrome 4. Perform chest
• Painful physiotherapy, if
• Anxiety necessary
• Perceptual/cognitive 5. Perform mucus
impairment suction for less
• Injury to the spinal cord than 15 seconds
• Neurological Immaturity 6. Perform
hyperoxygenation
before
endotracheal
suctioning.
 7. Remove solid
obstruction with
McGill forceps
8. Give oxygenif
necessary

Education

1. Recommend fluid
intake of 2000
ml/day, if there are
no
contraindications.
2. Teach effective
coughing
techniques

Collaboration

1. Collaboration in
administering
bronchodilators,
expectorants,
mucolytics, if
necessary.

3. Ineffective peripheral After nursing care was Circulation Care

perfusion carried out, the following (I.02079)
criteria were obtained: Observation
Definition:decreased • Check peripheral
peripheral blood circulation 1. Peripheral pulse circulation (eg:
which can harm health. strength is increased peripheral pulses,
2. Pale skin color edema, capillary
Characteristic limitations: decreases refill, color,
• No pulse 3. Capillary refill temperature, ankle-
• Changes in motor improves brachial index)
function • Identify risk factors
4. Akral is getting better
• Changes in skin 5. Skin turgor improves for circulatory
characteristics disorders (eg:
• TD changes in the diabetes, smoking,
extremities elderly,
• CRT>3 seconds hypertension, and
• Decreased pulse
• Edema high cholesterol
• Extremity pain levels)
• Peresthesia • Monitor for heat,
• Pale skin color on redness, pain, or
elevation swelling in the
Related factors: extremities.
• Lack of knowledge Therapeutic
about aggravating • Avoid
factors administering IV
• Lack of knowledge drips, or taking
about the disease blood in areas of
process limited perfusion.
• DM • Avoid measuring

• Hypertension blood pressure in

• Smoke extremities with
limited perfusion.
• Avoid applying
pressure and
tourniquet to the
injured area.
• Take infection
prevention
measures
• Do foot and nail
care
• Do hydration
Education
• Advise to stop
smoking
• Recommend
regular exercise
• Recommend
checking bath
water to avoid skin
burns.
• Recommend using
blood pressure
lowering drugs,
anticoagulants, and
cholesterol
lowering drugs, if
necessary.
 • Recommend taking
blood pressure
control medication
regularly
• Recommend
avoiding the use of
beta blockers
• Recommend
proper skin care
(eg: moisturizing
dry skin on feet)
• Recommend a
vascular
rehabilitation
program
• Teach a diet
program to
improve
circulation (eg: low
saturated fat,
omega 3 fish oil)
• Inform emergency
signs and
symptoms that
should be reported
(eg: pain that does
not go away with
rest, wounds that
do not heal, loss of
sensation).

4. Nutritional Deficit After nursing care was Nutrition Management

carried out, the following (I.03119)
Definition:nutritional intake criteria were obtained: Observation
is insufficient to meet • Identification of
1. The portion of food
metabolic needs consumed increases nutritional status
• Identifying food
2. Weight gain
Characteristic limitations: 3. Body mass index allergies and
• Abdominal cramps (BMI) improves intolerances
• Abdominal pain • Identify preferred
• Avoiding food foods
 • Body weight 20% or • Identify calorie
more below ideal body needs and nutrient
weight types
• Capillary fragility • Identify the need
• Diarrhea for nasogastric tube
• Hyperactive bowel use
sounds • Monitor food
• Lack of food intake
• Weight monitor
• Weight loss with
• Monitor laboratory
adequate food intake
test results
• Pale mucous
Therapeutic
membranes
• Perform oral
• Inability to eat food
hygiene before
• Decreased muscle tone
eating, if necessary
• Facilitate
Related factors:
determining
• Biological factors
dietary guidelines
• Economic factors
(eg: food pyramid)
• Inability to digest food • Serve food
• Inability to swallow attractively and at
food the right
• Psychological factors temperature.
• Provide high fiber
foods to prevent
constipation.
• Provide foods high
in calories and high
in protein
• Givefood
supplement, if
necessary
• Discontinue
nasogastric tube
feeding if oral
intake can be
tolerated.
Education
• Teach sitting
position, if able.
• Teach programmed
diet
Collaboration
 • Collaboration in
administering
medication before
meals (eg: pain
relievers,
antiemetics), if
necessary.
• Collaborate with a
nutritionist to
determine the
number of calories
and types of
nutrients needed, if
necessary.

5. Activity Intolerance After nursing care was Energy Management

carried out, the following (I.05178)
Definition :physiological or criteria were obtained: Observation
• Identify body
psychological insufficiency
function disorders
of energy to continue or 1. Fatigue Complaints
that cause fatigue
complete required or daily Decreased • Monitor physical
activities. 2. Dyspnea on and emotional
decreased activity fatigue
Characteristic 3. Dyspnea after • Monitor sleep
Limitations: decreased activity patterns and hours
• Monitor location
• Abnormal response of 4. Pulse rate improves
and discomfort
blood pressure and during activities
heart rate to activity Therapeutic
• ECG changes • Provide a
indicating arrhythmia comfortable, low-
and ischemia stimulus
environment (eg,
• Presence of dyspnea light, noise, visits)
during activity • Perform passive
• Verbally report fatigue and/or active range
and weakness of motion
exercises.
• Provide calming
Risk Factors
distraction
• Bed rest activities
• Overall weakness • Bedside seating
• Imbalance between facility, if unable to
oxygen supply and move or walk
demand Education
• Recommend bed
• Immobilization
rest
 • Recommend doing
activities gradually
• Advise to contact a
nurse if signs and
symptoms of
fatigue do not
improve.
• Teach coping
strategies to reduce
fatigue
Collaboration
• Collaborate with a
nutritionist on how
to increase food
intake
 BIBLIOGRAPHY
Brunner & Suddarth. 2002. Buku Ajar keperawatan medikal bedah, edisi 8 vol 2. Jakarta: EGC.

Baradero,M,et,al. Klien Gangguan Ginjal. (2008). Jakarta : EGC.

Fabiana Meijon Fadul. (2019). Artikel Chronic Kidney Disease. Komplikasi CKD. Francisco,
A. R. L. (2013). Anatomi Fisiologi Ginjal. Journal of Chemical Information and
Modeling, 53(9), 1689–1699. http://repository.unimus.ac.id/1148/3/BAB II.pdf

PPNI DPP Pokja SDKI. (2017). Standar Diagnosis Keperawatan Indonesia (SDKI). In
Persatuan Perawat Nasional Indonesia (1st ed.)

Price, Sylvia A. 2006. Patofisiologi Konep Proses-Proses Penyakit. Jakarta: EGC.

Ns. Tarwoto, Skep,et,al. (2009). Anatomi dan Fisiologi Untuk Mahasiswa

Keperawatan.Jakarta: Trans Info Media.
Sudoyo. W. Aru,et,al. (2006). Buku Ajar Ilmu Penyakit Dalam.Jakarta. FKUI.
Suharyanto,Toto,et,al. (2009).Asuhan Keperawatan Pada Klien Dengan Gangguan Sistem
Perkemihan. Jakarta: Trans Info Media.