I.

Concept of CKD (Cronic Kidney Disease) / GGK

A. Definitions
Chronic Kidney Disease (CKD) or chronic renal failure is defined as kidney damage
with decreased glomerular filtration rate (GFR) (Nahas & Levin, 2010). Chronic
renal failure is usually the result of late kidney function loss gradually (Doengos,
1999: 626). Chronic renal failure occurs when the kidneys are unable to maintain an
internal environment that is consistent with life and the restoration of functionality
does not begin. In most individuals the transition from healthy to chronic status or
persistent disease is very slow and waits for several years (C.Long, 1996: 368).

CKD or chronic renal failure (GGK) is defined as a condition in which the kidneys
experience slow, progressive, irreversible, and faint (insidious) function in which the
body's ability fails to maintain metabolism, fluid, and electrolyte balance.
(Smeltzer,2009).

Chronic renal failure is a failure of kidney function to maintain metabolism and fluid
and electrolyte balance due to progressive destruction of renal structure with the
manifestation of the accumulation of metabolite (toxic uremic) residues in the blood
(Muttaqin, 2011).
B. Kidney Anatomy and Physiology
1. Macroscopic
The kidney is located at the back of the upper abdomen, behind the peritoneum,
in front of the last two ribs and three large muscles (transverses abdominalis,
lumborum quadratus and psoas major). The kidneys are normally shaped like
peas or beans, the adult kidney is about 12x6x3 cm (adult fist) weighing about
150 grams. The left kidney is generally longer and smaller than the right kidney.
2. Microscopic
The kidneys are composed of 1-25 million nephrons. Nephrons are functional
units of the kidney consisting of glomerolus and renal tubules that function to
maintain fluid and electrolyte balance. Nephron has a length of ± 3cm.
a. Renal vascularization
The blood flow to the kidney through the renal artery is directly out of the
abdominal aorta. The renal artery becomes small to the arteriole or afferon
that enters the glomerulus and exits the glomerulus called the afferon.
b. Kidney physiology
Kidney function is to remove toxic substances or toxins, maintain fluid
balance, maintain the balance of acid and alkaline levels of body fluids,
remove other substances in the body, remove the rest of the metabolism of
the end result, protein, ureum, creatinine, and ammonia.
a) Filtration
Urinary formation begins with plasma filtration of the glomerulus, like
other body capillaries, glomerular capillaries are actively imhermeable to
large plasma proteins that are sufficiently permeable with water and
smaller solutions, such as electrolytes, amino acids, glucose and nitrogen
residues. RBF (renal blood flow) is about 25% of cardiac output, about
1200 ml / min.
b) Reabsorption
The substances in the kidney filtration are divided into 3 parts:
electrolytes, non electrolytes, and water. After filtration the second step
is selective reabsorption of these substances and then back again
substances already in filtration.
c) Excretion
The ultimate transport of molecules from the bloodstream through the
 tubules into citrate. Many substances secreted act into naturally in the
body such as penicillin. Substances naturally occur in the body including
uric acid and potassium and hydrogen ions.

C. Etiology
The etiology of chronic renal failure is various and complex, such as:
1. Kidney infections (glomerulonephritis, pyelonephritis)
2. Polycystic kidney disease
3. Renal obstruction (neoplasm), and prostate
4. Neephotoxic (analgesic, kanamycin)
5. Systemic diseases such as (DM, Hypertension, SLE, Gout).

D. Signs And Symptoms

1. According to Long, 1996: 369 you and symptoms of CRC are, among others;
a. Early symptoms:
Lethargi, headache, physical and mental fatigue, reduced weight,
irritability, depression
b. Further symptoms:
Anorexia, nausea accompanied by vomiting, shallow breath or shortness of
breath whether there is activity or not, udem accompanied indentation,
pruritis may not exist but may also be very severe.
2. According to Smalzer, 2001; 1449
Hypertension: due to fluid and sodium retention of the activity of the renin
angiotensin-aldosterone system
Congestive heart failure and polymar udem: due to excessive fluid
Pericarditis: due to irritation of the pericardial lining by toxic, pruritis, anorexia,
nausea, vomiting, and hiccups, muscle twitching, seizures, altered
consciousness, unable to concentrate.
3. Suyono signs and symptoms of 2001 are as follows:
a. Cardiovascular
Such as Hypertension, pitting edema, periorbital edema and venous
enlargement.
b. Polymer system
Krekel, shallow breath, kusmaul and thick sputum.
 c. Gastrointestinal System
Anorexia, nausea, vomiting, GI tract bleeding, ulceration and oral bleeding
and ammonia-breathing breath.
d. Muskuloeskeletal system
Muscle cramps, loss of muscle strength, bone fracture.
e. System integument
Skin color yellowish or greyish shine, prurinity, dry and scaly skin,
ecchymosis / bruises, thin and brittle nails, thin and coarse hair.
f. The reproductive system
Aminore, testicular atrophy.

E. Pathophysiology
In the event of kidney failure some nephrons (including glomerulus and
tubules) are suspected intact while others are damaged (whole nephron hypothesis).
Whole nephrons are hypertrophied and produce an increased volume of filtration
with reabsorption even in the case of a decrease in GFR / filter power. This adaptive
method allows the kidneys to function until ¾ of the damaged nephrons. The burden
of the material to be dissolved becomes greater than that which can be reabsorbed by
osmotic diuresis accompanied by polyuri and thirst.

Furthermore, as the number of damaged nephrons increases, many oliguri arise

with retention of residual products. The point where the onset of symptoms in the
patient becomes clearer and there are typical symptoms of kidney failure when
approximately 80 - 90% of renal function is lost. At this rate the renal function is
thus the creatinine clearance value down to 15 ml / min or lower (C Long, 1996).

Renal function decreases, the end product of protein metabolism (which is

normally excreted into the urine) is buried in the blood. There is uremia and affects
every body system. The more heaps of waste products the more severe the
symptoms. Many uremia symptoms improve after dialysis (Brunner & Suddarth,
2001: 1448).
 The general course of progressive renal failure can be divided into three stages:

1. Stage 1 (decrease in kidney reserve)

Marked with serum creatinine and normal Blood Ureum Nitrogen (BUN)
levels and asymptomatic sufferers. Kidney Faal <100-75%.
2. Stage 2 (renal insufficiency).
Kidney disease 75-25% of functioning tissue has been damaged (Glomerulo
filtration Rate is 25% of normal). At this stage Blood Ureum Nitrogen begins
to rise above normal, serum creatinine levels begin to increase beyond
normal levels, mild azotemia, nocturia and polyuri occur.
3. Stage 3 (end stage renal failure / uremia).
Occurs when 90% of the mass of the nephron has been destroyed, the
glomerulo filtration rate is 10% of normal, 5-10 ml per minute or less of
serum creatinine clearance. At this stage, serum creatinine and blood ureum
nitrgen levels rise very prominently and oliguri (Price, 1992: 813-814).

F. Investigations
1. Laboratory:
Ureum / Creatinine, Hemoglobin, blood gas analysis (AGD), CCT, (Na, K, Ca,
P), albumin, blood sugar and triglycerides.
Diagostics such as kidney biopsy
2. Radiology
3. BNO / plain abdominal photo, IVP (intra vena pielografi), ultrasound,
renogram, ECG / heart photo, lung photo and bone photo.
4. ECG

G. Complications
1. Hyperkalemia
Due to decreased excretion of metabolic acidosis, catabolism and excessive diit
input.
2. Pericarditis, perincardial effusion and cardiac temponade.
3. Hypertension
Due to fluid and sodium retention as well as mal function of rennin
angioaldosteron system.
 4. Anemia
Due to decreased erythroprotein, age range of red blood cells, bleeding
gasstrointestina due to irritation.
5. Bone disease
Due to phosphate retention of low serum potassium levels of vitamin D
metabolism, abnormal and elevated levels of aluminum.

H. Management
The goal of management in chronic renal failure is to maintain renal function
and homeostasis for as long as possible. All factors that play a role in the occurrence
of chronic renal failure are sought and addressed.
1. Conservative management includes:
Liquid and electrolyte balance settings
a. Detention of potassium and phosphorus may occur GGK rice (orally with
CaCo3)
b. Control can be done by reducing potassium intake in the diit.
c. Administration of aluminum hydroxide → binding phosphor
d. Giving laxatives
e. Provision of vitamin D
f. The balance of transfor oxygen
g. Anemia always accompanies CTR → client quickly fatigue and shortness
of breath
Provides comfort, rest and sleep
h. Generally discomfort to CRA includes pruritus, muscle cramps, thirst,
headache, dry skin, stress, emotional, insomnia.
i. Reducing serum phosphate levels with alhydrokside → reducing itching
j. Keeps skin moist
k. Provides anti-itching drugs
2. Dialysis: dialysis / hemodialysis
3. Medicines
Anti-hypertension, iron supplements, phosphate binding agents, calcium
supplements, furosemide (help urinate).
 4. Diets low in protein and high in carbohydrates.
5. Blood transfusion.
6. Renal transfusion

I. Pathway

↓ jumlah nefron fungsional

Nefron yang masih utuh

Nefron yang hancur

90 % nefron hancur 75% nefron hancur adaptasi

Tidak dapat mengkompensasi GFR ↓ Nefron hipertropi

(ketidakseimbangan cairan BUN dan kreatinine ↑
elektrolit )

↑kecepatan filtrasi ,
↑beban solute, ↑reabsorbsi
Adaptasi

GFR ↓10 % dari normal

(BUN dan creatinine ↑)
Keseimbangan cairan dan
↑ elektrolit dipertahankan
Kecepatan filtrasi dan
beban solute ↑

Urine isoosmosis

Fungsi ginjal rendah

Ketidakseimbangan dalam
glomerulus dan tubulus
Kegagalan proses
filtrasi
↓ cadangan ginjal
 Poliuri nokturi azotemia

Oliguria

Infusiensi ginjal Argiotensin ↑

Uremia ↑

Gagal ginjal Retensi Na +

Penumpukan kristal
urea dikulit

↓ eritopoetin di Kelebihan
ginjal volume cairan

Proritus

SDM ↓ Intoleransi
aktivitas
Gangguan
integritas kulit

Pucat, fatique,
malaise, anemia

Gangguan nutrisi kurang

dari kebutuhan

J. Client care plan with CKD / GGK interference

1. Assessment
a. Nursing history
a) Key complaints
b) Current disease history
c) Past medical history
d) Family disease history (genogram if present)
b. Physical examination: focus data
a) Activity and Rest
 Fatigue, weakness, malaise, sleep disorders, muscle weakness and tone,
decreased ROM
b) Circulation
History of old or severe hypertension, palpitations, chest pain,
increased JVP, tachycardia, orthostatic hypotension, friction rub
c) Ego Integrity
Stress factor, feelings of helplessness, no strength, refuse, anxiety, fear,
anger, irritable.
d) Elimination
Reduced frequency of urine, oliguri, anuri, changes in urine color, dark
urine red / brown, cloudy, diarrhea, constipation, abdomen bloated.
e) Food / liquid
BB increase due to edema, BB decrease due to malnutrition, anorexia,
nausea, vomiting, metallic taste in the mouth, ascites, decreased
muscle, decreased subcutaneous fat.
f) Neurosensory
Headache, blurred vision, muscle cramps, convulsions, numbness,
tingling, mental status disorder, decreased field of attention, inability to
concentrate, memory loss, chaotic, decreased level of consciousness,
coma
g) Pain / comfort
Pelvic pain, headaches, muscle cramps, leg pain, distraction, anxiety
h) Respiratory
Cusmaul respiration (fast and shallow), paroxysmal nocturnal dyspnea
(+), productive cough with frotty sputum in the event of pulmonary
edema
i) Security
Itchy skin, recurrent infections, pruritus, fever (sepsis and dehydration),
petechiae, ecchymosis, bone fracture, phosphate deposits of kalsieum
on the skin, limited ROM
j) Sexuality
Decreased libido, amenorrhea, infertility
k) Social Interaction
Unable to work, unable to perform the usual role
 c. Investigations
Ureum and creatinine usually increase

K. Possible Nursing Diagnoses

Diagnosis 1: Activity intolerance
a. Definitions
Inadequate physiological or psychological energy to continue or complete daily
activities that want or should be done.
b. Character restrictions
Discomfort or dyspnea during the move
Reporting verbal fatigue or weakness
Cardiac frequency or abnormal blood pressure in response to activity
ECG changes that indicate arrhythmias or ischaemia
c. Related factors
Bed rest and immobilization
Common weakness
Imbalances between supply and oxygen demand
Lifestyle lack of movement

Diagnosis 2: Ineffectiveness of the breath pattern

a. Definitions
Inspiration or expiration that does not provide adequate ventilation
b. Character restrictions
Subjective:
Disepnea
Shortness of breath
Objective:
Chest excursion change
Taking the position of three fulcrums (tripod)
Bradipnea
Decrease in inspiration and expiratory pressure
Decrease in ventilation a minute
Decrease in vital capacity
Deep breath
 An increase in anterior and posterior diameter
Breath of the nostrils
Ortopnea
Expiratory phase menmanjang
Speed of respiration
Tachypnea
Time ratio
Use of auxiliary aids to breathe
c. Related factors
Anxiety
Body position
Bone deformity
Deformity of chest wall
Reduced energy and fatigue
Hyperventilation
Hypoventilation syndrome
Muskuluskletal Damage
Neurological immaturity
Neuromuscular dysfunction
Obesity
Pain
Perceptual or cognitive impairment
Fatigue muscle fatigue
Spinal cord injury
 L. Planning
Destination &
No. Results Criteria Intervention (NIC) Rational
(NOC)
1. Aim : 1. Monitor the client for 1. Observe the extent to
Increase activity activities which the ability of the
or tolerate movement of the client
activities that can to be trained
be done 2. Assess the factors that 2. Know the agent,
cause fatigue factors and causes of
Results criteria: weakness and fatigue on
1. Activity the client
tolerance 3. Encourage physical 3. To maximize the
2. Resilience to exercise of passive and client's motion members
complete the active ROM 4. Maximize the giving
activity 4. Monitor client O2 repons of client O2
5. Maximize the
5. Monitor adequate nutrition provision of adequate
nutrition
2. Aim : 1. 1. Management of airway 1. 1. Facilitate client's
Normal / administration of O2 airway patency
effective 2. Teach the client to cough 2. Cleaning the airway
breathing patterns effectively and facilitate the flow
of O2
Results criteria: 3. Remove the
Airway immunity 3. Aspiration of breath secretions on the
1. Respiratory client's airway so as
status: ventilation not to get clogged
of air movement 4. Set client position 4. Enhance the
into and out of occurrence of
the lungs well 5. Monitor the client's shortness of breath
2. Normal vital breathing 5. Ensuring client's
signs airway patency
 6. Monitor client TTV 6. Ensure the client's
TTV to determine and
prevent further
compilation. \
7. Limit heavy activity 7. Reduce workload
and prevent shortness
of breath
8. Give the family penkes 8. Provide information
about deep breathing
relaxation techniques,
information about the
disease process and
reduce symptoms.
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Carpenito, Lynda Juall. (2000). Buku Saku Diagnosa Keperawatan Edisi 8. Jakarta: EGC.

Doengos E, Morilynn, dkk. (1999). Rencana Asuhan Keperawatan: Pedoman Untuk

Perencanaan Dan Pendokumentasian Perawatan Pasien Edisi 3. Jakarta: EGC.

Long, B. C. (1996). Perawatan Medikal Bedah. Suatu Pendekatan Proses Keperawatan

Jilid 3. Bandung: Yayasan Ikatan Alumni Pendidikan Keperawatan

Muttaqin, A. (2011). Asuhan Keperawatan Pada Sistem Perkemihan. Jakarta: Salemba

Medika.

Price, Sylvia A dan Lorraine M Wilson. (1995). Patofisiologi Konsep Klinis Proses-Proses
Penyakit. Edisi 4. Jakarta: EGC.

Smelzer, Suzanne C. dan Brenda G Bare. (2001). Buku Ajar Keperawatan Medikal Bedah
Brunner dan Suddart Edisi 8. Jakarta: EGC.