CHAPTER I

INTRODUCTION

A. BACKGROUND
The kidney is a vital organ that plays a very important very important
in maintaining the stability of the environment in the body. The kidneys
regulate the balance of fluids and electrolytes and acid base by way of filtering
the blood through the kidneys, selective reabsorbsi of water, electrolytes and
non-electrolytes, as well as his excellence as a urinary mengekskresi.

Chronic renal failureis a clinical syndrome caused by a decrease in

kidney function that is chronically, lasting progressive and such. This happens
when the glomerular filtration rate (LFG) of less than 50 ml/min. Chronic
renal failure in accordance with the stages can be reduced, mild, moderate or
severe. End stage kidney failure (end stage renal failure) is the stadium failing
kidneys that can result in death unless a replacement therapy done
(Suhardjono, 2001).

Chronic renal failure is characterized by a decrease in the rate of

screening glumerulus (GFR), so the increased blood urea levels, increase
blood urea levels and increasing screening process by nefron undergoing
hypertrophy, third charge that solut kemasing each of these tubules that are
still functioning will be greater than the normal state (William E,2009).

Based on some of the things above constituents interested in taking the

title of "Nursing care of Chronic renal failure" in this paper.

B. FORMULATION OF THE PROBLEM

This paper we arrange by on the development of some of the subject
matter of the following, namely:
1. What is the sense of chronic kidney failure?
2. How the classification of chronic kidney failure?
3. What is the etiology of chronic kidney failure?
 4. How can the pathophysiology of chronic kidney failure?
5. How is the manifestation of chronic kidney failure?
6. What is the examination of supporting of the chronic renal failure?
7. How is the treatment of chronic renal failure?
8. What are the complications of chronic renal failure?
9. How about the prognosis of chronic renal failure?
10. How the nursing care of patients chronic kidney failure?

C. The PURPOSE of
This paper we arrange to find out:
1. Understanding of chronic renal failure
2. Classification of chronic renal failure
3. The etiology of chronic renal failure
4. Pathophysiology of chronic renal failure
5. Manifestations of chronic renal failure
6. Complementary Examination of chronic renal failure
7. Treatment of chronic renal failure
8. Complications of chronic kidney failure
9. The Prognosis of chronic renal failure
10. Nursing care of patients of chronic renal failure
 CHAPTER II

TINJAUAN TEORI

A. ANATOMI GINJAL
Secara anatomi, kedua ginjal terletak pada setiap sisi dari kolumna
tulang belakang antara T12 dan L3. Ginjal kiri terletak agak lebih superior
dibanding ginjal kanan. Permukaan anterior ginjal kiri diselimuti oleh
lambung, pancreas, jejunum, dan sisi fleksi kolon kiri. Permukaan superior
setiap ginjal terdapat kelenjar adrenal.
Posisi dari kedua ginjal di dalam rongga abdomen dipelihara oleh ( 1 )
dinding peritoneum, ( 2 ) kontak dengan organ – organ visceral, dan ( 3 )
dukungan jaringan penghubung. Ukuran setiap ginjal setiap orang dewasa
adalah panjang 10 cm; 5,5 cm pada sisi lebar; dan 3 cm pada sisi sempit
dengan berat setiap ginjal berkisar 150 g.
Lapisan kapsul ginjal terdiri atas jaringan fibrous bagian dalam dan
bagian luar. Bagian dalam memperlihatkan anatomis dari ginjal. Pembuluh –
pembuluh darah ginjal dan drainase ureter melewati hilius dan cabang sinus
renal. Bagian luar berupa lapisan tipis yang menutup kapsul ginjal dan
menstabilisasi struktur ginjal. Korteks ginjal merupakan lapisan bagian dalam
sebelah luar yang bersentuhan dengan kapsul ginjal. Medula ginjal terdiri atas
6-18 piramid ginjal. Bagian dasar pyramid bersambungan dengan korteksdan
diantara pyramid dipisahkan oleh jaringan kortikal yang disebut kolum ginjal.
B. UNDERSTANDING
Chronic renal failure (GGK) is the decline of kidney function that causes
the inability to maintain the substance of the body under normal conditions
(Betz Sowden,2002).

Chronic renal failure occurs when the kidneys are not able to maintain an
internal environment that is consistent with the life and the restoration of
function is not started. On most individual transition from healthy to chronic
status or disease who settled very slowly and wait a few years. (Barbara c.
Long, 1996; 368)

Chronik renal failure progressive kidney damage was fatal and

characterized by uremia (urea and other nitrogen wastes that circulate in the
blood and its complications if not done dialysis or a kidney transplant).
(Nursalam. 2006).

Chronic renal failure or end stage renal disease (ESRD) is a progressive

renal function disorders and such where the ability of the body to fail to
maintain metabolism and balance of fluids and electrolytes, causing uremia
(urea retention and other nitrogen waste in the blood). (Brunner & Suddarth,
2001; 1448).

then it can be inferred that the Cronik Kidney Desease is a progressive

renal function disorders such that are caused by the presence of a metabolic
waste deposits in the blood, so that the ability of the body is not able to
mengekskresikan the remains of rubbish metabolism and maintain the balance
of fluids and electrolytes in the body.

C. ETIOLOGY
Chronic renal failure is generally caused by diffuse intrinsic kidney
disease and chronically. But almost all the bilateral and progressive
nephropathy will end up with chronic renal failure. Generally the disease
 outside the kidney, missal obstructive nephropathy may cause kidney
abnormalities intrinsic and end up with chronic kidney failure.

Glomerulonefritis hypertension and life as pyelonephritis most often is

the cause of Chronic renal failureis approximately 60%. Chronic renal failure
associated with polycystic kidney disease and obstructive nephropathy only 15
– 20%. Glomerulonefritis parenkim kidney disease is a chronic progressive
and diffuse, often end up with chronic kidney failure. Men more often than
women, age 20 – 40 years. Most of the patients were relatively young and is
the main candidate for a kidney transplant. Glomerulonefritis may be
associated with diseases system (Glomerulonefritis secondary) such as Lupus
Eritomatosus Sitemik, Poliarthritis Nodosa, Granulomatosus Wagener.
Glomerulonefritis (Glomerulopati) associated with diabetes mellitus
(Glomerulosklerosis) are not rare and it can end up with chronic kidney
failure. Glomerulonefritis related Amyloidosis is often found in patients with
chronical diseases such as tuberculosis, leprosy, rheumatoid arthritis, and
osteomyelitis, and myeloma.

Hipertensif kidney disease (arteriolar nefrosklerosis) is one of the

causes of chronic kidney failure. The incidence of hypertension berekhir
weight life with Chronic renal failureless than 10%. Approximately 10 -15%
of patients-patients with Chronic renal failurecaused by kidney disease

In adults, chronic renal failure associated with urinary tract infections

and kidney (as pyelonephritis) type uncomplicated rare, except tuberculosis,
multiple abscess, Necrotizing papilla left who do not get treatment adekuat.

As is known, interstitial nephritis shows abnormalities of

histopathology in the form of fibrosis and inflammatory reactions or
inflammation of the tissue interstitial with etiology. Sometimes also found
abnormalities-abnormalities about the glomerulus and blood vessels, vascular.
Uric acid nephropathy ranks first of interstitial nefrotis etiolgi.

D. PATHOPHYSIOLOGY
 The kidney has a real ability to compensate for the persistent nefron
loss that occurs in chronic renal failure. If the number decreased to glomerolus
filter 5-20 ml/min/1.73 m2, this capacity is starting to fail. This led to various
problems related to biochemical main ingredients handled the kidneys.
Sodium and fluid Imbalance occurs due to the inability of the kidney to
memekatkan urine. Hiperkalemia occur due to a decrease in the secretion of
potassium. Metabolic acidosis occurs due to damage of reabsorbsi bicarbonate
and ammonia production. Demineralisasi bones and growth disorders occur
due to the secretion of parathyroid hormone, increased plasma phosphate
(decreased serum calcium, acidosis) causes the release of calcium and
phosphorus into the blood stream and impaired intestinal absorption of
calcium. Anemia occurs due to impaired production of red blood cells, a
decrease in red blood cell life span, increased bleeding tendency (due to
damage to the function of platelets). Growth Changes associated with changes
in nutrients and various biochemical processes.

E. CLINICAL MANIFESTATIONS
According to Suhardjono (2001), clinical manifestations which appear in
patients with chronic renal failure are:
1. Disorders of the gastrointestinal system
a. Anorexia, nausea, and vomitus are associated with disorders of
metaboslime
b. proteins in the intestine.
c. Mouth odor of ammonia caused by ureum excessive saliva.
d. Hiccups (hiccup)
2. Erosif Gastritis, ulcer, colitis and peptik Diathesis.
a. Integumentary System
1) Pale colored Skin due to anemia. Itching with ekskoriasi due to
toxin Diathesis.
2) Ekimosis due to disorders of hematologis
 3) Urea frost due to crystallization of urea
4) Former scratching because of itching
5) Dry scaly Skin
6) Thin and brittle Nails
7) Thin and coarse Hair
b. Hematologic System
1) Anemia
2) Disorders of platelet function and thrombocytopenia
3) Malfunctioning leukocytes
c. The nervous system and muscles
1) Restles leg syndrome
2) Burning feet syndrome
3) Metabolic Encephalopathy
4) Myopathy
d. Cardiovascular System
1) Hypertension
2) Due to the hoarding of fluids and salt.
3) Chest pain and shortness of breath
e. Heart rhythm Disorders
1) Edema due to fluid build-up.
2) The Endocrine System
3) Sexual Disorders: libido, fertility and decreased erections in males.
4) Gangguan metabolisme glukosa, resistensi insulin, dan gangguan
sekresi insulin.
5) Gangguan metabolisme lemak.
6) Gangguan metabolisme vitamin D.

Clinical manifestations in General:

1. Fluid Imbalance
a. Excess fluid: edema, oliguri, hypertension, congestive heart failure
 b. Vascular volume Depletion: poliuria, decreased fluid intake,
dehydration
2. Electrolyte imbalance
a. Hiperkalemia: disorder, heart rhythm dysfunction stranded DNA
genome
b. Hipernatremia: thirst, tachycardia, stupor, the membrane is dry, the
increase in tendon reflexes, decreased level of consciousness deep
lobes
c. Hypokalemia and hiperfosfatemia: irritability, depression, muscle
cramps, parastesia, psychosis, and symptoms
d. Hypokalemia: a decrease in the reflected tendon of deep lobes,
hipotonia, ECG changes
3. Encephalopathy and neuropathy Diathesis
a. Itchy scratchy
b. Cramps and muscle weakness
c. Talk is not clear
d. Parastesia palms and soles of the feet
e. Poor Concentration
f. Sleepy
g. Signs of increased intracranial pressure
h. Comma
i. Seizures

F. COMPLEMENTARY EXAMINATIONS
1. Radiology
Aimed at assessing the State of the kidneys and assess the degree of
complications occur.
2. Photos plain abdomen to assess the form and magnitude of the kidney
(a/stone obstruction). Dehydration will worsen the State of kidney
sufferers therefore are expected not to fast.
3. IVP (Intra Venous Pielografi) to assess the system of pelviokalises and
ureter
This examination has the risk of decreased kidney faal in certain
circumstances, for example: elderly, DM, and uric acid Nephropathy.
4. ULTRASOUND to assess the magnitude and shape of the kidney, kidney
parenkim thick, density parenkim the kidneys, antomi pelviokalises
system, proximal Ureteral, bladder and prostate.
5. Renogram to assess kidney function right and left, the location of the
disorder (vascular, parenkim, excretion), as well as the remaining kidney
function.
6. Cardiac Radiology Examination to look for pericardial effusion,
kardiomegali.
7. Radiology Examination of bones to look for osteodistrofi (especially for
falanks fingers), metastasik calcification.
8. Radilogi pulmonary Checks to find the left lung Diathesis; this is considered
a dam.
9. Examination Pielografi Retrograde when suspected obstruction that is
reversible.
10. ECG to see possible: hypertrophy of the left ventricle, the signs of
perikarditis, arrhythmia, electrolyte disturbances (hiperkalemia).
11. Kidney Biopsy
12. Laboratory Examination is generally thought to support, the possibility of
a Chronic kidney failure:
- The rate of Creep blood: Increases the diperberat by the presence of
anemia, and hipoalbuminemia.
- Normositer normokrom anemia, and a low reticulocyte number.
- Ureum and creatinin: Rises, usually a comparison between ureum and
creatinin approximately 20:1. Remember the comparison could be
rising because of bleeding channel of indigestion, fever, extensive
burns, steroid treatment, and urinary tract obstruction. This
 comparison is reduced: smaller than the Ureum Kreatinin, in a diet
low in protein, and Klirens Test Creatinin decreases.
- Hiponatremi: generally due to excess fluid.
- Hiperkalemia: usually occurs in advanced kidney failure along with
declining diuresis.
- Hypocalcemia and Hiperfosfatemia: occurs because of decreased
synthesis of 1.24 (OH) 2 vit D3 at GGK.
- Lindi phosphatase metabolism disorder its bones phosphatases lindi
Isoenzim, especially bone.
- Hipoalbuminemis and Hipokolesterolemia; metabolic disorders and
generally caused a diet low in protein.
- The elevation of blood sugar, carbohydrate metabolism disorders
result in kidney failure, (resistance to insulin's influence on the
network ferifer)
- Hipertrigliserida fat metabolism disorders, as a result, due to elevation
hiormon inslin, somatotropik hormone and decreased lipoprotein
lipase.

G. MANAGEMENT
1. Medical Treatment
a) Anti hypertensive Drug that is often used is Metildopa (Aldomet),
propanolol and klonidin. The drug is diuretic furosemid is used (lasix).
b) Hiperkalemia acute can be treated by administering intravenous glucose
and insulin that K+ into the cell, or by administering intravenous
Calcium Gluconate 10% carefully while the ECG is constantly
supervised. When the levels of K+ can not be derived by dialysis, then
it can use sodium cation exchanger resin polistiren sulfonat
(Kayexalate).
c) Treatment for anaemia are: recombination eritropoetin (r-EPO) was
widespread, the current treatment for Uremic anemia: by reducing
 blood loss, vitamins, androgens to women, depotestoteron for men and
blood transfusions.
d) Acidosis can erupted when an acute acidosis occurs in people with
previous ones already experiencing chronic mild acidosis, on heavy
diarrhea accompanied by loss of HCO3. When severe acidosis will be
corrected by administering administering NaHCO3 parenteral.
e) Dialysis: a process in which water flows and solut passively diffusion
through a porous membrane of a liquid compartment towards the other
compartment.
f) Peritoneal Dialysis: is an alternative to hemodialysis on acute renal
failure handling and Chronicle.
g) In adults, 2 L sterile dialysis liquid is allowed to flow into the peritoneal
cavity through a catheter for 10-20 minutes. Usually the balance of
fluid and membranes are permeable and semi-peritoneal dialysis that
many vaskularisasinya will be achieved after the left for 30 minutes.
h) Kidney transplantation: procedure default is turning the kidney donor
and placing it on the contralateral side of the patient's iliac. Thus the
ureter is located at the anterior of the blood vessels of the kidney, and
more easily dianastomosis or implanted into the bladder recipients as
well.
2. Nursing Management
a) Maintaining the balance of fluids and electrolytes
b) weighing per day
c) Bcorrect the mEq of potassium to input 40-60/hr
d) Mengkaji area of edema.
e) Do skin care
f) Do oral hygiene care
g) Do the measurement of ECG, indicates the existence of a hiperkalemia
3. Diit Treatment
High carbohydrate, low protein, low sodium, low in protein to diit
limit approaching 1 g/oliguri phase kgBB. To minimize the breakdown
 of proteins and to prevent the buildup of toxic end result. Limit foods
and liquids containing potassium and phosphorus (banana, fruit and
juice-jusan and coffee).

H. COMPLICATIONS
1. Hypertension.
2. Infection traktus urinarius.
3. Obstruction traktus urinarius.
4. Electrolyte Disturbances.
5. Impaired perfusion to the kidneys.
 CHAPTER III
COVER

A. CONCLUSION

Chronic renal failure (GGK) is the decline of kidney function that

causes the inability to maintain the substance of the body under normal
conditions.
On early renal failure disease (Microalbuminuria) already had
cardiovascular morbidity and mortality prognostic. By memberatnya of kidney
abnormalities, accompanied by a decrease in kidney functions, the prognosis
proved to be getting worse, leading to kidney failure that requires dialysis,
target organ complications that reduce quality of life and increase the
mortality rate.
B. ADVICE
1. In performing nursing care should include aspects of biopsikososiospiritual
patients.
2. Each completed nursing action should document them, for legality.
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