FAKULTAS KEDOKTERAN Makassar, 30 Desember 2021

UNIVERSITAS MUSLIM INDONESIA

BLOK URONEFROLOGI

PROBLEM BASED LEARNING

MODUL 2

URONEFROLOGY

TUTOR: dr. Sri Wahyuni Gayatri, M. Kes

GROUP 5A

MUH. ALIF FADILLAH S 110 2019 0002

CINDY OKTAVIANI IBRAHIM 110 2019 0008
EGA FADILA 110 2019 0010
SALSABILA TIRTA APRILIA 110 2019 0021
FARHA AMALIA IMRAN 110 2019 0028
NATASYA WIDIYANA PUTRI 110 2019 0031
GITHA KETRINA YULIA SIHOTANG 110 2019 0032
INDRI SUHARAINI IWAN 110 2019 0042

FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2021
 KATA PENGANTAR

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tutorial ini dapat diselesaikan tepat pada waktunya. Aamiin.

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saran yang sifatnya membangun senantiasa kami harapkan guna memacu kami menciptakan
karya-karya yang lebih baik.

Semoga Allah SWT dapat memberikan balasan setimpal atas segala kebaikan dan
pengorbanan dengan limpahan rahmat dari-Nya. Aamiin yaa Robbal A’lamiin.

Makassar, 30 Desember 2021

Kelompok 5A
 SCENARIO 4

A 43-year-old man was admitted to the hospital with the chief complaint of right flank pain that
he had experienced since 2 months. Complaints accompanied by nausea, vomiting, weakness,
decreased urine output since the last 2 days. History of high uric acid since 5 years ago but not
taking regular treatment. On physical examination, blood pressure was 130/80 mmHg, pulse
100x/minute, RR 20x/minute, temperature per axilla 36.7 °C, right costovertebral tenderness.

A. Difficult word : -

B. Keywords :
- A man 43 years old
- Chief complaint of right flank pain that he had experienced since 2 months
- Complaints accompanied by nausea, vomiting, weakness, decreased urine output since
the last 2 days
- History of high uric acid since 5 years ago but not taking regular treatment.
- Physical examination, blood pressure was 130/80 mmHg, pulse 100x/minute,
RR 20x/minute, temperature per axilla 36.7 °C, right costovertebral tenderness.

C. Questions :
1. What is the pathomechanism of each symptom in the scenario?
2. What is the interpretation of the results of the physical examination in the scenario?
3. What diseases cause a decrease in the amount of urine?
4. Diagnostic steps according to the scenario!
5. What are the differential diagnoses according to the scenario?
6. How is the initial management of the scenario
7. What is the Islamic perspective based on the scenario?
D. Answers :

1. What is the pathomechanism of each symptom in the scenarioi?

Right Waist Pain

Often, the symptoms of right flank pain are caused by disorders of the urinary system. However,
apart from that, there are also several other causes of the pain.
1. Kidney stones
Humans have two kidneys located on the left and right. Blockage of stones in the right
kidney will trigger pain in the right waist. Usually the pain due to kidney stones is very
intense, especially when some of the stones move into the ureters or tubes that connect the
kidneys to the bladder.
Complaints of right flank pain in patients with kidney stones are often accompanied by
nausea and vomiting. In addition, complaints are also accompanied by red urine.
2. Kidney infection (pyelonephritis)
Pyelonephritis is an infection of the kidneys that causes the kidneys to enlarge and can be
permanently damaged. This disease can be life threatening. One of the symptoms of
infection is right back pain. Other accompanying complaints are usually fever up to 38.9
"C, pain or burning sensation when urinating, until the urine is cloudy and smells fishy.
3. Inflammation of the appendix (appendicitis)
Inflammation of the appendix or appendicitis has complaints of pain in the right abdomen.
The pain in patients with appendicitis usually increases with time and makes the sufferer
only able to hold the painful part to form a lying position curled up as a kanab. If not
detected and treated quickly, this inflammation can lead to intestinal rupture and a
widespread infection that can be life-threatening.
4. Muscle injury
Injuries to the waist can cause pain. This injury can be obtained from lifting heavy objects,
heavy, or falling. Usually the muscle pain that arises can be felt during activities and when
touched. Resting or not moving the affected area will reduce the pain. Right flank pain due
to muscle pain will usually subside on its own or can be relieved with painkillers or cold
compresses.

Nauseous vomit
Nauseous
Is a psychic sensation due to stimulation of the visceral organs, labyrinth and emotions.
Does not always progress to retching and expulsion. This condition is characterized by
the urge to vomit that is felt in the throat or stomach, often accompanied by symptoms of
hypersalivation, pallor, sweating, tachycardia and anorexia.
During periods of nausea, there is a decrease in tone of the greater curvature, body and
fundus. The antrum and duodenum contract repeatedly, while the duodenal bulb relaxes
causing reflux of duodenal fluid into the stomach. In this phase of nausea, active
peristalsis has not occurred.

Vomiting and Weakness

Vomiting is triggered by afferent impulses that travel to the vomiting center, which is
located in the medulla of the brain. These impulses are received from sensory centers such
as the chemoreceptor trigger zone (CTZ), the cerebral cortex, and visceral afferents from
the pharynx and gastrointestinal tract. Afferent impulses that have been integrated with the
vomiting center will produce efferent impulses to the salivation center, respiratory center,
gastrointestinal tract, pharynx, and abdominal muscles, all of which synergize to trigger
the vomiting process. Well, here it can be seen that when vomiting occurs, there is irregular
breathing, gasping for air, weakness, sweating, stomach contractions, or saliva coming out.

Causes of vomiting:

1. Pregnancy
2. Poisoning, pain, irradiation
3. Smells and touches the mouth
4. Brain pressure
5. Gastritis
6. Rotational movement
Decreased Urine Amount (Oligouri)
The pathophysiology of oliguria can involve prerenal, renal, and postrenal processes. The
most common prerenal cause is decreased blood flow to the kidneys, for example from
dehydration or heart failure. The cause of renal oliguria will trigger tubular injury, for
example in the case of glomerulonephritis. Meanwhile, in post-renal causes, urine
production is normal but there is obstruction of the urine output pathway.

Prerenal

Prerenal processes that can cause oliguria include decreased blood volume due to fluid loss
(diarrhea, bleeding, vomiting, use of diuretics); lack of fluid intake; third spacing liquid as
inpleural effusion; Burns, anaphylaxis, sepsis, and nephrotic syndrome.

Cardiac disorders can also cause a lack of fluid volume in the kidneys, as inheart failure,
myocardial infarction, and cardiac tamponade. Renal artery-venous thrombosis,
thromboembolism, and stenosis can also cause oliguria.

Decreased renal blood flow will cause activation of neurohormonal mechanisms, which
causes an increase in renin, angiotensin, aldosterone, catecholamines, and prostaglandins,
which will then increase the reabsorption of water and salt, so that the amount of urine
decreases. Continuous conditions without fluid correction will causeacute kidney failure.
In addition to circulatory changes, immunological and inflammatory conditions will cause
endothelial injury, which will increase vascular permeability and interstitial edema.

Renal

Abnormalities in the renal parenchyma can cause oliguria, as

inglomerulonephritisscleroderma, vasculitis, acute tubular necrosiscaused by ischemia and
nephrotoxicity. Tubular damage can impair kidney function in producing urine and
excreting metabolites.

Post-renal

Post-renal conditions that can cause oliguria include upper urinary tract obstruction, lower
urinary tract obstruction as inBenign prostatic hyperplasia, tumors, and urinary tract
stones. In these cases, urine production is normal, but urine output is impaired due to the
obstruction.

Reference:

1. Hakiqi, Zaki Ahmad. 2020. Causes of Right Back Pain.

https://www.scribd.com/document/455389079/Cause-Pain-Pain-Selangit-Kanan

2. Agustin, Andini. 2012. Mechanism of Nausea and Vomiting.

https://www.scribd.com/doc/139221125/MEKANISM-MUAL-MUNTAH
 3. Flubber, Squartic. L. 2016. Oligouri Pathomechanism

4. Klein SJ, Lehner GF, Forni LG, Joannidis M. Oliguria in critically ill patients: a narrative
review. J Nephrol. 2018 Dec 1:31(6):855–62.

5. Haider MZ, Aslam A. Oliguria. [Updated 2020 Aug 4]. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK560738/

6. Rimmel T, Kellum JA. Oliguria and fluid overload. Contrib Nephrol. 2010;164:39-45.
doi: 10.1159/000313719. Epub 2010 Apr 20. PMID: 20427992.

2. Interpretation of Physical examination on the scenario

Early scoring gives a simple combined measure of the extent of physiological abnormalities
in a person, usually based on vital signs, e.g. heart rate, blood pressure, breathing rate. In
addition, they are easily interpreted by clinical staff and can be calculated manually or by
electronic systems (Wong, 2015). The normal body temperature for adults is 36°-38°C (96.8°-
100.4°F). This body temperature can be measured with thermometers (glass thermometers,
electronics, typani) and various routes (oral, rectal, axilla, tympani). The abnormal body
temperature for adults is 40°C (104°F).

In adults, the normal pulse rate is 60-100 beats/min. While the abnormal pulse is <45 beats
/ min and >130 beats / min. For adults, the normal breathing rate is 12-20 breaths/min. While
the abnormal respiratory rate is <10 breaths / min and >26 breaths / min. Normal blood oxygen
saturation (SpO2) for adults is 95-100%. Abnormal oxygen saturation is <90%. In adults,
normal blood pressure systolic values are 90-130 mm Hg and diastolic values are 60-90 mm
Hg. While abnormal blood pressure systolic values ><80 mm Hg and >200 mm Hg. And
abnormal diastolic values <55 mm Hg, >120 mm Hg (Schriger, 2012).

The range of normal and abnormal values associated with vital signs for adults can be seen
in more detail in Table 1.

Table 1. Normal and abnormal range of adult vital signs

Usual Abnormal
 Temperature 36°-38° C 40° C
Pulse 60-100 <45
beats/min beats/minute,
>130
beats/minute
Breathing 12-20 <10
breaths/min breaths/min
>26
breaths/min
Oxygen 95-100% <90%
Saturation
Systolic 90-130 mm <80 mmHg
Blood Hg >200 mm Hg
Pressure
Diastolic 60-90 mm Hg <55 mmHg
Blood >120 mm Hg
Pressure

Normal blood pressure in the systolic value range < 120 mmHg and diatsolic values <80
mmHg. Prehypertension is defined as systolic blood pressure that has a value of 130-139
mmHg or diastolic 80-90 mmHg. Patients with prehypertension have twice the risk of
becoming hypertensive than individuals with lower blood pressure. Hypertension is defined
as systolic blood pressure that is worth 140 mmHg or more or diastolic which is worth 90
mmHg or more and is classified (by its severity) as stage 1 or 2. Systolic hypertension alone
(isolated systolic hypertension) is defined as systolic blood pressure that is worth 140 mmHg
or more and diastolic blood pressure that is 90 mmHg or less and should be further classified
according to its severity (e.g. 170/82 means stage 2 systolic hypertension) (JNC-VII, 2003).

The classification and management of blood pressure for adults can be seen in more detail
in Table 2.

Tabel 2

Classification Systolic TD Diastolic TD (mmHg)

(mmHg)
Usual <120 And <80
Prehypertension 120-139 Or 80-89
Hypertension 140-159 Or 90-99
degree 1
Hypertension >/=160 Or >/=110
degree 2
Reference:

- National High Blood Pressure Education Program.

Bethesda (MD): National Heart, Lung, and Blood Institute (US); 2004 Aug.
- Ahrens, T. 2008. The most important vital signs are not being measured. Aust. Crit. Care
21 (1), 3–5. (https://www.sciencedirect.com/science/artic le/abs/pii/S1036731407002044,
accessed August 9, 2019).

3.What diseases can cause a decrease in urine production?

Prerenal: Caused by decreased renal perfusion and the effects of filtration pressure. (a)
Hypovolemia, such as severe bleeding, serious dehydration, hypoproteinemia, cirrhosis and
nephrotic syndrome; (b) Cardiovascular diseases, including shock, heart failure, pericardial
tamponade, acute coronary syndrome (ACS), pulmonary embolism (PE), and serious arrhythmias;
(c) Kidney vascular disease, including renal artery stenosis, polyarteritis, renal artery thrombosis,
hypertensive crisis.
Renal parenchym: The location of the injury can cause oliguria and anuria due to decreased
permeability of glomerular filtration and glomerular filtration area. (a) glomerular diseases: such
as acute glomerulonephritis, rapid progressive glomerulonephritis, chronic nephritis with acute
attacks, Goodpasture syndrome, lupus nephritis (LN), Wegener granulomatosis, thrombotic
thrombocytopic purpura (TTP), accelerated hypertension; (b) tubular and interstitial diseases: such
as acute tubular necrosis, necrotic renal papyilitis, acute hyperuricemia, Hematosepsis; (c) kidney
vascular disease: such as malignant arteriole nephroclerosis, renal venous thrombosis; (d) others:
such as acute rejection after renaltasi transplan.
 Postrenal: This is always caused by obstructed urine flow but normal urine production. (a)
ureter obstruction: mechanical blockade (such as stones, tumors, blood clots, pus or chylous
blocks) or narrowing of adhesions (such as chronic tuberculosis infections) are both the result of
oliguria and anuria. Other causes include renal torsion, ureter injury and edema or external
pressure. (b) urethral blockages such as ureter calculus and vesikalic calculus, urethra strictures,
hyperplasia or prostate tumors, vesical ruptures, bladder nerves.
Reference: Chen J., Zeng R. (2020) Oliguria, Anuria and Polyuria. In: Wan XH., Zeng R. (eds)
Handbook of Clinical Diagnostics. Springer, Singapore.

4. Diagnostic steps according to the scenario!

Diagnostic steps based on scenario

A. Anamnesis
1. Asking for identity:
Nbut : X
Umur : 43th
Alamat: -
Pekerjaan :-
2. Ask the main complaints and dig into the current history of the disease.
Ask:
 Onset and duration of major complaints: since when?
 The shape, color and amount of urine, there are stones or not, sandy urine,hematuria.
 Other symptoms related: nausea, low back pain, pain when urinating, bad feeling
in the abdomen, pressure pain in the right abdomen.
3. Ask for additional complaints related to the main complaint
4. Perform anamnesis related to the system.
 Cardiovascular (history of myocardial infarction, coronary intervention, and heart
failure provide evidence of cardiorenal relationships and renal perfusion disorders)
 Respiration: dyspnea (e.g. secondary pulmonary edema due to kidney failure)
 Immunological/Infectious (for autoimmune or CKD-causing infections)
 Gastrointestinal (history of hepatitis, cirrhosis, and abdominal pain (e.g. peritoneal
dialysis-related infections)
  Genitourinaries (frequency of urinary tract infections, recurrent kidney stones, and
urinary symptoms associated with bladder obstruction provide evidence of
pyelonephritis, obstruction, and stones).
 Musculoskeletal: muscle wasting (in end-stage kidney failure)
 Dermatology: uraemic frost (in end-stage kidney failure)
5. Digging into previous and related diseases: history of hypertension or diabetes,
glomerulonephritis at an early age, previous episodes of acute kidney injury, urological
intervention)
6. Asking for a history of treatment: frequent use of NSAIDs or pain relievers, long-term
exposure to nephrotoxic antibiotics, exposure to radiocontras agents, use of chemotherapy)
7. Asking for a family history: the disease suffered causes difficulty urinating disorders.

B. Physical Examination
1. Assessment of the patient's general health, nutritional status, appetite, and weight changes
should be determined.
2. Blood pressure and pulse check
3. General Inspection
1) Decreased level of awareness: can be a feature of end-stage kidney disease.
2) Clear scars: can provide clues about previous abdominal surgery.
3) Pale: a pale color on the skin that may signal underlying anemia (e.g. erythropoietin
deficiency).
4) Shortness of breath: possibly due to secondary pulmonary edema due to advanced
kidney disease. Notypnea can also be caused by metabolic acidosis due to kidney
failure.
5) Edema: usually appears as swelling of the legs and abdomen (i.e. ascites). In the
context of examination of the kidney system, possible causes can include nephrotic
syndrome and end-stage kidney disease (due to anuria).
6) Uremic skin: the yellow color of the skin caused by uremia in advanced chronic
kidney disease.
7) Eye: Conjunctival examination to look for paleness that indicates anemia. Anemia
often occurs in patients with chronic kidney failure due to erythropoietic deficiency.
 8) Mouth: Seeing the absence or absence of uraemic fetor is a urine-like breath odor
(i.e. ammonia) that is usually associated with end-stage kidney disease.
4. Chest Examination
 Blunt percussion indicates pleural effusion that can occur in patients with excess
fluid (e.g. end-stage kidney disease) or nephrotic syndrome (hypoalbuminaemia)
 Accusculation of the lung field in the posterior
 Rough ronki signifies pulmonary edema (e.g. excess fluid in end-stage kidney
disease, hypoalbuminemia in nephrotic syndrome).
5. Abdominal Examination
 Scar inspection: there are different types of abdominal scars that can provide clues
about the patient's previous surgical history. Abdominal distension: can be caused
by a persistent intrabdominal mass (e.g. polycystic kidney), ascites (e.g. secondary
nephrotic syndrome), or a settled peritoneal dialysis fluid.
 Mild palpation to assess the presence of pressure and mass pain.
 Deep palpation with greater pressure to identify deeper masses. If any mass is
identified during palpation within, the following characteristic values:
1. Location: Kidney mass is usually palpable in the pelvis.
2. Size and shape: the approximate value of the size and shape of the mass.
3. Consistency: consistency of mass (e.g. enlarged polycystic kidneys may be
irregular consistency).
4. Mobility: The kidney mass will move to superior and inferior with respiration.
 Percussion can also be used to assess the presence of ascites by identifying shifting
dullness.
 Perform auscultation over the renal artery to identify vascular bruite that shows
turbulent blood flow i.e. auscultation 1-2 cm higher than the umbilicus and slightly
lateral from the midline on each side. Noise at this location may be associated with
renal artery stenosis (a possible cause of hypertension and kidney failure).
6. Assessing the absence of peripheral and sacral edema
Lower limbs and sacrum patients from pitting edema may indicate hypoalbuminemia (e.g.
end-stage kidney disease, nephrotic syndrome).
C. Supporting Check
1. Blood Test
This test is to find out the work of the kidneys by looking at the level of waste in the blood,
such as creatinine and ureum.
1) Creatinine
Creatinine is a product of endogenous waste from skeletal muscles that is excreted
through glomerular filtration and not reabsorption or secreted renal tubules.
If there is an increase in creatinine levels of 2.5 mg / dL can indicate kidney damage.
Serum creatinine examination is very functional to evaluate glomerular function.
2) Urea
Ureum is a substance formed from the breakdown of proteins mainly derived from
food. Here are the normal ureum scores in some age categories according to Centers
for Disease Control and Prevention (CDC) data:
Age 0-5 years: 5-18 mg/dL
Age 5-15 years: 7-18 mg/dL
Age over 15 years: 6-23 mg/dL
2. Urinalisis
1) Urinalysis can observe the color and clarity of urine
2) An assessment of urine odor.
3) Acidity measurements (normal urine pH of 4.5-8.0 and average 6.0) and (normal
urine type weight (normal 1,025 or more)
4) Tests to check the presence of protein (proteinuria) proteinuria is normally 150
mg/day, mild proteinuria levels less than 1 gram/day and tend to be associated with
kidney disease such as chronic pyelonephritis and severe proteinuria secreting
protein 3.5grams/day and is the laboratory's definition of nephrotic syndrome,
glucose (glucosuria), ketone body in the urine (ketonuria).
5) Examination of urine sediment microscope after grinding to detect red blood cells
(hematuria), pus (piuria), bacteria (bacteriauria).
3. Examination of kidney function
 Kidney function tests are performed to evaluate the severity of kidney disease and
follow the patient's clinical journey. This examination will also provide information about
the effectiveness of the kidneys in carrying out their excretory functions.

1) Kidney bonding ability (weight type and osmslality of urine) This examination will
show early impaired kidney function.
2) Creatinine clearance examination. Useful for the progress of kidney function status.
3) Examination of serum creatinine levels. Normal levels 0.7-1.5/100ml. Examination
of kidney function that reflects the balance between production and filtration by the
glomerulus.
4) Check the serum ureum.normal rate of 10-20mg/100ml.
Serves as an index of urinary excretion capacity.
4. Stone Analysis
Analysis of stones that have been removed from the urinary tract is done analysis.
The use of stone analysis is to find out the type of stone to prevent recurrence in the future.
Prevention can be in the form of dietary regulation and the administration of drugs.

5. Urine Culture
Urine cultures are examined to look for urinary tract infections, determine the type
of germs and the sensitivity of germs to some of the atibiotics tested.

6. Sistografi
Cystography is the imaging of jars by wearing contrast. This photo can be done in several
ways, among others Through photos Of contrast insertion through a urethra catheter
directly into the thread - thread Inserting contrast through a cystotomy catheter or through
a suprapubic insertion.

7. Uretrografi
Uretrography is urethra imaging using contrast material. Contrast material is inserted
directly through the meatus urethral externa so that if there is a intriguetura in the urethra
will appear a narrowing or contrast barrier in the urethranya extravasasi contrast in the
trauma of the urethra, or the presence of filling defect if there is a tumor in the urethra.

8. Pielografi Retrograde (RPG)

 Retrograd pielography or pyelography is imaging of the upper urinary system by
inserting radiopatic contrast material directly through a ureter catheter inserted in the
urethra contrast.

9. USG
The principle of ultrasound examination is to capture ultra sound waves reflected by
organs (tissues) of different densities. This examination is not inphasive and does not cause
radiation effects. Ultrasound can distinguish between solid period (hyperecoid) and the
period of curxoid, while non-opiate stones that cannot be detected X-ray photos will be
detected by ultrasound as echoic shadow. Ultrasound is widely used to look for
abnormalities in the kidneys, jars, prostate, testicles and examination in cases of
malignancy.

10. MRI
This examination is better than ultrasound but it is still very expensive. Both of
these examinations are widely used in the field of oncology to determine the limits , infasi
to the organs around the tumor and look for the presence of metastases to the lymph glands
as well as to other organs.

Reference:

1. Potter,Lewis. Urological History Taking. Adapted by Geeky

Medics. https://geekymedics.com/urological-history-taking/.
2. Building team. Guide to Learning Skills Clinical Urogenital System. Faculty of Medicine
Hasanuddin University.
3. Arici, Mustafa. 2014. Clinical Assessment of a Patient with Chronic Kidney Disease.
Department of Nephrology, Faculty of Medicine , Hacettepe University.
4. Rachmadi, D. 2010. Chronic kidney disease. Department of Children's Health Sciences
Faculty of Medicine Padjajaran University -RS. Dr. Hasan Sadikin Bandung.
5. Callan,Paul dan Logan, I. Renal System Examination. Adapted by Geeky
Medics. https://geekymedics.com/renal-system-examination-osce-guide/
6. BATES' GUIDE TO PHYSICAL EXAMINATION & HISTORY TAKING,8fr Ed. by
Lynn S. Bickley
 7. Indonesian Association of Internal Medicine Experts. 2015. Book of teaching disease
science in volume I Ed IV. Jakarta : FKUI publishing hall.
8. Siti, Setiati. et al. 2015. Teaching Disease Science in Volume I. Edition VI. Jakarta:
Interna Publishing

5. What are the differential diagnoses according to the scenario?

1. ACUTE KIDNEY INJURY

A. Definition

Acute renal impairment is a specific clinical condition with very varied manifestations,
ranging from mild without symptoms, to very severe with multiple organ failure. Acute renal
failure itself is a condition in which there is a sudden decline in kidney function, within hours to
several weeks, followed by kidney failure to excrete nitrogenous metabolic wastes with or without
fluid and electrolyte balance disorders. Sudden decrease in renal function within 48 hours, i.e. an
increase in serum creatinine level 0.3 mg/dl (≥26.4 mol/l), a presentation of an increase in serum
creatinine ≥ 50% (1.5x increase from baseline), or a decrease in urine output (documented
oliguria). 0.5 ml/kg/hour for more than 6 hours

B. Etiology

The etiology of acute renal impairment (ARF) is classically divided into 3 main groups
based on the location of the pathophysiological abnormality, namely before the kidney (pre-renal),
inside the kidney (renal/intrinsic), or after the kidney (post-renal). The incidence of pre-renal
etiology reaches 70% of all ARF that occurs outside the hospital and 40% that occurs in the
hospital.

a. Pre-renal

- Loss of body fluid volume

- Decreased effective volume of blood vessels

- Fluid redistribution

- Primary intra-renal vasoconstriction

b. Intra-renal

- Acute tubular necrosis

- Acute interstitial nephritis

 - Acute glomerulonephritis

- Microcapillary/glomerular occlusion

- Acute cortical necrosis

c. Post-renal

- ureteral obstruction

- Bladder or urethral obstruction

C. Epidemiology

Epidemiological data regarding ARF is very rarely reported, even though ARF is a disease
with a high mortality rate. The difficulty in making this data is partly because there is no uniform
definition and the wide variety of clinical symptoms. Since the use of the RIFLE criteria, the
definition of a diagnosis has become more uniform and more sensitive. The results of the meta-
analysis conducted by Tariq Ali, et al. A study using RIFLE as a diagnostic criterion showed that
the incidence of ARF was far above what was previously thought. According to Hoste &
Schurgers, the high incidence of ARF is a hidden threat because the mortality rate is much higher,
especially when accompanied by sepsis or acute lung injury.

In developing countries, the incidence of ARF in the general population is rarely reported,
because not all patients are admitted to hospital. Mild acute renal impairment can resolve on its
own outside the hospital, while severe ARF often does not reach the hospital because of geographic
or economic problems. Wang, et al. in China reported an ARF incidence of 0.54/1000 patients
treated, whereas Kohl et al. in India reported 6.6/1000 patients treated. In developed countries, the
incidence of ARF in the hospital is much higher in the elderly or after heart surgery. The meta-
analysis conducted by Needham (2005) showed that the incidence of ARF in the intensive care
unit (ICU) was 1-5% of all hospitalized patients and the mortality rate was 50-70%. Meanwhile,
Lamier's meta-analysis using the RIFLE criteria showed that the incidence of ARF in the ICU
varied between 5-67% of all hospitalized patients.

D. Pathophysiology

Figure 1. Pathophysiology of Acute Kidney Disorders

ARF is a syndrome with a broad spectrum of etiology, several mechanisms including

ischemic/hypoxic, nephrotoxic and inflammatory contributing to ARF. Sepsis is the leading cause
of ARF in the ICU.

E. Diagnosis
History

1. Suspected pre-renal azotemia: vomiting, diarrhea, polyuria due to glycosuria, history of taking
medications including diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin
converting enzyme (ACE) inhibitors, and angiotensin receptor blockers (ARBs).

2. Lumbar colic radiating to the genital area 7 suggestive of ureteral obstruction

3. Frequent urination at night (nocturia) and other urinary disorders; may occur in prostate disease

4. History of prostate disease, kidney stones, or pelvic or paraaortic malignancies. suspected post-
renal

Physical Examination

1. Orthostatic hypotension, tachycardia, decreased jugular venous pressure, decreased skin

turgor, and dry mucous membranes.

2. Abdominal bloating and suprapubic pain, bladder enlargement

3. AKI with palpable purpura, pulmonary hemorrhage, or sinusitis, suggestive of systemic

vasculitis

4. Idiosyncratic reactions (fever, arthralgia, itchy red rash), suspected allergic interstitial nephritis

5. Ischemic signs positive lower extremity, suspected rhabdomyolysis

Supporting Examination

1. Laboratory: complete peripheral blood, urinalysis, urine sediment, serum urea, creatinine, uric
acid, creatine kinase, electrolytes, lactate dehydrogenase (LDH), blood urea nitrogen (BUN),
antinuclear antibodies (ANAs), antineutrophilic cytoplasmic antibodies (ANCAs),
antiglomerular basement membrane antibodies (AGBM), and cryoglobulins.

2. Radiological: Ultrasound of the kidneys and urinary tract, CT scan, antegrade or retrograde
pyelography, MRI

F. Management

The main goals of management of AKI are to prevent further kidney damage and keep the
patient alive until renal function returns to normal. There are two types of treatment in the
management of AKI, namely conservative (supportive) therapy and renal replacement therapy
(RRT). Conservative therapy is carried out with drugs or fluids with the aim of preventing or
reducing the progressive decline in renal function, morbidity, and mortality due to complications
of AKI. If conservative therapy fails to treat any complications of AKI, RRT (dialysis) should be
considered. Priority for the management of AKI:

1. Find and correct pre- and post-renal factors

 2. Evaluate medications that have been given

3. Optimize cardiac output and renal blood flow

4. Improve and/or increase urine flow

5. Monitor fluid intake and output, Weigh daily

6. Look for and treat acute complications (hyperkalemia, hypernatremia, acidosis,

hyperphosphatemia, pulmonary edema)

7. Adequate nutritional intake early on

8. Locate the focus of infection and treat infection aggressively

9. Good comprehensive care

10. Promptly initiate dialysis therapy before complications arise

11. Give the drug with the right dose according to the renal clearance capacity

Table 1. Conservative Management of ARF

G. Complications

a. Disorders of body fluid balance

b. Electrolyte balance disorders
c. Metabolic acidosis
d. heart failure
e. Respiratory failure
f. Azotemia

H. Prognosis

Mortality due to ARF depends on clinical conditions and the degree of renal failure. It is necessary
to pay attention to the age factor, the older the worse the prognosis, the presence of accompanying
infections, gastrointestinal bleeding, severe causes will worsen the prognosis. The most common
causes of death are infection (30-50%), bleeding, especially the gastrointestinal tract (10-20%),
heart (10-20%), respiratory failure (15%), and multiorgan failure with a combination of
hypotension, septicemia, and so on. Patients with ARF who undergo dialysis have a mortality rate
of 50-60%, therefore prevention, early diagnosis, and early therapy need to be emphasized.

Reference:

1. Triastuti Indriana and Ida Bagus Gde Sujana.2017. Acut Kidney Injury (AKI). Section of
Anesthesia and Intensive Therapy at Sanglah Hospital, Faculty of Medicine, Udayana University

2. Surachno, RG et al. 2016. Textbook of Internal Medicine: Acute Kidney Disorders.

Jakarta: InternaPublishing Management in Internal Medicine: Clinical Practical Guide: Acute
Kidney Disorders. 2015

3. Melyda. 2017. Diagnosis and Management of Acute Kidney Injury in Septic Shock. CDK
Journal Vol.44 No.12

2. Chronic Kidney Failure

1) Definition
Chronic kidney disease is a pathophysiological process with various etiologies,
resulting in a progressive decline in kidney function, and generally ending in kidney
failure. Furthermore, renal failure is a clinical condition characterized by an
irreversible decline in kidney function, to a degree that requires permanent renal
replacement therapy, in the form of dialysis or kidney transplantation. And is
characterized by the presence of uremia (retention of urea and other nitrogenous
wastes in the blood). Chronic Kidney Disease (Chronic Kidney Disease) is a kidney
disease in which there is a decline in kidney function over a period of months to years,
which is characterized by a gradual decrease in the glomerular filtration rate (GFR)
over a long period. There are no early symptoms of chronic kidney disease,
Kidney function indicates the condition of the kidney and its function in renal
physiology. Glomerular Filtration Rate (GFR) indicates the amount of fluid filtered
by the kidneys. Creatinine Clearance Rate (CrCl) indicates the amount of blood
creatinine filtered by the kidneys. CrCl is a useful parameter to determine the GFR of
the kidney.
Causes of chronic kidney disease can be diabetes mellitus, high blood pressure
(hypertension), glomerulonephritis, polycystic kidney disease (Polycystic Kidney
 Disease). Risk factors for chronic kidney disease can be in the form of a patient's
family history of the disease. The diagnosis of chronic kidney disease is generally in
the form of a blood test that serves to determine the Glomerulus Filtration Rate (GFR),
and a urine test to determine whether there is albuminuria. Further examination can be
in the form of ultrasound and kidney biopsy to determine the cause of chronic kidney
disease
2) Epidemiology
In the United States, data from 1995 to 1999 stated that the incidence of chronic
kidney disease was estimated at 100 cases per million population per year, and this
figure was increasing by about 8% every year. In Malaysia, with a population of 18
million, it is estimated that there are 1800 new cases of kidney failure annually. In
other developing countries, the incidence is estimated at around 40-60 cases per
million population per year.

3) Criteria
 Kidney damage that occurs more than 3 months, in the form of structural or
functional abnormalities, with or without a decrease in the glomerular filtration rate
(GFR), with manifestations:
 Pathological abnormalities
 There are signs of kidney abnormalities, including abnormalities in the
composition of the blood or urine, or abnormalities in imaging tests
 Glomerular filtration rate less than 60 ml/min/1.73m2 for 3 months, with or without
kidney damage.

4) Classification
Classification of Chronic Kidney Disease on the basis of the degree of disease
Level Explanation GFR (ml/min/1.73m2)
1 Kidney damage with normal GFR or 90
2 Kidney damage with mild GFR 60 – 89
3 Kidney damage with moderate GFR 30 – 59
 4 Kidney damage with severe GFR 15 – 29
5 Kidney failure < 15 or dialysis

Classification on the basis of disease, made on the basis of GFR, which is calculated
using the Kockcroft-Gault formula as follows:
LFG (ml/min/1.73m2) = (140 – age) X weight *)
72 X plasma creatinine (mg/dl)
*) on women times 0.85

Classification of Chronic Kidney Disease on the Basis of Etiological Diagnosis

Disease Major type (example)
Diabetic kidney disease Diabetes type 1 and 2
Non-diabetic kidney Glomerular disease (autoimmune disease, systemic
disease infection, drugs, neoplasm)
Vascular disease (large vessel disease, hypertension,
microangiopathy)
Tubulointerstitial disease (chronic pyelonephritis, stones,
obstruction, drug poisoning)
Cystic disease (polycystic kidney)
Diseases in transplant Chronic rejection
Drug poisoning (cyclosporine/tacrolimus)
Recurrent (glomerular) disease
Transplant glomerulopathy

5) Etiology
The two main causes of chronic kidney failure are type 1 and type 2 diabetes
mellitus (44%) and hypertension (27%). Diabetes mellitus is a condition in which
there is an increase in glucose levels in the blood, causing damage to vital organs such
as the kidneys and heart as well as blood vessels, nerves and eyes. While hypertension
is a condition where there is an increase in blood pressure which if not controlled will
 cause heart attacks, strokes, and chronic kidney disease. Chronic kidney failure can
also cause hypertension. Other conditions that can cause kidney problems include:
 Inflammatory diseases such as glomerulonephritis (10%), can cause inflammation
and damage to the renal filtration unit. It is the third most common cause of chronic
kidney failure
 Hereditary diseases such as polycystic kidney disease (3%) cause enlarged cysts
in the kidney and damage surrounding tissues, and tubular acidosis.
 Malformations acquired by the baby while in the mother's womb. For example,
narrowing of normal urine flow resulting in backflow of urine to the kidneys. This
causes infection and damage to the kidneys.
 Lupus and other diseases that have an effect on the immune system (2%)
 Obstructive kidney disease such as urinary tract stones, tumors, enlarged prostate
gland in men and ureteral reflux.
 Recurrent urinary tract infections such as chronic pyelonephritis.
Long-term use of analgesics such as acetaminophen (Tylenol) and ibuprofen
(Motrin, Advil) can cause analgesic neuropathy, which can lead to kidney damage.

 Hypertensive vascular disease eg nephrosclerosis and renal artery stenosis.

 Other causes are HIV infection, sickle cell disease, heroin abuse, amyloidosis,
gout, hyperparathyroidism and cancer.
6) Risk factor
Risk factors for chronic kidney failure include: patients with diabetes mellitus or
hypertension, obesity or smokers, aged more than 50 years, individuals with a history
of diabetes mellitus, hypertension and kidney disease in the family and population
groups that have high rates of diabetes or hypertension such as African Americans. ,
Hispanic Americans, Asians, Pacific Islanders, and American Indians.

7) Pathophysiology
The pathophysiology of chronic kidney disease initially depends on the underlying
disease, but in later development the process is more or less the same. In chronic renal
failure there is a reduction in kidney mass resulting in structural and functional
hypertrophy of the remaining nephrons. This results in hyperfiltration, which is
followed by an increase in capillary pressure and glomerular blood flow. This
adaptation process lasts a short time, finally followed by a maladaptation process in
the form of sclerosis of the remaining nephrons. This process is eventually followed
by a progressive decline in nephron function. Changes in neuronal function remaining
after kidney damage lead to the formation of connective tissue, Meanwhile, intact
nephrons will experience an increase in the excretory load, resulting in a vicious cycle
of hyperfiltration and increased glomerular blood flow. And so on, this situation
continues like a cycle that ends with Terminal Kidney Failure (GGT) or End Stage
Renal Disease (ESRD). The presence of increased intrarenal renin-angiotensin-
aldosterone axis activity, systemic hypertension, nephrotoxin and renal
hypoperfusion, proteinuria, hyperlipidemia also contribute to the occurrence of
hyperfiltration, sclerosis, and progression.
With a decrease in GFR, there will be:
 Anemia
Disorders of erythropoietin formation in the kidneys cause a decrease in
erythropoietin production so that the process of formation of erythrocytes does not
occur causing anemia characterized by a decrease in the number of erythrocytes, a
decrease in Hb levels and followed by a decrease in blood hematocrit levels. In
addition, CKD can cause gastric mucosal disorders (uremic gastritis) which often
causes gastrointestinal bleeding. The presence of uremic toxins in CKD will affect
the half-life of red blood cells to be short, in normal circumstances 120 days to 70-
80 days and this uremic toxicant can have an erythropoiesis inhibition effect.
 Out of breath
In my opinion, it was caused by damage to the renal filtration unit, causing
decreased renal perfusion, eventually leading to renal ischemia. This causes the
release of renin contained in the juxtaglomerular apparatus, thereby converting
angiotensinogen to angiotensin I. Then by converting enzyme, angiotensin I is
converted to angiotensin II. Angiotensin II stimulates the release of aldosterone and
ADH thereby causing retention of NaCl and water increased extracellular
volume (hypervolemia)  excessive fluid volume  left ventricle fails to pump
 blood to the periphery  LVH  increased left atrial pressure  increase in
pulmonary venous pressure  increased pressure in the pulmonary capillaries 
pulmonary edema  out of breath
 Acidosis
In chronic renal failure, metabolic acidosis can occur due to a decrease in the ability
of the kidneys to excrete H+ ions accompanied by a decrease in bicarbonate
(HCO3) levels and plasma pH. The pathogenesis of metabolic acidosis in chronic
renal failure includes decreased excretion of ammonia due to loss of a number of
nephrons, decreased excretion of phosphate, loss of bicarbonate in the urine. The
degree of acidosis is determined by a decrease in blood pH. If the decrease in blood
pH is less than 7.35, it is said to be metabolic acidosis. Metabolic acidosis can cause
gastrointestinal symptoms such as nausea, vomiting, anorexia and fatigue. One of
the typical symptoms of metabolic acidosis is Kussmaul breathing, which occurs
because of the need to increase carbon dioxide excretion to reduce the severity of
the acidosis.
 Hypertension
Caused by damage to the renal filtration unit, causing decreased renal perfusion,
eventually leading to renal ischemia. This causes the release of renin contained in
the juxtaglomerular apparatus, thereby converting angiotensinogen to angiotensin
I. Then by converting enzyme, angiotensin I is converted to angiotensin II.
Angiotensin II has a strong vasoconstrictive effect that increases blood pressure.
 Hyperlipidemia
Decreased GFR causes a decrease in the breakdown of free fatty acids by the
kidneys, causing hyperlipidemia.
 Hyperuricemia
Kidney excretion disorders occur so that uric acid accumulates in the blood
(hyperuricemia). High uric acid levels will cause the deposition of urate crystals in
the joints, so the joints will look swollen, inflamed and painful.
 Hyponatremia
Increased sodium excretion can be caused by the release of natriuretic peptide
hormone which can inhibit sodium reabsorption in the renal tubules. If renal
 function continues to deteriorate accompanied by a decrease in the number of
nephrons, natriuresis will increase. Hyponatremia accompanied by excessive water
retention will lead to dilution of sodium in the extracellular fluid. The state of
hyponatremia is characterized by digestive tract disorders in the form of cramps,
diarrhea and vomiting.
 Hyperphosphatemia
Decreased kidney function results in a decrease in phosphate excretion so that a lot
of phosphate is in the blood circulation. If the solubility is exceeded, the phosphate
will combine with Ca2+ to form calcium phosphate which is poorly soluble.
Precipitated calcium phosphate will settle in joints and skin (causing joint pain and
pruritus, respectively)
 Hypocalcemia
This is because Ca2+ forms a complex with phosphate. Hypocalcemia
stimulates the release of PTH from the parathyroid glands, thereby mobilizing
calcium phosphate from bone. The result is bone demineralization (osteomalacia).
Usually PTH is able to keep the plasma phosphate concentration low by inhibiting
its reabsorption in the kidneys. Thus, despite the mobilization of calcium phosphate
from bone, its production in plasma is not excessive and the concentration of Ca2+
may increase. However, in renal insufficiency, the excretion through the kidneys
cannot be increased so that the plasma phosphate concentration increases.
Furthermore, the concentration of CaHPO4 precipitated and the concentration of
Ca2+ in the plasma remained low. Therefore, the stimulus for PTH release persists.
In this state of constant stimulation, the parathyroid glands are hypertrophied and
release even more PTH. Disorders associated with hypocalcemia are
hyperphosphatemia, renal osteodystrophy and secondary hyperparathyroidism.
Because PTH receptors are not only found in the kidneys and bones, but also in
many other organs (nervous system, stomach, blood cells and gonads), it is
suspected that PTH plays a role in the occurrence of various disorders in these
organs.
Decreased calcitriol formation in renal failure also plays a role in causing
mineral metabolism disorders. Usually this hormone stimulates the absorption of
 calcium and phosphate in the intestine. However, due to a decrease in calcitriol, it
causes decreased absorption of phosphate in the intestine, this exacerbates the
hypocalcemia state.
 Hyperkalemia
In a state of metabolic acidosis where the plasma H+ ion concentration increases,
the hydrogen ions will diffuse into the kidney cells, resulting in leakage of K+ ions
into the plasma. An increase in the concentration of H+ ions in kidney cells will
cause an increase in hydrogen secretion, while potassium secretion in the kidneys
will decrease, causing hyperkalemia. The clinical picture of this potassium disorder
is related to the nervous system and cardiac, skeletal and smooth muscles so that it
can cause muscle weakness and loss of deep tendon reflexes, gastrointestinal
motility disorders and mental disorders.
 Proteinuria
Proteinuria is a marker to determine the cause of kidney damage in CKD such as
DM, glomerulonephritis and hypertension. Glomerular proteinuria is associated
with a number of kidney diseases involving the glomerulus. Several mechanisms
cause an increase in glomerular permeability and trigger glomerulosclerosis. So
that large protein molecules such as albumin and immunoglobulin will be free to
pass through the filtration membrane. In the state of severe proteinuria will occur
spending 3.5 g protein or more which is called the nephrotic syndrome.
 Uremia
High levels of urea in the blood is called uremia. The cause of uremia in CKD is
due to impaired filtration function in the kidneys so that urea accumulation in the
blood can occur. Urea in the urine can diffuse into the bloodstream and cause
toxicity that affects the glomerulus and microvascularization of the kidney or renal
tubules. If the glomerular filtration rate is less than 10% of normal, then clinical
signs of uremia begin to appear. Patients will show symptoms of gastrointestinal
tract irritation, neurological disorders, breathing such as ammonia (fetor uremic),
uremic pericarditis and uremic pneumonitis. Cerebral disturbances can occur in
conditions of very high urea and cause uremic coma.
8) Diagnosis
 Clinical Symptoms
In chronic kidney failure, the symptoms develop slowly. At first there were
no symptoms at all, kidney function abnormalities can only be identified from
laboratory tests. As the disease progresses, over time there will be an increase in
blood urea levels (uremia). At this stage, the patient shows physical symptoms
involving abnormalities of various organs such as:
o Gastrointestinal disorders: decreased appetite, nausea, vomiting and uremic
fetor
o Skin disorders: urea frost and itching on the skin
o Neuromuscular disorders: weak limbs, paraesthesia, muscle cramps, decreased
concentration power, insomnia, restlessness
o Cardiovascular disorders: hypertension, shortness of breath, chest pain, edema
o Sex disorders: decreased libido, nocturia, oliguria
In the earliest stages of chronic kidney disease, there is a loss of renal
reserve power, in which the basal GFR 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 creatinine levels. Up to GFR, 60%
of patients still have no complaints (asymptomatic), but there has been an increase
in serum urea and creatinine levels. Up to 30% GFR, complaints began to occur
such as nocturia, weakness, nausea, poor appetite and weight loss. Up to a GFR of
less than 30% of patients show signs and symptoms of real uremia such as anemia,
increased blood pressure, phosphorus and calcium metabolism disorders, pruritus,
nausea, vomiting and so on. Patients are also susceptible to infections such as
urinary tract infections, respiratory infections, and gastrointestinal infections. There
will also be water balance disorders such as hypo or hypervolumia, electrolyte
balance disorders such as sodium and potassium. If the GFR is below 15%, more
serious symptoms and complications will occur and the patient will require renal
replacement therapy, including dialysis or kidney transplantation. In this condition,
the patient is said to have reached the stage of renal failure. If the GFR is below
15%, more serious symptoms and complications will occur and the patient will
 require renal replacement therapy, including dialysis or kidney transplantation. In
this condition, the patient is said to have reached the stage of renal failure. If the
GFR is below 15%, more serious symptoms and complications will occur and the
patient will require renal replacement therapy, including dialysis or kidney
transplantation. In this condition, the patient is said to have reached the stage of
renal failure.
 Laboratory Overview
Laboratory features of chronic kidney disease include:
o According to the underlying disease
o Decreased kidney function in the form of increased levels of serum urea and
creatinine, and decreased GFR
o Blood biochemical abnormalities include decreased hemoglobin levels,
increased uric acid levels, hyper or hypokalemia, hyponatremia, hyper or
hypochloremia, hyperphosphatemia, hypocalcemia, metabolic acidosis.
o Urinalysis abnormalities include proteinuria, hematuria, leukosuria, casts,
isostenuria
 Radiological Picture
Radiological examination of chronic kidney disease includes:
o Plain photo of the abdomen, radio-opaque stones can be seen
o Intravenous pyelography is rarely performed because the contrast is often
unable to pass through the glomerular filter, in addition to concerns about the
toxic effect of contrast on the already damaged kidney.
o Antegrade or retrograde pyelography as indicated
o Renal ultrasound may show reduced kidney size, cortical thinning, presence of
hydronephrosis or kidney stones, cysts, masses, calcifications.
o Kidney scan or renography if indicated
 Kidney Biopsy and Histopathological Examination
Performed on patients with kidney size that is still close to normal, where a
noninvasive diagnosis cannot be established and aims to determine the etiology,
determine therapy, prognosis and evaluate the results of the therapy that has been
given. Contraindicated in reduced kidney size, polycystic kidney, uncontrolled
 hypertension, perinephric infections, blood clotting disorders, respiratory failure,
and obesity.
9) Complications
Chronic kidney failure can cause various complications as follows:
 Hyperkalemia
 Metabolic acidosis
 Cardiovascular complications (hypertension and CHF)
 Hematologic disorders (anaemia)
 Renal osteodystrophy
 Neurological disorders (peripheral neuropathy and encephalopathy)
 Without treatment, a uremic coma will occur

10) Management
Management of chronic kidney disease includes:
 Specific therapy for underlying disease
The right time to treat the underlying disease is before the GFR declines. When
GFR has decreased to 20-30% of normal, therapy for the underlying disease is not
much benefit.
 Prevention and treatment of comorbid conditions
It is important to follow and record the rate of decrease in GFR to identify comorbid
conditions that may worsen the patient's condition.
 Slows down the deterioration of kidney function
The main factor causing worsening of kidney function is the occurrence of
glomerular hyperfiltration. Ways to reduce glomerular hyperfiltration are:
o Restriction of protein intake
Because excess protein cannot be stored in the body but is broken down into
urea and other nitrogenous substances, which are mainly excreted through the
kidneys, high-protein foods containing hydrogen ions, phosphates, sulfates, and
other inorganic ions are also excreted through the kidneys. Therefore, the
administration of a high-protein diet in patients with chronic renal failure will
result in the accumulation of nitrogenous substances and other inorganic ions
 and lead to uremia syndrome. Restriction of protein intake is also related to
restriction of phosphate intake, because protein and phosphate always come
from the same source and to prevent hyperphosphatemia.
Restriction of Protein and Phosphate Intake in Chronic Kidney Disease
LGF ml/min Protein intake g/kg/day Phosphate g/kg/day
>60 Not recommended Unlimited
25 – 60 0.6 – 0.8/kg/day, including > < 10 g
0.35 gr/kg/day high
biological value
5 -25 0.6 – 0.8/kg/day, including > < 10 g
0.35 g/kg/day high
biological value protein or
additional 0.3 g essential
amino acids or ketones
<60(syndromic 0.8/kg/day (+1 g protein/g < 9 g
nephrotic) proteinuria or 0.3 g/kg
additional essential amino
acids or ketones

o Pharmacological therapy
To reduce intraglomerular hypertension. The use of antihypertensive drugs
(ACE inhibitors) besides being useful for reducing cardiovascular risk is also
very important to slow the worsening of nephron damage by reducing
intraglomerular hypertension and glomerular hypertrophy.
 Prevention and therapy of cardiovascular disease
By controlling DM, controlling hypertension, controlling dyslipidemia,
controlling anemia, controlling hyperphosphatemia and treating fluid overload and
electrolyte balance disorders.
 Prevention and therapy of complications of disease:
o Anemia
 Evaluation of anemia begins when the hemoglobin level is <10 g% or
hematocrit <30% includes an evaluation of iron status (serum iron
level/serum iron, total iron binding capacity, serum ferritin), looking for
sources of bleeding, erythrocyte morphology, possibly hemolysis, etc.
Administration of erythropoitin (EPO) is recommended. The target
hemoglobin is 11 – 12 g/dl.
o Renal osteodystrophy
Renal osteodystrophy can be treated by:
 Overcoming hyperphosphatemia
 Restriction of phosphate intake 600 – 800 mg/day
 Administration of phosphate binders, such as salt, calcium,
aluminum hydroxide, magnesium salt. It is given orally to
inhibit the absorption of phosphate from food. The most widely
used calcium salts are calcium carbonate (CaCO3) and calcium
acetate
 The administration of calcium plucking substances, which can
block Ca receptors in the parathyroid glands, is called sevelamer
hydrochloride.
 Administration of calcitriol
Use is limited in patients with normal blood phosphate levels and
parathyroid hormone (PTH) levels > 2.5 times normal because it can
increase the absorption of phosphate and potassium in the
gastrointestinal tract, resulting in the buildup of calcium carbonate
salts in the tissues, which is called metastatic calcification. excessive
pressure on the parathyroid glands.
 Fluid and electrolyte restriction
Restriction of fluid intake to prevent edema and cardiovascular
complications is necessary. So the recommended intake of water is
500-800 ml plus the amount of urine. The electrolytes to watch out
for are potassium and sodium. Potassium restriction is performed
because hyperkalemia can lead to fatal cardiac arrhythmias.
 Therefore, the administration of drugs containing potassium and
foods high in potassium (such as fruits and vegetables) should be
limited. The recommended blood potassium level is 3.5 – 5.5
mEq/lt. Sodium restriction is intended to control hypertension and
edema. The amount of sodium salt given is adjusted to the high
blood pressure and the degree of edema that occurs.
 Kidney replacement therapy in the form of dialysis or kidney transplant
Performed on chronic kidney disease stage 5, namely the GFR < 15 ml/min. In the
form of hemodialysis, peritoneal dialysis or kidney transplantation.

11) Prognosis
CKD is incurable, so the long-term prognosis is poor, unless a kidney transplant is
performed. The current management is aimed only at preventing the progression of
CKD itself. In addition, usually CKD often goes unnoticed until it reaches an advanced
stage and causes symptoms so that treatment is often too late.
c. The Difference Between the Two Differential Diagnosis Judging from the Ultrasound Results

Renal ultrasound can also be used to help determine whether kidney failure is acute or
chronic. Normal-sized kidneys usually indicate acute kidney failure, but when both kidneys
are smaller than normal, it means chronic kidney failure.
1) BATTERY
The current diagnosis of AKI is made on the basis of an elevated serum creatinine
and a decreased blood urea nitrogen (BUN) and urine output, although there are limitations.
On ultrasound examination of AKI, performed to determine kidney size, presence
or absence of obstruction, abnormal renal parenchymal texture

2) CKD
Ultrasound examination in CKD is performed to determine the size of the kidney
is shrinking, cortical thinning, the presence of hydronephrosis or kidney stones, cysts,
masses, calcifications, proximal ureters, bladder, and prostate.
Blood chemistry examinations obtained in patients with CKD are increased
urea/BUN, increased serum creatinine, hypoalbunemia, dyslipidemia, hyperphosphatase
can occur.
Reference :

Sherwood, Lauralee. Urinary System. Human Physiology from Cells to Systems. Edition 2. Jakarta:
ECG Medical Book Publisher; 2014. p. 463 – 503.

Sudoyo, A. W et al. Chronic Kidney Disease. Internal medicine textbook. Volume II. Edition V.
Jakarta: FK UI IPD Publishing Center; 2019. p. 1035 – 1040.

Kamaludin Ameliana. 2016. Chronic Renal Failure. Jakarta : UPH Internal Medicine Department.

Clinical practice guidelines for chronic kidney disease: evaluation, classification and stratification,
New York National Kidney Foundation, 2012

Silbernagl, S and Lang, F. Chronic renal failure. Pathophysiology Color Text & Atlas. Printing I.
Jakarta: EGC Medical Book Publisher; 2017. p. 110 – 115.

6. What is the initial procedure related to the scenario?

The main goal of management isto prevent further kidney damage and keep the
patient alive until his kidney's faal returns to normal function.
Two types of treatment, namely conservative therapy (supportive) and
renalreplacement therapy(PRC). Conservative therapy is done with medications or fluids
with the aim of preventing or reducing the progressionivity of decreased kidney function,
morbidity, and mortality due to complications. If conservative therapy fails to address
any complications, it is necessary to consider PRC (dialysis).
AKI management priorities:
1. Find and correct pre- and post-renal factors

2. Evaluation of drugs that have been given

3. Optimize cardiac output and blood flow to the kidneys

4. Repair and/or increase urine flow

5. Monitor fluid intake and expenditure, weigh daily

6. Find and treat acute complications (hyperkalemia, hypernatremia, acidosis,

hyperphosphatemia, pulmonary edema)
7. Adequate nutrient intake early on
8. Find the focus of the infection and address the infection aggressively

9. Good thorough care

10. Immediately start dialysis therapy before complications arise

11. Give the drug with the right dose according to the capacity of the kidney cleanness

Monitoring of fluid intake and expenditure should be done regularly. Some patients
may experience significant fluid deficits, so close monitoring and regulation of fluid and
electrolyte balance should be done carefully. Fluid substitution should be closely
monitored with serially measured urine volume guidelines, as well as urinary electrolytes
and serums. AKI causes disturbances in renal excretion of sodium, potassium, calcium
and water, divalent hemostasis cation and urinary mechanisms. Therefore, AKI often
causes hyperkalemia, hyponatremia, hyperposfatemia, hypocalcemia,
hypermagnesemia, and metabolic acidosis. Management of complications can also be
done with renal replacement therapy (haemodialysis) indicated in the states of oligouria,
anuria, hyperkalemia (K>6.5 mEq/l), severe acidosis (pH<7.1), azotemia (ureum>200
mg/dl), pulmonary edema, encephalopathy uremicum, uremicum pericarditis,
neuropathy or uremicum myopathy, severe dysnatremia (Na>160 mEq/l or <115 mEq/l),
hyperthermia, over-dosing of dialysis-free medications. There is no definitive guidance
on when is the right time to stop kidney replacement therapy. In general, therapy is
stopped if the condition that is an indication has been resolved.
 But in the early phases, we can suggest adequate rest, a diet withregulated
fluid input, obtrusion surgery, and dialysis.

Reference :
Haryanti, I. A. P., & Berawi, K. N. (2015). Erapi Conservative and Kidney
Replacement Therapy as Management in Chronic Kidney Failure. Journal
Majority, 4(7), 49-54.
• Sinto, R., & Nainggolan, G. (2010). Acute kidney injury: clinicaland governance
approach. Maj Kedokt Indon, 60(1), 2.

7. What is the Islamic perspective based on the scenario?

ْ‫سعدِب ِنْ عَن‬ َ ‫ن ا َ ِبي ِْه عَنْ َو َّقاصْ ا َ ِبى‬ ِْ ‫ع‬

َ ِ‫ي‬ْ ‫صلَّى النَّ ِب‬
َ ‫سلَّ َْم الل ُهعَلَي ِْه‬ َّْ ِ‫للاَ ا‬
َ ‫ن َو‬ ْ ‫ب‬ َ ْ‫ب يُحِ ب‬
ْ ‫ط ِي‬ َّ ‫ظافَ ْةَ نَظِ يفْ ال‬
َْ ‫ط ِي‬ َ َّ‫ك َِريمْ يُحِ بالن‬
ْ‫َج َواديُحِ بال َج َوا َدفَنَظِ فُوااَفنَيتَكُمْ الك ََر َْم يُحِ ب‬

Meaning: "Indeed, Allah Ta'ala is good (and) loves goodness, clean (and) loves cleanliness,
noble (and) loves glory, good (and) loves goodness. Therefore, clean up your environment.
”(HR. Tirmidzi).