FAKULTAS KEDOKTERAN

UNIVERSITAS MUSLIM INDONESIA

BLOK SISTEM URONEFROLOGI Makassar, 26 December 2019

MODUL 2
URONEFROLOGI SYSTEM
“DECREASE URIN PRODUCTION”

Created By
Group 4
Tutor : dr. Nur Aisyah
dr. Irmayanti HB, Sp. PK
Muh. Akram Mu’fid 11020170085
Wa Ode Nur Fatimah Rifaat 11020170118
Vania Almira 11020170121
Nurul azizah An’naajiyyah 11020170148
Nurlana Zamaun 11020170162
Noor Qadriyanti Ramadhani 11020160090
Muh. Muslim Purnomo Sukman 11020170012
Tebi 11020170020
Miftahul Janna 11020170042
Andi Ishmah Faza 11020170056

FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2019
 FOREWORD

Our gratitude to Allah SWT for His blessings and guidance so that the report on
the results of this tutorial can be resolved properly. And do not forget we send our
greetings and blessings to the Prophet Muhammad who brought us from a world
full of ignorance to a world full of intelligence. We would also like to thank those
who helped make this report and the tutors who guided us throughout the tutorial
process. Hopefully the report on the results of this tutorial can be useful for
everyone who has read this report and especially for the drafting team itself.
Hopefully, after reading this report can broaden the knowledge of readers about
the face and stomach swelling.
Makassar, 26 December 2019

Group 4

2
SCENARIO 2
A woman, 30 years old, was hospitalized with complaints of reduced urine
production since yesterday afternoon. Complaints accompanied by low back pain.
In addition, patients feel very weak, vomiting often, and decreased appetite.
History of taking Ibuprofen for the past 1 week due to headaches. On physical
examination obtained HR 100/80 mmHg.

DIFFICULT WORD
-
KEYWORDS
- 30-years-old woman
- Urinary production has decreased since yesterday afternoon
- Low back pain, weakness, frequent vomiting and decreased appetite
- History of taking Ibuprofen medicine for the past 1 week
- HR 100/80 mmHg

QUESTIONS
1. Explain the anatomy, physiology and pathomechanism of decreased urine
production!
2. What are the factors that cause a decrease in urine production?
3. Explain the pathomechanism of weakness, vomiting, and decreased appetite
related to the scenario!
4. Explain the relation of the use of Ibuprofen drugs to patients based on the
scenario!
5. Explain diagnostic steps!
6. Explain the differential diagnosis related to the scenario!
7. Explain the initial management of the scenario!
8. Write down the Islamic perspective related to the scenario!

3
ANSWER
1) KYDNEY ANATOMY
Including the excretory system that produces urine, and drains out of the
body. Urine is the result of continuous blood filtration.1
a. Ren
There are two pieces, the shape of red beans with size 11 cm, width 6 cm
and thickness 3 cm Localization in the abdominis cavity, located on the
left and right vertebral columna. The cranial end is called the superior
polus (= cranial pollus) and the caudal tip is called the inferior polus (=
caudal polus), forming the anterior facies and posterior facies. Both
surfaces form lateral margo and medial margo. In the medial margo there
is the hilum renale, which is the site of entry and exit of the venous renal
artery, renalis, ureter and nerve fibers. In the superior pollus there is
suprarenalis gland.1
b. Ureter
Ureter is a channel formed by smooth muscle tissue with a size of
25 30 cm, connecting ren with vesica urinaria. Some are in the cavum
abdominis called pars abdominalis, and some are in the cavum pelvicum
called pars pelvina. The base of the ureter is a continuation of the pelvic
renis, separated from the ren through the hilal renale, located next to the
dorsal vasa renalis.1
The two ureters lead into the urinary vesica 5 cm apart from each
other. Walking obliq along 2 cm in the walls of the urinary vesica before it
empties into the vesica uinaria, called the ureteral os there are 3 ureteric
constriction sites, namely at the transition of the pelvic rena to the ureter,
(2) the compilation crosses the ailliaca communis, (3) mixed in the urinary
urinary.1
c. Vesica urinaria
A bag used by connective tissue and smooth muscle, which
functions as a storage area for urine. Volume 2000 3000 cc. Morphology
varies greatly, determined by time, sex and volume.1

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 d. Urethra
A fibromuscular canal, passed by urine from the urine vesica. This channel
closes when empty. In men also passed by semen (spermatozoa) There are
some between the urethra feminina and urethra masculina. Urethra in
women is called Urethra Feminina while in men it is called urethra
Masculina.1

Picture 1. Organs of The Urinary System

Vascularisation
The renal artery is branched by the abdominal aorta, the dexter renal artery
runs alongside the dorsal inferior vena cava. The superior vesical artery and the
inferior vesical artery are branched by the internal iliac artery. Giving
vascularisation to the urine, ureters and urethra pars prostatica. The renal vein
empties into the inferior vena cava.1,2
Innervation
Ren gets innervation from the renal plexus formed by the branching of the
coelicalicu plexux. Ureters receive innervation from n.thoracalis 10-12, n.lumbalis
1- sacralis 4. Urethral Vesica is preserved by vesicalis plexus originating from
n.sacralis 2-4.1

5
 Picture 2. Innervation of Kidney

KIDNEY PHYSIOLOGY (URIN FORMATION)

KYDNEY FUNCTION
Kidney is one of the organism that functions to maintain homostasis. In
maintaining renal homeostasis performs a variety of different functions.
Including:3,4
1. As organ endocrine
2. Art pressure regulator
3. Water and electrolyte balance
4. Acid Balance management
5. Vitamin D metabolism
6. Glucose metabolism
Glomerulus Filtration
The filtration process is taken over by the glomerulus. Capillaries in
glomerulus are relatively impermeable to proteins, where the results of filtration
will be free of protein and do not contain cellular elements, including red blood
cells. The structure of the glomerular membrane takes a role in the results of
filtration.3

6
 Picture 3. Glomerulous membrane
Glomerular membrane consists of three layers, from the outside starting
from the endothelial capillary membrane, glomerular basement membrane and
epithelial layer. The capillary endothelial lining of the fenestra is a pore, which
functions to filter substances with large molecules. In the second layer there is a
basement membrane, which is a network of collagen and proteoglycan fibers,
which are selective towards small molecules. This basal membrane consists of
three layers, from the outside in, the external lamina, lamina densa and internal
lamina. Small substances that can pass through capillaries, if they contain small
molecules, will not pass through the basement membrane. After passing through
the basement membrane the substance will pass through the epithelial layer. In
this layer there are long protrusions called podocytes. In these podocyte
protuberances there is a protein structure that causes the filtration gap that exists
between the podocytes to be polar, which if there are substances that contain
proteins there will be a process of repulsion so that the protein cannot pass
through the filtration gap . In the filtration gap there is a diaphragm through which
bacilli and filtration pass.3
The result of filtration is called glomerular filtrate liquid. The amount of
glomerular filtrate fluid is influenced by net filtration pressure. The net filtration
pressure is the pressure produced by the difference in hydrostatic pressure and the
oncotic pressure that is the agglomerular and bowman capsules. Hydrostatic
pressure on the glomerulus is determined one of them by arterial pressure where

7
the higher the arterial pressure, the greater the gromerulus hydrostatic pressure.
The hydrostatic pressure on the bowman capsule will increase in obstruction of
the urinary tract. Glomerular oncotic pressure is the pressure that works against
hydrostatic pressure, determined by the number of molecules, especially proteins
found in plasma. An increase in plasma protein will cause an increase in
concomglomerular pressure.3
Under normal circumstances, the glomerular hydrostatic pressure is 60
mmHg while the bowman's capsular hydrostatic pressure is 18 mmHg. This
causes the pressure of the glomerulus to be greater so that filtration is possible.
The oncotic pressure on the glomerulus holds back the filtration rate while the
oncotic pressure of the bowman capsule increases the filtration rate. However, due
to the oncotic pressure of the bowman capsule so little it can be said to be non-
existent. So the glomerular oncotic pressure which is normally 32mmHg will
withstand the glomerular filtration rate. If it can be concluded that the net
filtration pressure is the glomerular hydrostatic pressure minus the hydrostatic
pressure of the bowman capsule minus the glomerular oncotic pressure.3

The net filtration pressure greatly affects the Glomerular Filtration Rate
(LFG). In addition to the filtration pressure, LFG is also influenced by the state of
the glomerular layer. This condition is called the filtration coefficient. The
coefficient of filtration is strongly influenced by the state of the kidney itself. For
example in a state of chronic hypertension or diabetes mellitus causes a decrease
of the filtration coefficient so that it causes LFG also decreases. In the case of
obstruction of the ducts, urine, causing an increase in the hydrostatic pressure of
the bowman's capsule so the LFG will decrease. If the blood volume decreases so
that blood flow to the kidneys decreases it will cause the oncotic pressure of the
bowman capsule to increase, so the LFG will decrease.3

Tubulus Reabsorption
The reabsorpsitubulus is a very selective process. All plasma protein
solutes have the same concentration of glomerular filtrate in plasma. In most
cases, the amount of each absorbed material is the sum needed to maintain the
appropriate composition and volume of the internal fluid environment. In general,

8
tubules have a large reabsorption capacity for materials needed by the body and
are small or absent for substances that are not useful.3
To be reabsorbed, a change must pass five separate barriers, namely:3
1. Material must leave bodily fluids by passing through the cellular luminal
membrane.
2. The material must pass through the cytosol from all the tubules in the rest
3. Material must pass through the basolateral membrane seltubulus to enter the
intersisium fluid.
4. Material must be diffused through liquid liquids.
5. Material must penetrate capillary walls to enter blood vessels.
Tubular Secretion
Like tubular reabsorption, tubular secretion involves transepithelial
transport, but now the steps are reversed. By providing a second entry route into
the tubules for certain materials, tubular secretion, the separate transfer of material
from the perirubular capillaries into the tubule lumen, becomes a complementary
mechanism that increases elimination. Any material that enters ketubulus, either
through glomerular filtration or tubular secretion, and is not reabsorbed will be
eliminated in the urine.3
Normal substances in the urine:3,4

a. Organic components: Urea, uric acid, creatinine, amino acid derivatives,

conjugates with sulfuric acid glucuronic acid, glycine. Metabolites from many
hormones, choriogonadotropins, and urochromes.
b. Inorganic components: in the urine there are cations Na +, K +, Ca2 +, Mg2 +,
and NH4 +, as well as the Cl, SO42-, and HPO42- anions. Pathologic
substances present in urine glucose, ketones, proteins, blood, bilirubin.
c. Kidney compensation :5
1. secretion of hydrogen ions
2. reabsorption of bicarbonate ions
3. new bicarbonate ion production
Metabolic Acidosis : Excretion of hydrogen ions,

9
 Extracellular bicarbonate liquid
Metabolic Alkalosis : Secretion of hydrogen ions in the tubules,
Extracellular bicarbonate liquid

The pathomechanism of urine production decreases

Oliguria is a condition in which a person's urine is released less than 1 mL

/ kg / hour in infants, less than 0.5 mL / kg / hour in children, and less than 400mL
/ day in adults. Oliguria is a clinical indication of kidney failure and has been used
as a criterion for diagnosing kidney failure. While anuria is a condition where
there is no urine issued by someone. In clinical practice, the indicator is less than
50 mL / day.6
Etiology of oliguria and anuriaOliguria can occur through 3 types of
pathophysiological processes: mechanisms that occur pre-renal, intra-renal and
post-renal.6
Pre-renal
Oliguria that occurs prerenal is the functional response of the normal
kidney to hypoperfusion. Decreased blood volume triggers a systemic response
which aims to normalize the volume of fluid in the blood vessels by reducing
GFR. Activation of the sympathetic nervous system and the renin-angiotensin
system results in vasoconstriction of blood vessels in the kidneys and results in
decreased GFR.6

Picture 4. Pre-renal mechanism of Urine Production

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Patogenesis oliguria pre-renal
The initial stage of pre-renal oliguria is compensation for reduced
perfusion to the kidneys. In this stage what happens is auto-regulation of the
kidney which maintains GFR through afferent arteriolar dilatation (through
myogenic response, tubuloglomerular feedback) and efferent arteriolar
constriction (via Angiotensin II).6
This initial stage also includes an increase in the reabsorption of salt and
water in the tubules (stimulated by the RAA system and the sympathetic
nervous system). Usually this pre-renal oliguria is reversible if perfusion to
the kidneys is immediately corrected. However, ongoing renal hypoperfusion
can result in a shift from a compensatory mechanism to decompensation.6
In this decompensation phase there is excessive stimulation of the
sympathetic nervous system and the RAA system, which results in
vasoconstriction of blood vessels in the kidneys and can cause ischemia in
kidney tissue. Consumption of vasoconstrictor drugs and prostaglandin
synthesis inhibitors can cause oliguria due to decreased renal perfusion.6
Intra-renal

Picture 5. Intra renal mechanism of Urine Production

11
 Oliguria caused intra-renal is more associated with structural kidney
damage. Which include structural damage such as primary glomerular
disease, acute tubular necrosis or vascular lesions.6
The pathophysiology of ischemia due to acute tubular necrosis has
been widely studied. Ischemia that occurs in tubular cells affects cell
metabolism and dead tubular cells resulting in cell desquamation, cast
formation, intratubular obstruction, backflow of tubular fluid, and oliguria.6

Picture 6. Pasca renal mechanism of Urine Production

In most clinical cases, the oliguria is also reversible and is associated

with repair and regeneration of tubular epithelial cells.6
Pasca-renal

Oliguria caused by post-renal impairment is a consequence of mechanical

or functional obstruction of urine flow. Obstruction can occur in the upper
part of the urinary tract (pelvis, ureter) or lower part (vesika urine until it
exits the body). The form of oliguria from this problem is usually corrected
by removing obstruction.6

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2) Factors causing the decrease in urine production
Pre-renal
Oliguria that occurs in the pre-renal is the functional response of the
normal kidney to hypoperfusion. Decreased blood volume triggers a systemic
response which aims to normalize the volume of fluid in the blood vessels by
reducing the Glomerular Filtration Rate (LFG). Activation of the sympathetic
nervous system and the renin-angiotensin system results in vasoconstriction of
blood vessels in the kidneys and results in decreased LFG.6
The initial stage of pre-renal oliguria is compensation for reduced
perfusion to the kidneys. In this stage what happens is auto-regulation of the
kidneys that maintains LFG through afferent arteriolar dilatation (through
myogenic response, tubuloglomerular feedback) and efferent arteriolar
constriction (via Angiotensin II).6
This initial stage also includes an increase in the reabsorption of salt and
water in the tubules (stimulated by the RAA system and the sympathetic nervous
system). Usually this pre-renal oliguria is reversible if perfusion to the kidneys is
immediately repaired. However, ongoing renal hypoperfusion can result in a shift
from a compensatory mechanism to decompensation.6
In this decompensation phase there is excessive stimulation of the
sympathetic nervous system and the RAA system, which results in
vasoconstriction of blood vessels in the ginnjal and can cause ischemia in kidney
tissue. Consumption of vasoconstrictor and prostaglandin inhibitors can cause
oliguria due to decreased renal perfusion.6
Intra-renal
Oliguria that is caused in the renal is more related to the damage to kidney
structure. Which includes structural damage such as primary glomerular disease,
acute tubular necrosis (due to prolonged ischemia, drugs and toxins) or blood
vessel lesions.6
Pathophysiology of ischemia due to acute tubular necrosis. Ischemia that
occurs in tubular cells affects cell metabolism and dead tubular cells resulting in
cell desquamation, cast formation, intratubular obstruction, backflow of tubular

13
fluid, and oliguria. Oliguria is reversible and is associated with repair of tubular
epithelial cells.6
Pasca-renal
Oliguria caused by post-renal disorders is a consequence of mechanical or
functional obstruction of urine flow. Obstruction can occur in the upper part of the
urinary tract (pelvis, ureter) or lower part (vesika urine until it exits the body). The
form of oliguria from this problem is usually corrected by removing obstruction.6

3) Pathomechanism of weakness, vomiting, and decreased appetite

related to the scenario!
WEAKNESS
The motor unit and cerebral cortex are central to understanding hese
symptoms. At the cellular level, the basic problem may be the delivery of
adequate amounts of oxygen and nutrients. As a result of inadequate oxygen and
nutrient intake into cells, a state of hypoxia occurs. In cells, ATP levels will
decrease and ATP-ase activity is disrupted. This can cause impulses to be sent to
the brain and is interpreted as weakness and fatigue.7
VOMIT
Vomiting is a way of the gastrointestinal tract to clean itself and its contents
when almost all of the upper gastrointestinal tract is widely irritated. Excesive
distension or irritation from the duodenum causes strong stimulation to vomit.8
Once the vomiting center has been sufficiently stimulated and vomiting
behavior arises, the first effect is (1) deep breathing, (2) rising of the hyoideus and
larynx to attract the upper esophageal sphincter so that it opens, (3) glottic closure
to prevent vomiting from entering the lungs, and (4) removal of the mole palate to
cover the posterior nares. Then comes a strong diaphragm contraction down along
with the contraction of all the abdominal wall muscles. This condition squeezes
the stomach between the diaphragm and the abdominal muscles, forming an
intragastric pressure to a high extent. Finally, the fully relaxed lower esophageal
sphincter makes the secretion of stomach contents upward through the esophagus
So, the action of vomiting comes from a work of squeezing the abdominal

14
muscles associated with contraction of the stomach wall and opening of the
esophageal sphincter so that the contents of the stomach up through the
esophagus.8
The relations between vomiting and reduced urine production is when a
situation occurs where urine production is reduced, the waste substances from the
body cannot be excreted. As a result the remaining substances are stored and
accumulate in the blood. A condition called azotemia occurred. This situation then
stimulates the vomiting center in the medulla oblongata called Chemoreseptor
Trigger Zone. This causes reflex vomiting.8
DECREASED APPETITE
The hypothalamus is the part of the brain that plays an important role in
regulating the processes of homeostasis, including regulating appetite. A number
of central neuropeptides are known to be involved in them. Anabolic peptides
such as Neuropeptide Y (NPY) and Agouti-related protein (AgRP) act as
accelerators that work to stimulate eating so that it will increase appetite. Whereas
catabolic peptides such as Cocain-and-Amphetamine-Regulated-Transcript
(CART) also pro-opiomelanocortin (POMC) have the opposite effect of inhibiting
eating so that it will reduce appetite. When one neuron is activated, the other
population will experience inhibition.8
Fat cells in adipose tissue secrete a hormone, leptin. Leptin levels in the
blood represent the amount of triglyceride fat stores in fat tissue. The more fat
reserves, the more leptin is released into the blood. The collaboration between IL-
1 and TNFα will also cause an increase in leptin levels in the blood.8
Leptin receptors are found in large quantities in the ventromedial
hypothalamus which is the center of satiety. The presence of leptin also causes
suppression of the desire to eat through the inhibitory pathway to NPY and
stimulation of POMC and CART in the hypothalamic arkuatus nucleus. All of this
will cause a decrease in appetite.8
The relations between decreased appetite and reduced urine production is
when a situation occurs where urine production is reduced, the risk of

15
inflammation increases. When inflammation occurs, the immune response in the
body will release inflammatory mediators, including IL-1 and TNF α.8
The collaboration between IL-1 and Alfa TNF will cause an increase in
leptin levels in the blood. The presence of leptin will suppress the desire to eat
through the inhibitory pathway to NPY and stimulation of POMC and CART in
the hypothalamic arctic nucleus. Finally, there was a decrease in appetite.8

4. The relations of ibuprofen drug use to patients based on the scenario

Non Steroidal Anti Inflamation Drugs are anti-inflammatory drugs that are
often used in pain management but have risks in the form of gastrointestinal
disorders (peptic ulcer), bleeding, and hypertension. Besides having anti-
inflammatory effects, NSAIDs as well has an analgesic and antipyretic effect.
Based on the selectivity of COX-1 and COX-2, NSAIDs are divided into two
types namely COX-2 selective and non-selective. NSAIDs work as an anti-
inflammatory drug by inhibiting the enzyme cyclooksigenase in the arachidonic
acid pathway. This inhibition results in inhibition of prostaglandin, thromboxan,
and prostacyclin synthesis which are mediators of inflammation. Side Effects of
NSAIDs on the Kidney As previously explained that NSAIDs result in inhibition
of prostaglandin synthesis and prostacyclin, while prostaglandins and prostacyclin
function as renal vasodilation agents. Besides prostaglandins also have effects on
the inhibition of sodium and water resorption in the kidneys. While prostacyclin
also has a stimulating effect on sodium expenditure kidney. When the synthesis of
both is inhibited by NSAIDs, it not only causes renal vasoconstriction, but also an
increase in sodium and water reabsorption and a decrease in sodium excretion in
the kidneys. An increase in sodium and water reabsorption and a decrease in
sodium excretion in the kidneys results in an increase in blood pressure in a
person. Under normal circumstances, inhibition of prostaglandin synthesis does
not greatly affect the physiological function of the kidneys, but when
hemodynamic disorders occur, such as in elderly patients, patients with a history
of chronic kidney disease, heart failure, cirrhosis and diabetic patients, NSAIDs
must be careful. Based on the mechanism of action of NSAIDs the inhibition of

16
prostaglandin synthesis not only produces anti-inflammatory effects but can also
cause vasoconstriction in the afferent kidney. The occurrence of renal afferent
vasoconstriction results in decreased blood flow to the kidneys and decreased
glomerular filtration rate which causes substances that should not be excreted in
urine. This causes decreased urine production and the presence of minimal
metabolic waste in urine and increased blood.9

5. Diagnostic steps related to scenario

ANAMNESIS10
a. Patient ID: A woman, 30 years old
b. Main Complaints: urinary production has declined since yesterday
afternoon
c. Accompanying complaints: low back pain, feeling very weak, frequent
vomiting, and decreased appetite
d. Disease history: -
e. Family history: -
f. Environmental History: -
g. Previous Treatment History: taking Ibuprofen for 1 weeks continuously
PHYSICAL EXAMINATION10

The patient's physical examination includes examination of the patient's

general condition and urology examination. Often abnormalities in the field of
urology provide manifestations of general (systemic) disease, or not infrequently
urology patients happen to suffer from other diseases.

1. General impression of the patient

a. General condition: good or disease
b. Body weight: obese, thin or normal
c. Temperature: warm, cold, moist
d. Vital signs: - HR = 130/80 mmHg

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2. Urological Examination
a. Kidney examination
Any enlargement of the upper lumbar or abdominal area must be
considered during the inspection. Enlargement may be caused by
hydronephrosis or tumors in the retroperitoneal region. Kidney
enlargement due to hydronephrosis or kidney tumors, may feel palpation
and pain in percussion.
In Urolithiasis: supra symphysis pain is found due to infection or
palpable mass due to urinary retention. Large bimanual stones that can
be touched.
b. Buli-Buli Examination
On the bladder examination note the presence of a lump / mass or
scar tissue as a result of the incision / surgery in the suprasymphysis. The
mass in the suprasymphysis area may be a malignant bladder tumor or
because the bladder is fully filled from a urine retention. With palpation
and percussion the upper limit of the bladder can be determined.
In Urolithiasis: urethra stones may experience sudden urination with
severe pain in the glans penis, shaft of the penis, perineum, and rectum.
c. External Genital Examination
In external genital inspection, the possibility of abnormalities in the
penis / urethra includes micropenis, macropenis, hypospadias, cordae,
epispadia, stenosis of the external urethral meatus, phimosis /
parafimosis, urethro-cutaneous fistula, and penile ulcer / tumor. Severe
anterior urethral strains cause fibrosis of the corpus spongiosum which is
palpated on the palpation next to the ventral penis, a hard tissue known as
spongiofibrosis. Palpable hard tissue in the penile corpus cavernosa may
be a disease of Peyrone.
d. Scrotum Examination and Its Contents
Note whether there is an enlargement of the scrotum, a feeling of
pain when touched, or there is scrotal skin hypoplation that is often found
in cryptorchidism. To distinguish between solid mass and cystic mass

18
 contained in the contents of the scrotum, transillumination (illumination)
checks on the contents of the scrotum. Inspection of light is carried out in
a dark place and illuminates the scrotum with bright light. If the contents
of the scrotum seem dreamy it means it contains cystic fluid and is said
to be positive transillumination or positive diaphanoscopy.
e. Plug in the Rectal Toucher
The digital rectal examination was assessed: (1) anal sphincter tone
and bulbo-cavernous reflex (BCR), (2) looking for possible mass in the
rectal lumen, and (3) assessing the state of the prostate. The assessment
of the bulbo-cavernous reflex is done by feeling the pinch reflexes on the
anal sphincter on the fingers due to pain stimulation that we give to the
glans penis or clitoris.
f. Neurology Examination
Neurological examination is intended to look for possible
neurological abnormalities that result in abnormalities in the urogenital
system, such as motor neuron lesions or peripheral nerve lesions that are
the cause of the neurogen bladder.
LABORATORY EXAMINATION11

Urinalisis

Urinalysis is the examination most often done in cases of urology. This

examination includes tests:

a. Macroscopic by assessing the color, odor, and specific gravity of the

urine
b. Chemistry includes checking the acidity / pH, protein and sugar in the
urine
c. Microscopic search for the possibility of cells, casts (cylinders), or
other formations in urine.
d. Urine has an acidic pH, which is average: 5.5 - 6.5. If you get a
relatively alkaline pH there may be an infection by urea-splitting

19
 bacteria, whereas if the pH is too acidic there may be acidosis in the
kidney tubules or uric acid stones.
e. Significantly obtained erythrocytes in the blood (> 2 per field of view)
indicates an injury to the urinary system; and the presence of significant
leukosituri (> 5 per field of view) or pyuria is a sign of urinary tract
inflammation.
f. On AKI (Acute Kidney Injury) obtained
Urine volume. Acute anuria or severe oliguria, prerenal ARF1 is
usually almost always accompanied by oliguria (<400ml / day), although
sometimes oliguria is not found. Renal and post-renal ARF1 can be
characterized by both anuria and polyuria.

Blood tests
Routine blood tests consist of examining the levels of hemoglobin,
leukocytes, blood sedimentation rate, leukocyte count, and platelet count.
Urine Culture
Urine culture examination is examined if there is a suspected
urinary tract infection. If germs are found in the urine, they are bred in
certain media to look for types of germs and at the same time the
sensitivity of germs to the antibiotics being tested.
Pathology Anatomy
In this examination can be determined a normal tissue, undergoing an
inflammatory process, benign growth, or malignant growth occurs.
Besides this examination can determine the pathological stage and the
degree of differentiation of a malignancy.
Kidney Function Test
An increase in blood urea and creatinine levels progressively with
serum creatinine levels> 0.3 mg / dl around 50%, and blood urea levels
around 10-20 mg / dl per day. Electrolyte disturbance:
- Hyperkalemia
- Hyponatremia (sodium loss <120 mmol / liter)

20
 - Hypocalcemia
- Hyperphosphatemia (accumulation of phosphoric acid so that serum
calcium ion levels go down which will stimulate parathyroid to
increase the hormone again so that excretion of phosphate increases
again.
In CKD (Chronic Kidney Disease):
- Decreased kidney reserve (LFG between 50% - 80%)
- Renal insufficiency (kidney function between 20% - 50%)
RADIOLOGICAL EXAMINATION (IMAGING)11
1. Plain abdominal photo
Plain abdominal photo or KUB (Kidney Ureter Bladder) is a screening
photo for examination of urological abnormalities. In addition, it should be noted
that there are other radio-opaque shadows, for example the shadow of needles
(implants) that are located around the paravertebra that are deliberately mounted
to reduce pain in the waist or back, or the shadow of a clip mounted during
surgery to clamp a blood vessel.
In Urolithiasis:
- The most radiopaque to radiolucent sequence in BNO is; calcium
phosphate, calcium oxalate, magnesium ammonium phosphate, cystine, gout, and
xanthine. On the bladder stones appear layers of stone layered like an onion,
located in the middle line, and if there is an enlarged prostate, the stone is located
higher.
2. Ultrasound (Ultrasonography)
Examination of the kidney is used: (1) to detect the presence and condition
of the kidney (hydronephosis, cysts, mass, or shrinkage of the kidney). In bladder,
ultrasound is useful for calculating the residual urine after micturition and
detecting stones or tumors in the bladder. In the prostate gland, through the
transrectal approach (TRUS) is used to look for nodules in the prostate
malignancy and determine the volume / size of the prostate. If a suspected prostate
malignancy is found, TRUS can be used as a guide in biopsy of the prostate gland.
In the testis, it is useful to distinguish between testicular tumors and testicular

21
hydrocele, and sometimes can detect the location of cryptorchid testes that are
difficult to be palpated with. In malignancy, in addition to knowing the presence
of a solid mass in the primary organ, also to detect the possibility of metastases in
the liver or gland the aorta.
3. CT scan and MRI
Both of these examinations are widely used in the field of oncology to
determine the tumor staging, namely: tumor boundaries, invasion of organs
around the tumor, and look for metastases to the lymph nodes and to other organs.

6. Differential diagnosis related to the scenario

A. ACID KIDNEY INJURY

DEFINITION
Acute Kidney Injury (AKI) is a rapid decrease (in hours to weeks) that the
glomerular filtration rate (LFG) is generally reversible, followed by kidney failure
to excrete nitrogen residual metabolism, with / without impaired fluid and
electrolyte balance. The Acute Dialysis Quality Initiative (ADQI) consisting of
nephrologists and intensivists in America in 2002 agreed to change the term ARF
to AKI. The replacement of the term renal to kidney is expected to help ordinary
people understand, while the replacement of the term failure to injury is
considered to more accurately describe the pathology of kidney disorders.12
Initial evaluation and management of patients with acute kidney injury
(AKI) should include: 1) an assessment of the causes that contribute to kidney
injury, 2) an assessment of the clinical course including comorbidity, 3) a careful
assessment of volume status, and 4) steps appropriate therapy designed to
overcome or prevent the deterioration of renal functional or structural
abnormalities. Initial assessment of patients with classic AKI includes differences
between prerenal, renal, and post-renal causes.12
Acute kidney injury (AKI) is characterized by a sudden decrease in kidney
function that occurs within a few hours to days. The current diagnosis of AKI is
made on the basis of increased serum creatinine and decreased blood ureanitrogen

22
 (BUN) and urine output, although there are limitations. It should be noted that
changes in BUN and serum creatinine can represent not only kidney injury, but
also normal responses from the kidneys to extracellular volume depletion or
decreased renal blood flow.12
Acute kidney injury is defined when one of the following criteria is met:12
a. Serum creatinine increases by ≥ 0.3 mg / dL or ≥ 26μmol / L within 48
hours or
b. Serum creatinine increased ≥ 1.5 times that of the reference value, which
is known or thought to have occurred within one week or
c. Urine output <0.5ml / kg / day for> 6 consecutive hours
ADQI issued an AKI classification system with RIFLE criteria consisting
of 3 categories (based on increasing serum Cr levels or decreasing LFG or UO
criteria) that describe the severity of kidney function decline and 2 categories that
describe the prognosis of renal impairment.12
Table 1. Clasification of AKI in RIFLE Chriteria, ADQI Revision 2007
Increased Decreased
UO Chriteria
Category
SCr LFG

>1,5 x of basic value > 25% basic value <0,5 mL/kg/hour,

Risk >6 hours

>2,0 x of basic value > 50% basic value <0,5 mL/kg/hour,

Injury >12 hours

>3,0 x of basic our > 75% basic value <0,5 mL/kg/hour,

or >4 mg/dL >24 hours or

Failure
With increased
Anuria ≥12 hours
Akut > 0,5 mg/dL

Decreased persistent kidney function for more than four weeks

Loss

Decreased persistent kidney function for more than four weeks

End Stage

23
 In 2005, the Acute Kidney Injury Network (AKIN), a collaboration of
international nephrologers and intensivisors, proposed modifications to the RIFLE
criteria. AKIN strives to increase classification sensitivity by recommending.
With some modifications, the R, I, and F categories of the RIFLE criteria are
sequentially in accordance with AKIN criteria stages 1, 2, and 3. Categories L and
E on the RIFLE criteria describe clinical outcomes (outcomes) so they are not
included in the stages.12
Table 2. Clasification AKI with AKIN

Increased SCr UO Chriteria

Steps

>1,5 x basic value or <0,5 mL/kg/hour, ≥6 hours

1 Increased >0,3 mg/Dl

<0,5 mL/kg/hour,
2 >2,0 x basic value ≥12hours

>3,0 x basic value or <0,5 mL/kg/hour, ≥24

hours or
>4 mg/dL with acute increased > 0,5

3 mg/dL or Anuria ≥12 hours

Initiation of kidney replacement
therapy

24
 Picture 7. Classification of AKI with AKIN
In the identification of patients these two criteria are used, thus providing a
more accurate evaluation. Then for determining the AKI degree must also be
accurate because with increasing degrees, the risk of death and TPG will increase.
In addition, there is a known long-term risk after the onset of AKI resolution of
cardiovascular disease or CKD and death. So in determining the degree of the
patient must be classified based on the highest degree. So if SCr and UO give
different degrees, patients are classified in higher degrees.12
EPIDEMIOLOGY
AKI becomes a complication in about 5-7% of acute care admission
patients and reaches 30% in patients admitted in the intensive care unit (ICU).
AKI is also a medical complication in developing countries, especially patients
with a background of diarrheal diseases, infectious diseases such as malaria,
leptospirosis, and natural disasters such as earthquakes. The incidence has
increased fourfold at United State since 1988 and an estimated 500 per 100,000
population per year. This incidence is even higher than the incidence of stroke.
Several world reports show incidents that vary between 0.5-0.9% in the
community, 7% in patients treated in hospitals, up to 36-67% in patients treated in

25
 intensive care units (ICU) and 5-6% ICU patients with AKI require Kidney
Replacement Therapy (TPG or Replacement Renal Therapy (RRT)).12
AKI RISK FACTORS
Understanding the risk factors owned by individuals can help to prevent
the occurrence of AKI. This is especially useful in hospitals, where risk factors
can be assessed before exposure such as surgery or administration of potentially
nephrotoxic agents.12
Table 3. Risk Factor of AKI : Exposure and Susceptibilitas in AKI
nonspesific KDGIO 2012

Exposure Susceptibilitas

Sepsis Dehydration and fluid depletion

Chritical illnes Elderly

Shock circulation Woman

Burns Black race

Trauma CKD

Heart surgery (especially CPB) Chronic disease (cardio, pulmo.

Liver)

Nonkardiak major surgery Diabetes Mellitus

Nefrotoxic drugs Cancer

Radiocontras Agents Anemia

26
 Finally, it is very important to screen patients who are exposed to prevent
AKI, it is even advisable to always assess the risk of AKI as part of the initial
evaluation of emergency admission accompanied by biochemical examination.
Monitoring is still carried out on patients with high risk until the patient's risk
disappears.12
PATHOPHYSIOLOGY
Under normal circumstances renal blood flow and glomerular filtration
rate are relatively constant which is regulated by a mechanism called
authoregulation. Two mechanisms that play a role in this autoregulation are:12
a. Myogenic strain receptors in afferent vascular arteriole smooth muscle
b. Reciprocal tubuloglomerular
In addition to hyporepinephrine, angiotensin II, and other hormones can
also affect autoregulation. Pre-renal renal failure is mainly due to renal
hypoperfusion. In a state of hypovolemia, there will be a decrease in blood
pressure, which activates cardiovascular baroreceptors which in turn activate the
sympathetic nervous system, the renin-angiotensin system and stimulate the
release of vasopressin and endothelin-I (ET-1), which is the body's mechanism to
maintain blood pressure and cardiac output. and cerebral perfusion. In this
situation the mechanism of renal authoregulation will maintain renal blood flow
and glomerular filtration rate (LFG) with afferent arteriolar vasodilation affected
by myogenic reflexes, prostaglandins and nitric oxide (NO), as well as afferent
arteriolar vasoconstriction which is mainly influenced by angiotensin-II and ET- 1
There are three main pathophysiologies of the causes of acute kidney injury
(AKI):12
a. Decreased renal perfusion (pre-renal)
b.Renal intrinsic disease
c. Acute renal obstruction (post renal)
- Bladder outlet obstruction (post renal)
- Stones, thrombus or tumors in the ureter

27
Pre Renal Acute Kidney Failure (Azotemia Pre Renal)
In severe renal hypoperfusion (mean arterial pressure <70 mmHg) and
lasting for a long time, the authorization mechanism is disrupted where afferent
arterioles undergo vasoconstriction, mesangial contractions and increased
reabsorption of sodium and water. This condition is called prerenal or acute
functional renal failure where structural damage from the kidney has not yet
occurred.12
Treatment of hypoperfusion will improve intrarenal homeostasis to normal
again. Kidney authority can be influenced by various drugs such as ACEI,
NSAIDs, especially in patients over the age of 60 years with a serum creatinine
level of 2 mg / dL so that pre-renal ARF can occur. This process is easier for
hyponatremic conditions, hypotension, diuretic use, cirrhosis of the liver and heart
failure. It should be remembered that elderly patients can develop conditions that
are a risk of pre-renal ARF such as narrowing of the renal arteries (renovascular
disease), polycystic kidney disease, and intrarenal nephrosclerosis. A study of
mice that prerenal acute renal failure will occur 24 hours after the closure of the
renal artery.12
Intra-Renal Acute Kidney Failure (Intrinsic Renal Azotemia)
Acute renal acute renal failure is a complication of several renal
parenchymal diseases. Based on the primary location of tubular damage causing
acute renal failure, namely:12
a. Large kidney blood vessels
b. Renal glomerulus
c. Renal tubules: acute tubular necrosis
d. Kidney interstitial
Acute renal acute renal failure that often occurs is acute tubular necrosis
caused by ischemia and nephrotoxins. In renal renal failure vascular abnormalities
often occur which causes acute tubular necrosis. Where in NTA vascular and
tubular abnormalities occur. In vascular abnormalities occur:12
a. increased cytosolic Ca2 + in afferent glomerolar arterioles which causes
sensitivity to vasoconstrictor substances and authorization disorders.

28
 b. an increase in oxidative stress that causes renal vascular endothelial cell
damage, which results in an increase in A-II and ET-1 as well as a
decrease in prostaglandins and the availability of nitric oxide from
endothelial NO-synthase.
c. an increase in inflammatory mediators such as tumor necrosis factor and
interleukin-18, which will further increase the expression of intracellular
adhesion molecule-1 and P-selectin from endothelial cells, thereby
increasing the attachment of inflammatory cells especially neutrophil cells.
This situation will cause an increase in oxygen free radicals. All of the
above processes together cause intrarenal vasoconstriction which will
cause a decrease in GFR.
One of the most common causes of intrinsic AKI is sepsis, ischemic and
nephrotoxic both endogenous and exogenous on the basis of pathophysiology,
namely inflammation, apoptosis and regional perfusion changes that can cause
acute tubular necrosis (NTA). Other causes that are rarely found and can be
conceptually anatomically depend on the major part of damage to the renal
parenchyma: glomerulus, tubulointerstitium, and blood vessels.12
AKS sepsis-associated
It is an important cause of MMR, especially in developing countries. A
decrease in LFG in sepsis can occur in the absence of hypotension, although most
cases of severe sepsis occur haemodynamic collapse that requires a vasopressor.
Meanwhile, it is known that tubular injury is clearly associated with AKI in sepsis
with manifestations of tubular debris and cast in urine.12
The hemodynamic effect on sepsis can reduce LFG due to generalized
arterial vasodilation due to increased regulation of cytokines which triggers NO
synthesis in blood vessels. So there is a lot of efferent arteriolar vasodilation in
early sepsis or renal vasoconstriction in sepsis which continues due to activation
of the sympathetic nervous system, the renin-angiotensus-aldosterone system,
vasopressin and endothelin. Sepsis can trigger endothelial damage resulting in
microvascular thrombosis, reactive oxygen activation of species and adhesion and
migration of leukocytes that can damage renal tubular cells.12

29
Post Renal Acute Kidney Failure
Post-renal renal failure, post-renal ARF is 10% of all ARF. Post-renal
ARF1 is caused by intra-renal and extrarenal obstruction. Intrarenal obstruction
occurs due to deposition of crystals (urate, oxalate, sulfonamide) and proteins
(myoglobin, hemoglobin). Extrarenal obstruction can occur in the ureteric
pelvis by intrinsic obstruction (tumor, stone, papilla necrosis) and extrinsic
(malignancy in the pelvis and retroperitoneal, fibrosis) as well as in the bladder
(stones, tumors, hypertrophy / prostate malignancies) and urethra (striktura).
Post-renal ARF1 occurs when acute obstruction occurs in the urethra, bladder
and ureter bilaterally, or obstruction in the unilateral ureter where the other
kidney is not functioning.12
In the initial phase of acute total ureteric obstruction an increase in renal
blood flow and an increase in renal pelvic pressure is caused by prostaglandin-
E2. In the second phase, after 1.5-2 hours, there is a decrease in renal blood
flow below normal due to the influence of thromboxane-A2 and A-II. Kidney
pelvic pressure continues to increase but after 5 hours begins to settle. Phase 3
or chronic phase, characterized by decreased kidney flow and a decrease in
renal pelvic pressure to normal within a few weeks. Kidney blood flow after 24
hours is 50% of normal and after 2 weeks of staying 20% of normal. During
this phase, the release of inflammatory mediators and growth factors begin to
cause renal interstitial fibrosis.12
ETIOLOGY
The etiology of AKI is divided into 3 main groups based on the
pathogenesis of AKI, namely: (1) disease that causes renal hypoperfusion
without causing interference with the renal parenchyma (prarenal AKI, ~ 55%);
(2) disease that directly causes interference with the renal parenchyma (renal /
intrinsic AKI, ~ 40%); (3) diseases associated with urinary tract obstruction
(pascarenal AKI, ~ 5%). The incidence rate of AKI is highly dependent on the
place where the AKI occurs.12

30
DIAGNOSIS
a. Diagnosis Approach
In patients who meet the diagnostic criteria for AKI in accordance with the
above, it must first be determined whether the condition is indeed an AKI or an
acute condition in CKD. Some general standards that can distinguish between
these two conditions include a history of etiology of CKD, a history of etiology
causing AKI, clinical examination (anemia, neuropathy in CKD) and course of
disease (recovery in AKI) and kidney size. The standard is not fully applicable.
For example, the kidneys are generally small in CKD, but can also be normal in
size or even enlarged as in diabetic neuropathy and polycystic kidney disease. The
diagnostic approach should also lead to the determination of the etiology, stage of
AKI, and determination of complications.12
b. Clinical Examination
Physical examination and support is to distinguish the pre-renal, renal and
post-renal. In establishing the diagnosis of acute kidney failure examined:12
1. A careful history and physical examination to find the cause such as
cardiovascular surgery, angiography, history of infection (skin
infection, throat infection, urinary tract infection), history of swelling,
history of urinary stones.
2. Differentiating acute kidney failure with chronic for example anemia
and small kidney size indicates chronic kidney failure.
To diagnose ARF, repeated checks of renal function are required, such as
urea, creatinine or glomerular filtration rate. In outpatients always checked fluid
intake and output, body weight to estimate the existence of loss or excess body
fluids. In severe ARF with reduced kidney function water and salt excretion is
reduced so that it can cause edema, even to the point where there is severe excess
water or pulmonary edema. Reduced acid excretion can also cause metabolic
acidosis with Kussmaul's respiratory compensation. Generally, manifestations of
ARF are more dominated by factors of precipitation or primary disease.13

31
 1. Assessment of patients with AKI
g. Serum creatinine level. Kidney physiology is assessed by repeatedly
checking serum creatinine levels. Creatinine serum levels cannot
accurately measure LFG because it depends on production (muscle),
distribution in body fluids, and excretion by the kidneys13
h. Urine volume. Acute anuria or severe oliguria is a specific indicator
for acute kidney failure, which can occur before changes in blood
biochemical values. However, urine volume in ARF can vary, prerenal
ARF is usually almost always accompanied by oliguria (<400 ml /
day), although sometimes there is no oliguria. Renal and post-renal
ARF1 can be characterized by both anuria and polyuria.13
2. Biological markers (biomarkers). The requirement for a biological marker
of ARF is to be able to detect before an increase in creatinine levels
accompanied by ease of examination techniques. Biological markers are
needed to diagnose ARF as soon as possible. These biological markers are
substances released by damaged kidney tubules, such as interleukin 18,
tubular enzymes, N-acetyl-B-glucosamidase, alanine aminopeptidase,
kidney injury molecule 1. In one study in children after open heart surgery
gelatinase -associated lipocain (NGAL) is proven to be detected 2 hours
after surgery, 34 hours earlier than the increase in creatinine levels.13
SUPPORTING INVESTIGATION
From the examination of urinalysis, can be found various markers of
glomerular inflammation, tubules, urinary tract infections, or crystal uropathy. In
prerenal AKI, the sediment obtained is acellular and contains transparent hyaline
cast. Postrenal AKI also shows a picture of inactive sediments, although
hematuria and pyuria can be found in intralumen obstruction or prostate disease.
The renal AKI will show a variety of casts that can lead to the cause of the AKI,
including pigmented "muddy brown" granular casts, casts containing tubular
epithelium that can be found on ATN; erythrocyte cast on glomerular damage or
tubulointerstitial nephritis; leukocyte cast and pigmented "muddy brown" granular
cast in interstitial nephritis.13

32
 Biochemical results of blood (Na, Cr, plasma urea) and urine (urine
osmolality, Na, Cr, urine urea levels) in general can lead to the determination of
the type of AKI.13
MANAGEMENT
By definition, prerenal AKI is reversible in correction of major
haemodynamic abnormalities, and postrenal AKI by removing obstruction. To
date, there is no specific therapy for establishing intrinsic renal AKI due to
ischemia or nephrotoxicity. Management of this disorder must focus on
eliminating hemodynamic abnormalities of causes or toxins, avoiding additional
symptoms, and prevention and treatment of complications. Specific treatment of
other causes of renal AKI depends on the underlying pathology.13
AKI Prarenal
The composition of the replacement fluid for the treatment of prerenal
ARFs due to hypovolemia must be adjusted according to the composition of the
lost fluid. Severe hypovolemia due to bleeding must be corrected with packed red
cells, whereas isotonic saline is usually an appropriate replacement for mild to
moderate bleeding or plasma loss (for example, burns, pancreatitis). Urinary and
gastrointestinal fluids can vary greatly in composition but are usually hypotonic.
Hypotonic solutions (for example, 0.45% saline) are usually recommended as an
early replacement in patients with prerenal ARF due to increased urinary or
gastrointestinal loss, although isotonic saline may be more appropriate in severe
cases. Subsequent therapy must be based on measuring the volume and isotonic of
the excreted fluid. Serum potassium and acid-base status must be monitored
carefully. Heart failure may require aggressive management with positive
inotropics, preload and afterload reducing agents, antiarrhythmic drugs, and
mechanical aids such as intraaortic balloon pumps. Invasive hemodynamic
monitoring may be needed to guide therapy for complications in patients whose
clinical assessment of cardiac function and intravascular volume is difficult.12,13
Intrinsic renal AKI
AKI due to other intrinsic kidney diseases such as acute glomerulonephritis or
vasculitis can respond to glucocorticoids, alkylating agents, and / or

33
plasmapheresis, depending on the primary pathology. Glucocorticoids also
accelerate remission in some cases of allergic interstitial nephritis. Aggressive
control of systemic arterial pressure is of crucial importance in limiting kidney
injury in malignant hypertension, nephrosclerosis, toxemia of pregnancy, and
other vascular diseases. Hypertension and AKI due to scleroderma may be
sensitive to treatment with ACE inhibitors.AKI postrenal.13
Postrenal AKI
Management of postrenal AKI requires close collaboration between
nephrologist, urology, and radiology. Disorders of the urethral neck or bladder are
usually managed initially by transurethral or suprapubic placement of the bladder
catheter, which provides temporary relief while obstructing lesions are identified
and treated definitively. Similarly, ureteral obstruction can be treated initially by
percutaneous catheterization of the renal pelvis. Indeed, blocking lesions can often
be treated percutaneously (for example, calculus, sloughed papilla) or bypassed by
the insertion of a ureteral stent (for example, carcinoma). Most patients experience
proper diuresis for several days after obstruction relief. About 5% of patients
develop transient salt-wasting syndrome which may require administration of
intravenous sodium to maintain blood pressure.13
Basically the governance of AKI is largely determined by the cause of
AKI and at what stage AKI is found. If found in the prarenal and initiation stages
(RIFLE R and I criteria), efforts that can be made are optimal management of
basic diseases to prevent patients from falling at the next AKI stage. These efforts
include rehydration if the cause of AKI is prarenal / hypovolemia, sepsis therapy,
cessation of nephrotoxic substances, correction of postcarenal obstruction, and
avoidance of nephrotoxic agents. Monitoring fluid intake and discharge must be
done routinely. During the polyuria stage (maintenance and initial repair stages),
some patients can experience significant fluid deficits, so close monitoring and
careful regulation of fluid and electrolyte balance must be carried out. Fluid
substitution must be closely monitored with guidelines for urine volume measured
serially, as well as urine and serum electrolytes.13

34
NUTRITION THERAPY
The nutritional needs of AKI patients vary depending on the underlying
disease and the comorbid conditions encountered. A classification system for
nutrition based on catabolism status was proposed by Druml in 2005.13
Table 4. Nutritional of Patient AKI
Katabolisme
Variabel
Mild Moderate Severe

Clinical state Toxic of drug Surgery +/- Sepsis, ARDS,

Infection MODS

Dialisis Rarely Based on needen Often

Route of Oral Enteral +/- Enteral +/-

Nutrition Parenteral Parenteral

20-25 25-30 25-30

Energy kkal/kg/BBari kkal/kg/BBari kkal/kg/BBari

Energy sources Glucose 3-5 Glucose 3-5 Glucose 3-5

g/kgBB/day g/kgBB/day g/kgBB/day

Fat 0,5-1 Fat 0,8-1,2

g/kgBB/day g/kgBB/day

0,6-1 0,8-1,2 1,0-1,5

Protein g/kgBB/day g/kgBB/day g/kgBB/day

Foods Enteral Enteral

Glucose
Nutrition supply Glucose formula 50- formula 50-

70% 70%

Fat 10-20% Fat10-20%

AA 6,5-10 % AA 6,5-10 %

Mikronutrien Mikronutrien

35
 The criteria for starting ginal replacement therapy in critical patients with
acute ginal disorders are:13
a. Oliguria: urine production <2000 ml in 12 hours
b. Anuria: urine production <50 ml in 12 hours
c. Hyperkalemia: Levels of potassium> 6.5 mmol / L
d. Severe acidemia (acid poisoning): pH <7.0
e. Azotemia: urea levels> 30 mmol / L
f. Uremic encephalopathy
g. Uremic neuropathy / myopathy
h. Uremic pericarditis
i. Sodium plasma abnormalities: concentrations> 155 mmol / L or
<120 mmol / L
j. Hyperthermia
k. Drug poisoning
COMPLICATIONS
Complications related to AKI depend on AKI's objections and mild and
moderate AKI related conditions may be overall asymptomatic especially at the
beginning.13
PREVENTION
The best prevention of AKI is to pay attention to the hemodynamic status of a
patient, maintain fluid balance and prevent the use of nephrotoxic substances or
drugs that can interfere with kidney compensation in someone with impaired
kidney function. Neither dopamine or diuretic dopamine has been proven
effective in preventing AKI.13
PROGNOSIS
Mortality due to ARF depends on the state of the clinic and the degree of
kidney failure. It should be noted that the age factor, the older the worse the
prognosis, the accompanying infection, gastrointestinal bleeding, severe causes
will worsen the prognosis. The most common causes of death are infection (30-
50%), especially gastrointestinal bleeding (10-20%), heart (10-20%), respiratory
failure (15%), and multiorgan failure with a combination of hypotension,

36
septicemia, and so on. Patients with ARF who undergo dialysis have a mortality
rate of 50-60%, so prevention, early diagnosis, and early therapy need to be
emphasized.13
B. UROLITHIASIS
DEFINITION
Urinary stones are hard masses that develop from crystals that separate from
the urine while in the urinary tract. Normally, urine contains chemicals to prevent
or inhibit the formation of these crystals. However, the block does not work on
everyone, so on those people the stone is still formed. If the crystals that are
formed are small enough, then the crystal stones will leave the body through the
urinary tract unnoticed. Urinary tracts can contain a mixture of various chemicals.
The most common type contains calcium in combination with oxalate or
phosphate. These chemicals are normal in a person's diet and form important body
parts such as bones and muscles.12
A more rare type is a type of stone that is formed due to infection of the
urinary tract. This type of stone is called struvite (infection stone). The other type
is uric acid stones which are quite rare and cystine stones are a rare type.12
Urolithiasis is a medical term used for stones that form in the urinary tract.
Another term commonly used is urinary tract stone disease and nephrolithiasis.
Doctors also use the term to describe the location of stones in the urinary tract.
For example, stones in the ureter are called uerterolithiasis.12
ETIOLOGY
Cystinuria and hyperoxaluria are two types of inherited and rare metabolic
disorders that can cause stone formation. In cystinuria, too many amino acids that
are not dissolved in the urine, bind together, causing the formation of stones
formed from cystine. In hyperoxaluria patients, the body produces too much
oxalate, which is a type of salt. When urine contains oxalate rather than dissolved,
the crystals then settle and form stones.12
Hypercalciuria is hereditary, and is likely to cause stone formation in more
than half of patients. Calcium is absorbed from food excessively and is excreted in

37
urine. High calcium levels in the urine cause the formation of calcium oxalate
crystals or calcium phosphate in the kidneys or elsewhere in the urinary tract.12
Other causes of urinary tract stones are hyperuricosuria, which is a disorder
of gout metabolism (gout), excessive intake of vitamin D, urinary tract infections,
urinary tract obstruction. Certain diuretics, commonly called water pills, and
calcium-based antacids can enhance the formation of urinary tract stones due to
increased calcium in the urine.12
Calcium oxalate stones can form in people who have chronic intestinal
inflammation or who have undergone intestinal bypass surgery, or ostomy
surgery.12
Calcium oxalate stones can form in people who have chronic intestinal
inflammation or who have undergone intestinal bypass surgery, or ostomy
surgery. As mentioned previously struvite stones can form in people suffering
from urinary tract infections. People who use indinavir protease inhibitors, drugs
used to treat HIV infection, also experience increased risk of kidney stone
formation.12
EPIDEMIOLOGY
Up to 10% of caucasian men will have urinary tract stones by the age of
70. Within 1 year calcium oxalate will form, 10% of men will form another
calcium oxalate stone, and 50% will form another type of stone in 10 years. The
prevalence of urinary tract stone disease is determined by individual intrinsic
factors (sex, age, heredity) and extrinsic factors (geographical location, climate,
and season of water intake, diet, occupation). The combination of these factors
often has a contribution in the formation of urinary tract stones.12
PATOMECHANISM
Stones can form because urine becomes too saturated with salts that can
form stones or urine lacks normal inhibitors of stone formation such as citrate.
Citrate can bind to calcium which is usually involved in stone formation. About
80% of urinary stones contain calcium and the rest can be various substances such
as uric acid, cystine, and struvite. Urinary tract stones are more common in people
with certain disorders (such as hyperparathyroidism and short bowel syndrome)

38
and in people on a diet high in protein or vitamin C or who do not consume
enough water or calcium. People with a family history of urinary tract stone
formation may have calcium stones and more often. Struvite stones are a mixture
of magnesium, ammonium, and phosphate, also called infection stones because
they only form in infected urine.12
CLINICAL MANIFESTATIONS
Symptoms and signs depend on the location of the stone. Patients with
glabal stones (nephrolithiasis) will feel achy and colic in the costovertebral angle
(costovertebra angle = CVAi). Physical examination showed tenderness and CVA
pain. If hydronephrosis occurs, a mass will be felt. An infection can occur and if
there is sepsis will be fever, chills and apathy. Symptoms of digestive tract such as
nausea, vomiting, and abdominal distension can occur due to paralytic ileus.
Hematuria can occur micro (90%) or macro (10%).12
In patients with ureteric stones (ureterolithiasis) there is sudden pain
caused by a stone passing, pain in the form of aches in the CVA or colic that
radiates to the lower abdomen according to the location of stones in the ureter. In
men the pain will radiate to the testes if the stone is in the proximal ureter or vulva
in women and the scrotum in the stones in the distal ureter. Digestive tract
disorders can also occur. When the stone has settled in the ureter, it is only found
aching in the CVA due to the dam. Patients who experience colic appear nervous
and their skin is wet and cold. On physical examination, tenderness and CVA
tenderness, spasm of the abdominal muscles, hypersensitive testes, and
hypersensitive scrotum. Tile stones settled in the ureter only found tenderness and
pain or not found any abnormalities at all.12
In patients with bladder stones (vesicolithiasis0 there are symptoms of
urinating which are suddenly stopped and painful pain radiating to the penis.
Stopped mictures can be smoothed back when the position is changed. If this
happens to children, they will roll around. and pulling on his penis, if there is an
infection, there are signs of cystitis to hematuria, on physical examination there is
supra symphysis pain due to infection or palpable mass due to urinary retention,
large stones that can be touched bimanual.12

39
 Patients with urethra stones may experience sudden urination with severe
pain in the glans penis, shaft of the penis, perineum, and rectum. The pain can
lead to the location where the stone can be held in the urethra:12
a. Glans penis - navicularis fossa
b. Anterior urethra - stone location
c. Perineum and rectum - urethra bulb and urethra pars prostatica
SUPPORTING INVESTIGATION12
a. Regional laboratory tests that should be performed are complete peripheral
blood and kidney function tests.
b. In the examination of urinalysis when pH> 7.6 is usually found urea splitting
which causes inorganic stones while acidic pH causes organic stones (uric
acid stones). Can also be found sediments, microscopic hematuria (90%), and
if there is a leukocyte infection will increase. Examination to look for causes,
among others, can be measured excretion of Ca, phosphorus, uric acid in
urine 24 hours.
c. During the BNO-IVP examination, the location, size, number of stones and
the presence of a dam were seen. The most radiopaque to radiolucent
sequences on BNO are; calcium phosphate, calcium oxalate, magnesium
ammonium phosphate, cystine, gout, and xanthine. On the bladder stones
appear layers of stone layered like an onion, located in the middle line, and if
there is an enlarged prostate, the stone is located higher.
In impaired kidney function, IVP is not carried out so that retrograde
pyelography is performed or if the results of retrograde pyelography are
inadequate followed by anthropadic pyelography.12
Helical (also called spiral) computed tomography (CT) can be done without using
contrast. CT can determine the location and determine where the stones clog the
urinary tract.12
Ultrasonography is an alternative examination other than CT and does not
expose patients to radiation. But with ultrasonography can pass a small stone
(especially the one lying on the ureter), the location of the blockage.12

40
MANAGEMENT
Management can be by:12
a. Open operation
b. Endoscopic surgery (PNCL, URS-lithotrpsy, mechanical lithotripsy, etc.)
c. Extra Corporeal Shockwave Lithotrpsy
Conservative therapy with diuretic administration can only be done on ureteral
stones <5mm in diameter with mild hydronephrosis whose colic pain has been
treated.12
PROGNOSIS
The prognosis of urinary stones depends on factors including:12
a. Big stone
b. Stone layout
c. An infection
d. Obstruction
The bigger the stone the worse the prognosis. Location of stones that can cause
obstruction can facilitate infection. The greater the tissue damage due to infection
due to obstruction will be able to cause a decrease in ginal function so that the
prognosis is getting worse.12
C. CHRONIC KIDNEY FAILURE
DEFINITION
Kidney is one of the main organs of the urinary system or urinary which is
responsible for filtering and removing metabolic waste fluid from the body. As is
known, after the cells of the body convert food into energy, waste will also be
produced as a byproduct of the metabolic process that must be removed
immediately so as not to poison the body. Some through the kidney with urine,
and the rest through the skin under sweat.13
The kidneys are tasked with filtering wastes carried by the blood to keep
the blood clean, and removing the metabolic waste so that the body's cells do not
become sluggish due to poisoning. These substances come from the normal
process of processing food consumed, and from the breakdown of muscle tissue
after carrying out a physical activity. The body will use food as energy and repair

41
body tissue. After the body has taken enough of the food according to the need to
support the activity, the rest will be sent into the blood to be filtered kidney.13
Chronic kidney failure is kidney damage that occurs for more than 3
months, based on pathological abnormalities or markers of kidney damage such as
proteinuria. The diagnosis of chronic kidney disease is when the glomerular
filtration rate (LFG) is less than 60ml / min / 1.73m². Classification of chronic
kidney disease is based on two things, namely on the basis of the degree of
disease and on the basis of etiological diagnosis. Classification based on the
degree of disease, made on the basis of LFG, which is calculated using the
Kockcroft-Gault formula:13,14
LFG (ml/minute/1,73m²) = ( 140 – age ) x weight *)
72 x kreatinin plasma (mg/dl)
*) in women multiplied by 0.85
Table 5. Criteria for chronic kidney disease
Kidney damage that occurs more than 3 months, in the form of structural or
functional abnormalities, with or without a decrease in glomerular filtration rate
(LFG), with manifestations:
- Pathological abnormalities
 There are signs of kidney abnormalities, including abnormalities in the
composition of blood or urine, or abnormalities in the imaging process
Glomerular filtration rate (LFG) is less than 60 ml / min / 1.73m² for 3 months,
with or without kidney damage.

42
 Table 6. Classification of Chronic Kidney Injury based on degree of disease
Degree Describe LFG
(ml/minute/1,73m²)
1 Kidney injury with normal or ≥ 90
increase LFG
2 Kidney injury with small decrease 60 – 89
LFG
3 Kidney injury with moderate LFG 30 – 59
4 Kidney injury with significant 15 – 29
decrease LFG
5 Kidney Injury < 15 or dyalisis

This distinction is not always the same throughout the world, but it is
better to be distinguished from one another to prevent confusion. The term
azotemia shows an increase in blood urea and creatinine levels, but there are no
obvious symptoms of kidney failure. Whereas uremia is a symptomatic phase of
kidney failure where kidney symptoms can be detected clearly.13,14
ETIOLOGY
Chronic kidney failure is a continuation of several types of diseases as follows:13
a. Chronic kidney tissue diseases such as glomerulonephritis.
Glomerulonephritis or commonly called inflammation of the glomerulus
(kidney filter unit) can damage the kidneys, so the kidneys can no longer
filter out the body's remaining metabolic substances and cause kidney
failure.
b. Endocrine diseases such as complications of diabetes, type 1 and type 2
diabetes.
c. Chronic infections, such as pyelonephritis and tuberculosis. Pyelonephritis
is a bacterial infection of one or both kidneys.
d. Congenital abnormalities such as kidney cysts.
e. Kidney obstruction, such as kidney stones.

43
 f. Vascular diseases such as nephrosclerosis and high blood pressure.
Malignant nephrosclerosis is a condition associated with high blood
pressure (malignant hypertension), malignant or excessive decrease in blood
pressure causes kidney blood flow to decrease so that the smallest arteries
(arterioles) in the kidneys are damaged and immediately kidney failure
occurs.
g. Binding tissue diseases such as lupus. This lupus occurs when antibodies
and complement are formed in the kidney which causes an inflammatory
process that usually causes nephrotic syndrome (large protein expenditure)
and can quickly cause kidney failure.
h. Drugs that damage the kidneys, for example, aminoglycoside therapy in the
long term
All of these factors will damage the kidney tissue gradually and cause kidney
failure. If a person suffers from acute kidney failure that does not respond to
treatment, chronic kidney failure will form.13
PATHOGENESIS
Decreased kidney reserve (LFG between 50% - 80%). This stage is the
mildest, where the kidney physiology is still good. At this stage this patient has
not yet felt the symptoms and LFG examination is still within normal limits.
During this stage serum creatinine and BUN (Blood Urea Nitrogen) levels are
within normal limits and asymptomatic sufferers. Impaired kidney function may
only be known by giving a heavy workload, such as a long bladder concentration
test or by conducting a careful GFR test.13
Renal insufficiency (renal physiology between 20% - 50%). At this stage
the patient can perform tasks as usual even though the power and concentration of
the kidneys decrease. At this stage the treatment must be fast in terms of
overcoming fluid deficiency, salt deficiency, heart problems and prevention of
administration of drugs that are disturbing kidney physiology. If these steps are
carried out as soon as possible correctly can prevent sufferers from entering more
severe stages. At this stage more than 75% of the functioning network has been
damaged. BUN levels have only just begun to rise above normal limits. This

44
increase in BUN concentration varies, depending on the protein content in the
diet. At this stage serum creatinine levels begin to rise above normal levels.13
Polyuria due to kidney failure is usually greater in diseases that mainly
attack the tubules, although polyuria is moderate and rarely more than 3 liters /
day. Usually found anemia in kidney failure with kidney physiology between 5%
- 25%. kidney physiology is clearly very decreased and symptoms of lack of
blood arise, blood pressure will rise, the patient's activities begin to be disrupted.
Uremi kidney failure (kidney function less than 10%). All symptoms are clear and
the patient enters into a state where he cannot perform daily tasks as he should.
Symptoms that arise include nausea, vomiting, decreased appetite, shortness of
breath, dizziness, headaches, reduced urine, sleep deprivation, convulsions and
finally a decrease in consciousness until coma. The final stage arises in about 90%
of the mass of the nephron has been destroyed. The GFR is 10% from normal and
creatinine levels may be 5-10 ml / min or less.13
In this situation serum creatinine and BUN levels will increase very
markedly as a decrease. In the final stage of kidney failure, sufferers begin to
experience symptoms that are quite severe because the kidneys are no longer able
to maintain light and electrolyte homeostasis in the body. Patients usually become
oliguric (urinary output) of less than 500 / day due to glomerular failure even
though the disease process initially attacks the kidney tubules.13
Complex attacks the kidney tubules, complex biochemical changes and
symptoms called uremic syndrome affect every system in the body. In the final
stage of kidney failure, the sufferer will surely die unless he gets treatment in the
form of a kidney transplant or dialysis.13
PATHOPHYSIOLOGY
The pathophysiology of chronic kidney disease actually depends on the
underlying disease, but in subsequent developments the process is more or less the
same.13
Reduction in renal mass results in structural and functional hypertrophy of
the nephron that remains as a compensatory effort, mediated by vasoactive
molecules such as cytokines and growth factors. This results in hyperfiltration,

45
which is followed by increased capillary pressure and glomelurus blood flow.
This adaptation process lasted a short time, finally followed by a maladaptation
process in the form of nephron sclerosis that still remains. This process is
eventually followed by a progressive decline in the function of the nephron, even
though the underlying disease is no longer active.13
An increase in the activity of the renin renin-angiostein-aldosterone axis,
partly mediated by growth factors such as transforming growth factor β. Some
diseases are also considered to play a role in the progression. Chronic kidney
disease is albuminuria, hypertension, hyperglycemia, dyslipidemia. There is
interindividual variability for both sclerosis and glomerular and tubulointerstitial
fibrosis.13
In the earliest stages of chronic kidney disease, there is a loss of kidney
spare power, in which circumstances the basal LFG is still normal or even
increased. Then slowly but surely, there will be a progressive decline in nephron
function, which is characterized by an increase in serum urea and creartinin levels.
Until the LFG is 60%, the patient still has no complaints (asymptomatic), but
there has been an increase in serum urea and creatinine levels. Until the LFG of
30%, began to occur complaints in patients such as, nocturia, weak body, nausea,
lack of appetite and weight loss.14
Until the LFG is below 30%, the patient shows symptoms and signs of
uremia such as anemia, increased blood pressure, impaired phosphorus and
calcium metabolism, pruritus, nausea, vomiting and so forth. Patients are also
susceptible to infections such as urinary tract infections respiratory infections or
gastrointestinal infections. There will also be disruption of water balance such as
hypo or hypervolemia, electrolyte balance disorders such as sodium and
potassium. If the LFG is below 15%, there will be more serious symptoms and
complications, and the patient will need kidney replacement therapy such as
dialysis or kidney transplantation. In this situation the patient is said to have
reached the stage of kidney failure13.

46
EPIDEMIOLOGI
The number of patients with chronic or asymptomatic chronic renal failure
makes it difficult to know the exact prevalence of chronic kidney failure. A more
precise number is the number of patients with chronic kidney failure who enter
the terminal phase because they require or are undergoing dialysis. From data
based on abnormal serum creatinine, it is currently estimated that patients with
chronic kidney failure are around 2000 per million population. Most of these
patients do not need replacement treatment, because they have already died from
other causes. Compared to coronary heart disease, stroke, DM, and cancer, this
number is much smaller, but it causes big problems because the treatment is very
expensive.13
Data and epidemiological studies on chronic kidney failure in Indonesia
can be said to be missing. Existing but also rare, are clinical epidemiological
studies or data. At this time, the prevalence patterns in Indonesia cannot be stated,
nor can the morbidity and mortality patterns. The available clinical data comes
from national referral hospitals, provincial referral hospitals and specific private
hospitals. Thus it can be understood that the data comes from special groups.13
CLINICAL SYMPTOMS14
a. Kidney and urinary system: initially changes in the form of low blood
pressure, dry mouth, lost skin tone, lethargy, fatigue, nausea and finally
confusion. Because the kidneys lose the ability to excrete sodium, sufferers
will experience sodium retention and excess sodium, so the sufferer
becomes irritated and becomes weak. Urine output decreases and affects the
chemical composition.
b. Heart and blood circulation: kidney failure continues to become high blood
pressure, heart rate becomes irregular, swelling of congestive heart failure.
c. Respiratory equipment: the lungs undergo changes with great susceptibility
to infections, fluid accumulation, pneumonia in pain and difficulty breathing
due to congestive heart failure.

47
 d. Gastrointestinal tract: inflammation and ulceration occurs in most digestive
tracts. Other symptoms are feeling metal in the mouth, ammonia breath,
decreased appetite, nausea and vomiting.
e. Skin: very characteristic of the skin becoming pale, bluish brown, dry and
scaly. Fingernails become thinner, brittle, hair dry and easy to pata,
discoloration and easy fall.
f. Nervous system: limb syndrome syndromes - a sign of nerve damage, pain,
such as burning, itching of the feet and legs. Can be reduced by moving or
twirling. Muscles also become cramped and move around, memory is
reduced, attention is reduced, drowsiness, irritability, confusion, coma, and
seizures. The doctor will check the brain waves to show the damage.
g. Endocrine glands: chronic kidney failure provides slow growth in children,
infertility and decreased sexual desire for both sexes, reduced menstruation
can even stop altogether, decreased impotence and sperm production and
increased blood sugar levels as in diabetes.
h. Blood changes: anemia, decreased age of red blood cells, blood loss during
dialysis and bleeding in the digestive tract, and blood clotting disorders.
i. Muscles and bones: mineral and hormone imbalances cause muscle and
bone pain, bone loss, breakage, calcium deposits in the brain, eyes, gums,
joints, inner heart, and blood vessels. Arterial classification will result in
coronary heart disease. Kidney is found in calcification of the kidneys.
LABORATORY DESCRIPTION
Laboratory tests are carried out to determine the presence of chronic
kidney failure, determine the presence or absence of emergencies, determine the
degree of chronic kidney failure, determine system disorders, and help establish
etiology. Laboratory features of chronic kidney disease include:14
a. In accordance with the underlying disease.
b. Decreased kidney function in the form of increased serum urea and
creatinine levels, and decreased LFG. Serum creatinine levels alone
cannot be used to estimate kidney function.
c. Biochemical abnormalities of blood.

48
 d. Urinalization disorders.
Tests that are generally considered to support the possibility of a chronic
kidney failure are:14
a. Elevated blood sedimentation rates are exacerbated by the presence of
anemia and hypoalbuminemia.
b. Normochrome normositer anemia, and decreased reticulocyte count.
c. Increased serum blood and creatinine levels.

Usually the ratio between ureum and creatinine is around 20: 1. This ratio
can be elevated (ureum> creatinine) in gastrointestinal bleeding, fever, extensive
burns, severe illness with hyperchabolism, steroid treatment and urinary tract
obstruction. This comparison is reduced (urea> creatinine), on a low protein diet
(TKU) and creatinine clearance test (TKK) decreases:14
a. Hyponatremia, generally due to excess fluid.
b. Hyperkalemia usually occurs in advanced kidney failure (TKK <5 ml /
min) along with decreased diuresis. Hypokalemia occurs in tubular
kidney disease or excessive use of diuretics.
c. Hypocalcemia and hyperphosphatemia. Hypocalcemia mainly occurs
due to reduced absorption of calcium in the small intestine due to
reduced synthesis of 1.25 (OH) 2. Hyperphosphatemia occurs due to
impaired kidney function so that the expenditure of phosphorus is
reduced. Between hypocalcemia, hyperphosphatemia, vitamin D,
parathormone and bone metabolism, there is a mutually influential
relationship.
d. Leachate phosphatase is elevated, due to bone metabolic disorders,
which are elevated especially bone leachate phosphatease isoensim.
e. Hypoalbuminemia and hypocholesterolemia are generally caused by
metabolic disorders and inadequate / low protein diets.
f. Elevation of blood sugar due to impaired carbohydrate metabolism in
kidney failure, which is thought to be caused by intolerance to glucose

49
 due to resistance to the influence of insulin on peripheral tissue and the
influence of somatotropic hormones.
g. Hypertriglyceridemia, due to impaired fat metabolism, which is caused
by the elevation of the hormone insulin, somatotropic hormone and
decreased lipoprotein lipapase.
h. Metabolic acidosis with respiration compensation shows decreased pH,
decreased "base exercise" (BE), decreased HCO³ and decreased PCO₂,
all caused by organic acid retention in kidney failure and lung
compensation.
DIAGNOSIS
If chronic kidney failure is symptomatic then the diagnosis is generally not
difficult to establish. Symptoms and signs of chronic kidney failure should be
discussed in accordance with system disorders that arise.14
System disorders in chronic kidney failure:14,15,16

a. Gastrointestinal
1. Anorexia, nausea, and vomitus, which are associated with disorders of
protein metabolism in the intestine, formation of toxic substances due
to metabolism of intestinal bacteria such as ammonia and methyl
guanidine, and swollen intestinal mucosa.
2. Foetor uremicum is caused by excessive urea in the saliva which is
converted by bacteria in the mouth to ammonia so that the breath
smells of ammonia. Another result is the emergence of stomatitis and
parotitis.
3. Hiccup, why is not yet known.
4. Erosevia gastritis, peptic ulcer and uremic colitis.
b. Skin
1. Pale skin due to anemia and yellowish - due to accumulation of
urochrome.
2. Itching - excoriation due to uremic toxins and the deposition of
calcium in the skin pores.

50
 3. Echymosis due to haematological disorders.
4. Urea fost: due to crystallization of urea in sweat.
5. Scars - scratching due to itching.
c. Hematologic
1. Normochrome anemia, normositer.
- Reduced erythropetin production, so erythropoesis stimulation in
the bone marrow decreases.
- Hemolysis, due to reduced lifespan of erythrocytes in the toxic
atmosphere of uremia.
- Iron deficiency, folic acid, due to decreased appetite.
- Bleeding in the skin digestive tract.
- Bone marrow fibrosis due to secondary hyperparatiroit.
2. Impaired platelet function and thrombocytopenia.
- The bleeding period is extended.
- Bleeding due to aggregation & adhesion of reduced platelets and
decreased platelet factor III ADP (adenosine phosphate).
3. Leukocyte disorders.
- Leukocyte hypersegmentation.
- Phagocytosis and chemotaxis are reduced, making infection easier.
d. Nerves and Muscles
1. "Restless Leg Syndrome": sufferers feel achy in their lower limbs and
always move their legs.
2. "burning feet syndrome": a sense of tingling and burning, especially in
the soles of the feet.
3. Metabolic ensofalotpati:
- Weak, unable to sleep, impaired concentration.
- Tremors, asterisks, myoclonus.
- Convulsions.
4. Myopathy: weakness and hypotrophy of the muscles especially the
proximal muscles of the extremities.

51
 e. Kardiovaskuler
1. Hypertension due to fluid and salt accumulation or increased activity
of the renin system - angiotensin - aldosterone.
2. Chest pain and shortness of breath due to pericarditis, pericardial
effusion, coronary heart disease (due to atherosclerosis arising early),
and heart failure (due to fluid retention and hypertension).
3. Disorders of heart rhythm due to early atherosclerosis, electrolyte
disturbances and metastastic classification.
4. Edema due to fluid retention.
f. Endocrine
1. Sexual disorders: decreased libido, fertility and erections in men due to
decreased testoserone production and spermatogenesis, also associated
with certain metabolites (zinc, parathyroid hormone). In women
arising from menstrual disorders, disorders of ovulation to ameorrhoe.
2. Impaired glucose tolerance.
3. Impaired fat metabolism.
4. Impaired metabolism of vitamin D.
g. Other disorders
1. Bone: osteoditrofirenal, namely osteomalacia, fibrous osteitis,
osteosclerosis, and metastatic classification.
2. Acid base: metabolic acidosis due to accumulation of organic acids as a
result of metabolism.
3. Electrolytes: hypocalcemia, hyperphosphatemia, hyperkalemia. Because in
chronic kidney failure there is a disruption of homeostatic balance in the
whole body, disruption in one system will affect other systems, so that a
metabolic disorder can cause abnormalities in various systems / organs of
the body.
IMPLICATIONS FOR NUTRITION
Chronic kidney failure is a disorder of kidney function that has lasted a long
time. The symptoms are generally called uremic syndrome, the main symptoms
are gastro intestinal symptoms such as nausea, vomiting and decreased appetite.

52
So that patients are generally in a nutritional status less. Limited research on the
nutritional status of patients with chronic renal failure without hemodialysis
shows that with anthropometric measurements 42.9% of patients with good
nutritional status, 50% of patients are in poor nutritional status and 7.1% are in
poor nutritional status.16
Food requirements that affect chronic kidney failure:16
Consistent and controlled protein intake is important.
1. Protein is still needed as a building block but too much intake can cause
BUN levels to rise and symptoms of uremia to return. Therefore,
portion sizes should be weighed or measured first and afterwards
periodically check for accuracy.
2. Protein needs are met throughout the day, not only in one dish.
Adequate calorie intake is important:16
1. Calories that are too low will increase catabolism.
2. Calorie source foods without protein, such as butter, oil and sweet cakes
that are allowed can be given freely.
For those who need fluid restrictions:16
1. Liquid sources include foods that thaw at room temperature.
2. An easy way to measure fluid intake is to use water that contains the
total fluid requirement per day and place it in the refrigerator. The liquid
consumed, according to the amount of water that is in it right.
3. To reduce thirst, try:
a) Hard candies.
b) Very cold water not ordinary water.
c) Gargle and maintain good oral hygiene.
For those who need potassium restrictions:16
1. Potassium requirements are based on laboratory data and clinical
symptoms, even food is adjusted to the patient's preferences / food
habits.
2. How to reduce the potassium content in vegetables and fruits: cut into
small pieces, soak one night, and boil in new water.

53
 3. Portion sizes are made so that each portion contains approximately the
same amount of protein, sodium and potassium.
4. Kidney failure patients who are recommended to eat lots of sweet foods
(high CHO) to cover calorie intake, need to be advised to pay attention
to oral hygiene to avoid dental caries.
5. One of the symptoms of uremic syndrome is decreased appetite, so
patients are encouraged to have a good breakfast. Because uremia can
cause a sense of taste, patients may choose foods that are highly
seasoned.
MENTOSA AND NUTRITION MEDICAL THERAPY
Mentosa medical therapy16
1. Treatment
The goal of treatment is to control symptoms, minimize complications and
slow the progression of the disease.
The steps taken are to look for aggravating factors in chronic kidney failure:
a. Urinary tract infection.
b. Urinary tract obstruction.
c. Hypertension.
d. Impaired renal perfusion / blood flow.
e. Electrolyte disturbances.
f. Use of nephrotoxic drugs, including chemicals and traditional medicines.
Alkalinization agents (such as sodium bicarbonate or Shohl solution), cation
exchange potassium binding potassium, antibiotics, aluminum hydroxide or
aluminum carbonate antacids to bind phosphorus, antihypertensive agents, and
diuretics are the most commonly used treatment measures.
Dialysis is needed if these steps, combined with dietary restrictions, are not
enough to prevent or control hyperkalemia, fluid saturation, symptomatic uremia
(drowsiness, nausea, vomiting and tremor), or a rapid rise in BUN and creatinine
levels. Although hemodialysis is widely used, an increasing number of patients
are taking CAPD (chronic ambulatory peritoneal dialysis) or CCPD (continuous

54
cycling peritoneal dialysis), which is done every day and is very popular because
it is easily done for outpatients.
2. Dialysis15
Dialysis is of 2 types, the principle works is based on the process of
osmosis diffusion:
a. Hemodialysis: an artificial semipermeable membrane (dialiser) is used.
b. Peritoneal dialysis: use the patient's own abdominal membrane
(peritoneum) as a semipermiable membrane.
The rest of metabolism (poisons such as urea and creatinine) will move from
the patient to dialysate fluid after passing through the membrane, so that the
patient's blood becomes clean.
In chronic kidney failure lifelong dialysis therapy is needed as a kidney
replacement therapy unless a kidney transplant operation is performed to replace a
damaged kidney.
Ideally dialysis is done 2-3 times a week. If the patient wants to reduce the
frequency of dialysis, he must restrict the diet of protein and water more
stringently, which has the consequence of malnutrition less advisable. Delays
dialysis can be at risk of complications such as swelling of the lungs, convulsions,
loss of consciousness, severe electrolyte disturbances, gastrointestinal bleeding,
heart failure can even cause death.
3. Kidney transplant or kidney transplant14
Kidney transplantation is a kidney replacement therapy that involves
kidney transplantation from living or dead people to people in need. Renal
transplantation is the treatment of choice for most patients with chronic kidney
failure. Kidney transplantation is the choice to improve the quality of life of
patients.
Renal transplantation is usually placed in the iliac fossa rather than placed
in the original kidney site, so that different blood supplies are needed, such as the
renal artery that is connected to the external iliac artery and the renal vein that is
connected to the iliac vein of the extreme.

55
 There are a number of complications after transplantation, such as
rejection (rejection), infection, sepsis, disruption of lymph polyperation post-
transplantation, electrolyte imbalance.

NUTRITION THERAPY
As patients with chronic kidney failure experience nausea and vomiting,
therefore a small portion of food is cultivated but is nutritionally valuable and is
given more frequently. Food is offered in an interesting, varied way, according to
the patient's needs. Because sufferers often experience malnutrition, it is
necessary to pay attention to energy and protein intake. Carbohydrates, protein,
and fat are energy sources. Fulfillment of energy intake is mainly obtained from
staple foods. Adequate input is needed to achieve optinal nutritional status.16

The nutritional condition of patients with chronic kidney failure is very

important to be maintained and improved. The diet goals for patients with chronic
kidney failure are:The nutritional condition of patients with chronic kidney failure
is very important to be maintained and improved. The diet goals for patients with
chronic kidney failure are:16

1. Enough protein needs to maintain nitrogen balance and also prevent excess
accumulation of metabolic waste between dialysis.
2. Provide enough energy to prevent catabolism in body tissues.
3. Regulate sodium intake to anticipate blood pressure and edema.
4. Limit potassium intake to prevent hyperkalemia.
5. Regulate fluid intake, to prevent excess fluid between dialysis.
6. Limiting intake of phosphorus.
7. To meet the needs of other nutrients, especially vitamins that are soluble in
the dialysis process.

Dietary requirements:16

1. Enough energy that is 30-35 kcal / kg BW. Energy intake must be optimal
from non-protein food groups. This is intended to prevent the disruption of

56
 protein as a source of energy, these ingredients are usually obtained from
oil, butter, margarine, sugar, honey, syrup, herbs and others.
2. Protein 0.6 - 0.75 g / kg BW. Protein restriction is based on body weight,
degree of renal insufficiency, and the type of dialysis to be undertaken.
Animal protein is recommended because its biological value is higher than
vegetable protein. The quality of protein can be improved by providing
pure essential amino acids.
a. Low protein diet I: 30 g protein, for BW 50 kg.
b. Low protein diet II: 35 g protein, for BW 60 kg.
c. Low protein diet III: 40 g protein, for BW 65 kg
The source of this protein is usually from animal groups such as eggs,
meat, chicken, fish, milk, etc. preformance in the amount recommended.
To increase levels of albumin given additional food ingredients such as
catfish extract or with egg white 4 times a day.
3. Enough fat 20-30% of the total total energy needs. Preferably
polyunsaturated fat. The ratio of saturated fat and saturated fat is 1: 1.
4. Carbohydrates are enough, namely the total energy needs minus the
energy derived from protein and fat. Carbohydrates given first are
complex carbohydrates.
5. Sodium given between 1-3 g. Sodium restriction can help overcome thirst,
thereby preventing excess fluid intake. Foods that are high in sodium that
are not recommended include: canned foods. Sodium salt added to foods
such as sodium bicarbonate or baking soda, sodium benzoate or fruit
preserves, sodium nitrite or belching used as preservatives of meat as in
"corner beff".
6. Potassium is restricted (40 - 70 mEq) if there is hyperkalemia (potassium
blood> 5.5 mEq), oligura, or anuria. Foods high in potassium are tubers,
fruits, avocados, ambon bananas, mangoes, tomatoes, bamboo shoots,
cassava leaves, papaya leaves, spinach, peanuts, green beans and
soybeans.

57
 7. Calcium and phosphorus should be controlled by hypocalcium and
hyperphosphatemic conditions, this is to avoid the occurrence of
hyperparathyroidism and to a minimum prevent the classification of bones
and body tissues. Intake of phosphorus 400 - 900 ml / day, calcium 1000 -
1400 mg / day.
8. Fluid is limited to the amount of urine a day plus the discharge of fluid
through sweat and breathing (± 500 ml)
9. Enough vitamins, if necessary supplemented with pyridoxine, folic acid,
vitamin C, and vitamin D.

7. Management related to the scenario

a. The fluid intake must be balanced with the output during oligouri
b. Electrolytes: concerned are Na and K intakes
c. If hyponatremia occurs, 3% NaCl / hypertonic can be given
d. If hyperkalemi arises, given:
- Ca gluconate 10%: 0.5 ml / kg body weight / day
- NaHCO3 7.5%: 3 ml / kgBB / day
- Kayexalate: 1 gr / kgBB / day (K exchange resin)
e. Protein: protein restriction must be as soon as possible.
Purpose of fluid restriction:
- Prevent protein catabolism, reduce the accumulation of traces of
nitrogen and limit the onset of uremia toxicity
- Reducing phosphate intake (by limiting milk intake) as a prevention
of secondary hyperparathyroidism and renal osteodystrophy
- Reducing the intake of H ions (because every 10 grams of protein
produces 7 mEq H ions) which means it helps prevent and improve
acidosis.
The type of protein given must be of high biological value, namely animal
protein such as eggs, cow's milk, meat, fish and poultry.14,16

58
 8. Islamic perspective based on scenario

It means: "It was narrated from Sa'ad bin Abi Waqas from his father, from
the Messenger of Allah. : Verily, Allah SWT is holy who likes holy things, He is
Clean, He likes cleanliness, He is Mahamulia who likes glory, He is Beautiful and
loves beauty, therefore clean your places "(Narrated by Tirmizi).

59
 REFERENCES

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