Case Report

CHRONIC KIDNEY DISEASE

Presenter

: Agus Salim (100100027)

Seprima Yenti (100100029)

Supervisor

: dr. Nelly Rosdiana, Sp.A (K)

INTRODUCTION
Chronic Kidney Disease (CKD) is a patophysiologic process with various etiology which
cause decrease renal function progressively. This is a clinical condition where the renal
dysfunction is irreversible and lasting until renal replacement therapy (dialysis, renal
transplantation) is needed.1
CKD is a serious public health problem with national surveys showing a condireably
gihger prevalence than appreciated previously.2 Recent evidence indicates that the outcomes can
be improved by early diagnosis and treatment. 3 Earlier stages of CKD can be detected through
routine laboratory measurements. The presence of CKD should be established, based on presence
of kidney damage and level of kidney function (glomerular filtration rate [GFR]).4
Children who have CKD may present to clinicians with a combination of problems
involving

growth,

nutrition,

electrolyte

disturbances,

renal

osteodystrophy,

anemia,

immunizations, hypertension, and renal transplantation. Children with CKD need a

comprehensive treatment. A teamwork consist of pediatric nephrologist,nutritionist, psikologist
or psychiatric and patient family.5

EPIDEMIOLOGY
Globally, the prevalence of chronic kidney disease (CKD) stage II or lower in children is
reported to be approximately 18.5-58.3 per million children.6 Data from the ItalKid study
reported a mean incidence of 12.1 cases per year per million in the age-related population (age
range, 8.8-13.9 y) and a prevalence of 74.7 per million in this population. 7 The frequency of
chronic kidney disease increases with age and is much more common in adults than children.
Among children, chronic kidney disease is more common in children older than 6 years than in
those younger than 6 years. The percentages in the NAPRTCS cohort were 19% in children aged
0-1 years; 17% in those aged 6-12 years; 33% in children aged 2-5 years; and 31% in those older
than 12 years.6
In Indonesia, there is no prevalence of CKD in children nationally. Based on study in 7
hospital in Indonesia, 2889 children who were treated with renal disease (years 1984-1988), 2%
of them are diagnosed with CKD.RSCM Jakarta found 4.9% from 668 of children who are
hospitalized with kidney disease are diagnosed with CKD. The incidence in the General Hospital
Dr. Soetomo for 5 years (1988-1992) is 0.07% of all patients hospitalized in the pediatric ward.5
DEFINITION AND STAGING
Chronic kidney disease (CKD) is the presence of kidney damage lasting for at least 3
months with or without a decreased GFR or any patient who has a GFR of less than 60 mL/min
per 1.73 m2 lasting for 3 months or more, irrespective of diagnosis (Tabel 1).4
Tabel 1. Criteria for definition of CKD
A patient has CKD if either of the following criteria are present :
1. Kidney damage for >3 month, as defined by structural or functional abnormalities of the
kidney, with or without decrease GFR, manifested by 1 or more of the following features:

Abnormalities in the composition of the blood or urine

Abnormalities in imaging tests

Abnormalities on kidney biopsy

2. GFR <60 mL.min/1.73 m2 for >3 month, with or without the other signs of kidney damage
described above.
Kidney Disease Outcomes Disease Initiative, 2012. Clinical Practice Guideline for Chronic
Kidney Disease : Evaluation, Clasification and Stratification.

The normal level of GFR varies according to age, gender, and body size. The normal
GFR in young adults is 120 to 130 mL/min/1.73 m 2, whereas the normal level of GFR is much
lower than this in early infancy, even when corrected for body surface area, and subsequently
increases in relationship to body size for up to 2 years.8 Staging of Chronic Kidney Disease based
on KDOQI is shown in tabel 2.
Tabel 2. KDOQI Classification of the stage of CKD
Stage

GFR

Description

Action Plan

(mL/min/1.73 m2)
1

>90

Kidney damage with normal or Treat primary and comorbid conditions,

increased GFR

slow CKD progression, CVD risk

reduction

60-89

Kidney damage with mild

Estimate rate of progression

reduction of GFR
3

30-59

Moderate reduction of GFR

Evaluate and treat complications

15-29

Severe reduction of GFR

Prepare for kidney replacement therapy

<15

End Stage renal failure

Kidney replacement therapy

Kidney Disease Outcomes Disease Initiative, 2012. Clinical Practice Guideline for Chronic
Kidney Disease : Evaluation, Clasification and Stratification.
ETIOLOGY
CKD has a prevalence of 1.5 to 3.0 per 1.000.000 among children younger than the age
of 16 years. In children, CKD may be the result of congenital, acquired, inherited, or metabolic
renal disease, and the underlying cause correlates closely with the age of the patient at the time
when the CKD is first detected. CKD in children <5 years old is most commonly a result of
congenital abnormalities such as renal hypoplasia, dysplasia, or obstructive uropathy. Additional
causes include congenital nephrotic syndrome, prune belly syndrome, cortical necrosis, focal
segmental glomerulosclerosis, polycystic kidney disease, renal vein thrombosis, and hemolytic
uremic syndrome. After 5 years of age, acquired diseases (various forms of glomerulonephritis
including lupus nephritis) and inherited disorders (familial juvenile nephronophthisis, Alport

syndrome) predominate. CKD related to metabolic disorders (cystinosis, hyperoxaluria) and

certain inherited disorders (polycystic kidney disease) can occur throughout the childhood years. 9
Overall, the most common causes of CKD in children are urologic abnormalities (30% to
33%) and glomerulopathies (25% to 27%). These two abnormalities account for more than 50%
of the reported causes of end-stage renal disease in children. The other major causes are
hereditary nephropathies (16%) and renal hypoplasia and dysplasia (11%). Data from the North
American Pediatric Renal Trial and Collaborative Studies 2006 demonstrate very similar
information (Table 3).10
Tabel 3.Common Cause of Chronic Kidney Disease in Children
Diagnosis

Incidence

Obstructive uropathy

22%

Aplasia/hypoplasia/dysplasia

18%

Glomerulonephritis

10%

Reflux nephropathy

8%

Dilys A. Whyte and Richard N Fine, 2008. Chronic Kidney Disease in Children.
PATOPHYSIOLOGY
Renal function decrease progressively despite the primary disease has been resolved or
have become inactive. This condition indicate a mechanism of secondary adaptation that has a
role in the ongoing damage in chronic kidney disease. One of the evidence about the mechanism
is the presence of renal histologic feature of CKD that caused by any primary disease. Change
and adaptation of the remaining nephron following renal damage in the beginning lead to
formation of connective tissue and further damage of the surviving nephrons. This condition will
continue until the end stage of renal failure.11

Figure 1. Cycle of the chronic kidney disease

Wassner SJ, Baum M (1999). Chronic Renal Failure. Physiology and Management. In: Barrat
TM, Avner ED, Harmon WE, Editors. Pediatric Nephrology, 4th edition. Baltimore: Lippincott
Williams & Wilkins, pp. 1155-1182.
Hyperfiltration injury may be an important final commonpathway of glomerular
destruction, independent of the underlying cause of renal injury. As nephrons are lost, the
remaining nephrons undergo structural and functional hypertrophy characterized by an increase
in glomerular blood flow. The driving force for glomerular filtration is thereby increased in the
surviving nephrons. Although this compensatory hyperfiltration temporarily preserves total renal
function, it can cause progressive damage to the surviving glomeruli, possibly by a direct effect
of the elevated hydrostatic pressure on the integrity of the capillary wall and/or the toxic effect of
increased protein traffic across the capillary wall. Over time, as the population of sclerosed
nephrons increases, the surviving nephrons suffer an increased excretory burden, resulting in a
vicious cycle of increasing glomerular blood flow and hyperfiltration injury.9

Proteinuria itself can contribute to renal functional decline, as evidenced by studies that
have shown a beneficial effect of reduction in proteinuria. Proteins that traverse the glomerular
capillary wall can exert a direct toxic effect on tubular cells and recruit monocytes and
macrophages, enhancing the process of glomerular sclerosis and tubulointerstitial fibrosis.
Uncontrolled can hypertension exacerbate disease progression by causing arteriolar
nephrosclerosis and by increasing the hyperfiltration injury. Hyperphosphatemia can increase
progression of disease by leading to calcium phosphate deposition in the renal interstitium and
blood vessels. Hyperlipidemia, a common condition in CKD patients, can adversely affect
glomerular function through oxidant-mediated injury.9
CLINICAL MANIFESTATION
Early clinical manifestation of CKD doesn't show specific symptoms such as dizziness,
letargis, anorexia, nausea.5 CKD patient from chronic glomerulonephritis can present with
edema, hypertension, hematuria, and proteinuria. Infants and children with congenital disorders
such as renal dysplasia and obstructive uropathy can present in the neonatal period with failure to
thrive, polyuria dehydration, urinary tract infection, or overt renal insufficiency. Congenital
kidney disease is diagnosed with prenatal ultrasonography in many infants, allowing early
diagnostic and therapeutic intervention. Children with familial juvenile nephronophthisis can
have a very subtle presentation with nonspecific complaints such as headache, fatigue, lethargy,
anorexia, vomiting, polydipsia, polyuria, and growth failure over a number of years.9
In physical examination we found a pallor, limp, and hypertension. The condition last for
along time and more day more severe. Uremia is a toxic syndrome caused by severe glomerular
damage, tubular dysfunction, and renal endocrine function.5
Clinical manifestation is the result of :
1. Fluid and electrolyte imbalance
2. overacumulation of uremic toxin.
3. Hormonal dysfunction (decrease of erytropoeitin and vitamin D3)
4. unresponse of end organ with growth hormone.

LABORATORY FINDING
Laboratory findings could be found :9
1. complete blood count normochromic, normocytic anemia.
2. Renal Function Test serum ureum and creatinine.
3. Electrolite hyperkalemia, hyponatremia (if volume overloaded), acidosis,
hypocalcemia, hyperphosphatemia.
4. Urinalisis proteinuria and hematuria if caused by glomerulonephritis in heavy
proteinuria could be found hypoalbuminemia.
Glomerular filtration rate (GFR) used for staging of CKD. In children, the formula to
estimate patient's GFR are shown below :12

Where k is :
1. 0.33 for low-birhtweiht infant <1 year old
2. 0.45 for term infant <1 year old whose weight is appropriate for gestational age
3. 0.55 for children (1-13 years old)
4. 0.57 for adolescent girls (13-21 years old)
5. 0.70 for adolescent boys (13-21 years old)
TREATMENT
Patients with CKD should be evaluated to determine:
1. Diagnosis (type of kidney disease)
2. Comorbid conditions (such as hyperlipidemia)
3. Severity, assessed by level of kidney function
4. Complications, related to level of kidney function
5. Risk for loss of kidney function
6. Risk for cardiovascular disease
Treatment of CKD should include:
1. Specific therapy, based on diagnosis
2. Evaluation and management of comorbid conditions

3. Slowing the loss of kidney function

4. Prevention and treatment of cardiovascular disease
5. Prevention and treatment of complications of decreased kidney function (eg,
hypertension, anemia, acidosis, growth failure)
6. Preparation for kidney failure therapy
7. Replacement of kidney function by dialysis and transplantation,
if signs and symptoms of uremia are present, a clinical action plan should be developed
for each.
1. Nutrition
Children who have CKD have nutrition and protein deficiencies for several reasons,
including anorexia, nausea and vomiting from the uremia, and an abnormal sense of taste. Young
children, in particular, need sufficient caloric intake to grow. Protein intake should be optimized
to allow for maintenance of nitrogen balance and preservation of lean body mass. Some patients
may require supplemental nasogastric or gastrotomy tubefeeding if they cannot maintain optimal
height and weight gain by oral feeding. However, if protein intake isexcessive, hyperfiltration
may occur, leading to increased damage to the renal parenchyma. Micropuncture studies
demonstrate an increase in the GFR (hyperfiltration) after an amino acid load due to reduction in
afferent arteriolar resistance.
Prostaglandins, which can alter vascular tone and increase the GFR, recently have been
implicated in the development of hyperfiltration because prostaglandin values have been noted to
increase in response to an increased amino acid load. Protein restriction was believed to slow the
progression of renal disease, but this effect has not been verified in children. Reducing protein
intake to 0.8 to 1.1 g/kg per day has not been shown to affect linear growth negatively. Because
many vitamins are lost during dialysis, pediatric patients undergoing this therapy should
supplement their diets with vitamins, especially folic acid, trace minerals, and B complexes.
Specialized formulas that have high energy contents and lower electrolyte contents have
been developed for infants and children who have CKD. These are reasonable formulas for an
older child already on dialysis who may be not be meeting his or her nutritional goal or who is
experiencing poor weight gain or growth.

2. Fluid and Electrolite Imbalance

Hyperkalemia is a complication of CKD. In the healthy kidney, potassium reabsorption
occurs in the proximal tubules and the loop of Henle, and secretion of up to 90% of the daily
intake of potassium occurs in the distal tubules. As renal disease progresses, the distal tubules of
the remaining nephrons continue to secrete potassium. Increased aldosterone also enhances
potassium secretion by stimulating sodium-potassium exchange in the kidneys and the colon.
However, hyperkalemia develops from an increase in dietary potassium that overwhelms the
compensatory mechanisms or by use of medications that alter potassium secretion
(spironolactone, amiloride, or angiotensin converting enzyme inhibitors). Table 4 lists
approaches to treating hyperkalemia. Hypokalemia also can occur in children who have CKD but
tends to develop in patients who have tubular defects such as seen with Fanconi syndrome.
Tabel 4. Treatment of hyperkalemia
Product

Dose

Sodium bicarbonate

([0.6

Potential adverse effects

X

BB]

[bicarbonate Hypocalcemia

desired-bicarbonated observed]) /2
0.5-1 mEq/kg IV over 1 hour
Calcium gluconate (10%)

0.5-1 mL/kg IV over 5-15 min

Arrhythmia

Glucose and insulin

Glucose 0.5 g/kg with insulin 0.1 Hypoglycemia

unit/kg IV over 30 min

Sodium

polystyrene 1g/kg per dose PR or PO

sulfonate
Beta agonist

5-10 mg aerosolized

Constipation/diarrhea
Tachycardia, hypertension

IV= intravenous, PO= orally, PR=rectally

Dilys A. Whyte and Richard N Fine, 2008. Chronic Kidney Disease in Children.
3. Acid-base imbalance
Metabolic acidosis develops in patients who have CKD because of abnormally decreased
bicarbonate reabsorption of filtered bicarbonate, reduction of renal ammonia synthesis, decreased
acidified tubular fluid, and decreased titratable acid excretion. Decline in GFR below 50% of

normal is accompanied by a decline in bicarbonate reabsorption. Reduced bicarbonate

reabsorption leads to systemic acidosis, which causes protein degradation and efflux of calcium
from bone. Such factors play a role in the poor linear growth observed in children who have
CKD.
Therapy should target maintaining a serum bicarbonate concentration of 20 to 22 mEq/L
(20 to 22 mmol/L). Bicarbonate replacement consists of administering sodium bicarbonate
supplements or phosphate binders. Most available binders have a base component such as
calcium carbonate.
4. Hypertension
Hypertension is diagnosed in children who have CKD by finding an elevated blood
pressure reading on three or more separate office visits at least 1 week apart. The diagnosis is
based on the child's age, sex, and height percentile. Grades of hypertension are as follows, based
on tables or graphs of normal values:
Prehypertension: Average systolic or diastolic pressuresare at the 90th percentile or
greater but at or less than the 95th percentile for age, sex, and height
Stage I hypertension: Average systolic or diastolic pressure is at or greater than the
95th percentile for age, sex, and height
Stage II hypertension: Average systolic or diastolic pressure is more than 5mmHg
higher than the 95th percentile
Hypertensive urgency and emergency: Average systolic or diastolic pressure is more
than 5 mm Hg higher than the 95th percentile and clinical symptoms of headache,
vomiting, seizures, or encephalopathy are present
In addition to determining the underlying cause of the hypertension, clinicians should
monitor patients at least annually with echocardiography to assess function and left ventricular
status. Medications are adjusted to improve cardiac function. Those children who fall into the
hypertensive urgency and emergency category require intravenous medications or a rapid-acting
oral medication (nifedipine or minoxidil) to reduce blood pressure.

5. Anemia
Anemia in CKD is caused by either an insufficient production of erythropoietin by the
diseased kidneys or by iron deficiency. Anemia is defined as a reduction in red blood cell volume
or hemoglobin concentration below the normal range for a healthy person. Morbidity, mortality,
and quality of life data from the KDOQI guidelines suggest that maintaining the hematocrit in
the range of 33% to 36% (0.33 to 0.36) and the hemoglobin at 11.0 to 12.0 g/dL (110.0 to 120.0
g/L) is important for children who have CKD. Prior to the development of recombinant human
erythropoietin, patients who had CKD had to undergo transfusions to increase their hematocrit
values. Transfusions not only exposed patients to various infectious agents but exposed and
sensitized them to human lymphocyte antigens, putting them at increased risk for rejection
should they undergo renal transplantation.
With improvement of anemia, children demonstrate improvement in cognitive
development, cardiac function, and exercise tolerance, as well as decreased mortality. As stated,
anemia is caused by either an insufficient production of erythropoietin by the diseased kidneys or
by iron deficiency. Due to decreased appetites, children who have CKD cannot increase their
iron stores adequately through an oral diet. Oral iron therapy should be administered at a dose of
2 to 3 mg/kg per day of elemental iron in two or three divided doses. Iron should be consumed
on an empty stomach and not concomitantly with phosphate binders because iron binds to the
phosphate binders.
Parenteral iron can be provided to those who continue to lose blood or who cannot
tolerate oral iron. Parenteral iron can be administered easily to patients receiving hemodialysis
because they already have vascular access. Intravenous iron also can be used for the peritoneal
dialysis patient who is resistant to oral iron or is noncompliant in taking oral iron.
Erythropoietin can be administered subcutaneously to children who have CKD, including
those undergoing peritoneal dialysis, or intravenously for those receiving hemodialysis.
Erythropoietin can be given one, two, or three times per week. The initial dose ranges between
30 and 300 units/kg per week, with the usual maintenance dosage between 60 and 600 units/kg
per week. The maintenance dose is determined and adjusted based on monthly hemoglobin
values. A new form of erythropoietin, darbepoetin alfa, which has a longer half-life and requires
dosing once every 2 weeks to once monthly, is being investigated for use in children.

6. Growth
Growth retardation is one of the major complications of a child who has CKD. The
degree of growth failure has been correlated with age of onset of CKD.
The cause of growth failure is believed to be multifactorial, including :
growth hormone (GH) and insulin-like growth factor-I (IGF-I) function
nutritional status
acid-base balance
bone mineralization.
When renal function is reduced, GH is increased because of decreased clearance by the
kidneys despite the normal pulsatile release of the hormone, which continues despite the
increased GH concentrations. Resistance to GH and to IGF-I also is believed to lead to growth
reduction. In some studies, serum GH concentrations are increased in patients who have CKD,
but the concentrations of GH receptors are reduced. Another cause may be the upregulation of
intracellular inhibitors, labeled suppressors of cytokine signaling (SOCS). The SOCS proteins
can alter the phosphorylation of GH receptors and may cause GH resistance.
Similarly, IGF-1 resistance probably is due to several causes. IGF-binding proteins, of
which six are now identified, increase with renal failure and most likely inhibit the actions of
IGF-1 by binding with it, thereby preventing IGF-1 from binding to its receptor. Other hormones
that play a role in pubertal growth and development have been found to be reduced in children
who have CKD, including luteinizing hormone, plasma testosterone, and free testosterone.
Treatment of growth failure initially involves resolving nutritional deficiencies and
improving the acid-base balance of children who have CKD. Once these tasks are accomplished,
affected children begin GH therapy if growth retardation persists. Most patients who have CKD
grow when given the recommended starting dose of 0.05 mg/kg per day, administered
subcutaneously daily. Whether patients in the pubertal age group require additional GH needs
additional investigation.

PROGNOSIS
About 70% of children with chronic kidney disease develop ESRD by age 20 years.
Children with ESRD have a 10-year survival rate of about 80% and an age-specific mortality rate
of about 30 times that seen in children without ESRD. The most common cause of death in these
children is cardiovascular disease, followed by infection. Of the deaths due to cardiovascular
causes, 25% were attributed to cardiac arrest (cause uncertain), 16% to stroke, 14% to
myocardial ischemia, 12% to pulmonary edema, 11% to hyperkalemia, and 22% to other
cardiovascular causes, including arrhythmia. But currently, survival rate of children with CKD is
more better. Data from the Australia and New Zealand (ANZ) registry revealed that the risk of
death was associated with the year in which renal replacement therapy was initiated, the age of
patients at the start of that therapy, and the type of dialysis used.11

CASE REPORT
Name
Age
Sex
Date of Admission

: F.A.Z
: 15 Tahun
: Male
: August, 12th 2014

Chief Complaint

: Loss of consciousness

History:
This has been happened by the patient + 4 days ago. Patient didnt respond when family asking
for conversation. Patient be more quite even the patient spoke, that was incoherent. Patient is a
oldterm patient in nephrology division pediaetric departemen. Last month, the patient was
recommended for hospitalization, but the patient refused.
History of vomit suffered by patient + 3 day, frequency five times per day, volume + spoon.
The content is what patient eat and drink. Now, the vomit was denied.
Diare wasnt found. last defecation three days ago. History of pale faeces was denied. Last
urination 2 days ago. History of urine like a tea was denied.
Fever wasnt found, history of fever also denied
History of seizure was found five months ago, frequency once a day. As soon as the patient
hospitalized at RSUP HAM.
History of weight loss was found, history of appetite loss was found
History of previous illness : History of drugs
: Spironolakton, Furosemide
Physical Examination
Generalized status
Body weight: 40 kg, Body length: 165 cm
Body weight according to age
: 40/56 = 71%
Body height according to age
: 165/170 =97%
Body weight according to body height : 40/51 = 78%
Interpretation : Undernutrition
Presens status
Consciousness: GCS : 13 (E4V4M5), Blood pressure 140/100 mmHg, HR: 98 bpm, RR: 24 bpm,
body temperature: 36,8oC, body weight : 40 kg, body height : 165 cm
Anemic (+); Icteric (-); Cyanosis (-); Edema (-). Dyspnea (-).
Localized status
Head :
Eye: isochoric pupil (3mm/3mm), light reflex (+/+) , conjunctiva palpebral inferior pale (+/+),
icteric sclera (-).

Nose: nasal septum : no deviation, mucosa color dark pink, polyps (-), sinus tenderness (-),
discharge (-).
Ear : External auditory canal: no discharge, tympanic membrant: intact, no inflammation,
Mouth: lips : color is red, fissures; Bucal : dark pink, glistening; tounge : dark pink, papilla
athropy (-), tremor (-)
Teeth and gums : twenty teeth, caries (-).
Tonsil : difficult to assess
Neck :
Lymph node enlargement (-), Neck rigidity (-)
Thorax:
Inspection
Palpation
Percussion
Auscultation

: Symmetrical fusiformis, epigastrial retraction (-), RR: 20 x/i, reguler

: SF right = left, normal
: Sonor
: rales (-/-) , stridor (-/-).

Abdomen:
Inspection
Palpation
Percussion
Auscultation

: Symmetrical fusiformis
: Soepel, Liver and spleen unpalpable
: Tympani
: Normoperistaltic

Extremities:
Extremitas superior : Pulse 98 bpm, regular, adequate pressure and volume, warm,
CRT < 3", spastic (-/-).
Extremitas inferior : Pulse 98 bpm, regular, adequate pressure per volume, warm,
CRT < 3", spastic (-/-).
Urogenital:
Male, within normal limit.

Laboratory Findings (August 12th 2014) :

Parameters
Complete Blood Count
Hemoglobin
Hematocrite
Erithrocyte
Leucocyte
Platelet
MCV
MCH
MCHC
RDW
MPV
PCT
PDW
Hitung Jenis

Value

Normal Value

7.20 gr%
17.40 %
2.37 x 106 /mm3
11.37 x 103 /mm3
420.000 /mm3
73.40 fl
30.40 pg
41.40 gr%
13.20 %
8.00 fl
0.34%
7.8%

13.2 17.3 gr%

43 49 %
4.20 4.87 x 106/mm3
4.5 11 x 103/mm3
150 - 450/mm3
85 95 fl
28 - 32 pg
33 - 35 gr%
11.6 14.8 %
7.0 10.2 fl

Neutrofil

86.90%

37-80

Limfosit

9.70%

20-40

Monosit

3.30%

2-8

Eosinofil

0.10%

1-6

Basofil

0.000%

0-1

Neutrofil absolute

9.88

1,9-5,4

Limfosit absolute

1.10

3,7-10,7

Monosit absolute

0.38

0,3-0,8

Eosinofil absolute

0.01

0,2-0,5

Basofil absolute

0.00

0-0,1

Parameters
Analisa Gas Darah
pH
PCO2
PO2
Bikarbonat
Total CO2
Kelebihan Basa (BE)
Saturasi O2
Carbohydrate Metabolism
Blood Glucose ad random
Renal Function Test

Value

Normal Value

7.31
27.9 mmHg
151.7 mmHg
29.5 mmol/L
15.1 mmol/L
-5.0 mmo/L
99.3%

7.35 7.45
38 42
85 100
22 26
19 25
(-2) (+2)
95 100

149.00 mg/dL

< 200

Ureum
Creatinine
Elektrolit
Kalsium
Natrium
Kalium
Klorida

178.00 mg/dL
4.97 mg/dL

< 50
0,17 0,42

8.9 mg/dL
98 mEq/L
1.7 mEq/L
56 mEq/L

9.2 11.0 mg/dL

135 155 meq/L
3,6 5,5 mEq/L
96 106 mEq/L

Radiologic imaging Juni 28th 2014

Figure 2. The chest x-ray of the patient

Chest x-ray interpretation;
KV is too high, good inspiration, middle trachea, both costophrenicus angels is sharp, smooth
diaphragm, Cardio Thoracic Ratio is more than 50%, bones and soft tissues in normal condition,
Result : Cardiomegaly
Working Diagnosis:
Chronic Kidney disease Stage IV

Management:,
Oxygen 1 2 L/i nasal canule (+), nasogastric tube (-)
IVFD D5% 5 gtt/i
Spironolakton 2 x 25 mg
Diet pediasure milk + Diet 1995 kkal + 80 g protein
Diagnostic Planning:
Chest X-ray
Complete blood count
Glucose ad random
Electrolyte (Na, K, Cl)
Blood gas analysis
Urin analysis
Nephrology consult
USG Doppler Of Kidney and Bladder

Follow Up Patients
August, 12 th 2014
S Loss of consciousness
O Sens: GCS 14 , Temp: 36.8oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-) Dyspnoe
(-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.
HR: 98 bpm, reguler; murmur (-)
RR: 28 x/i, regular, rales (-)
Abdomen
Soepel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 98 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
140/100 mmhg
Genital
Male; within normal limit.
A Chronic Kidney Disease Stage IV
P Management:
O2 1-2 L/i
IVFD D5% 5 gtt/I mikro
Spironolakton 2x25 mg
Diet Milk Pediasure + Diet 1995 kkal + 32 g protein
Hiponatremia correction
Fast Correction = (120-98) x 40 x 0.6 = 501.6 mEq (finished in 6 hours. With NaCl
3% = 501.6/513 =977cc = 160 gtt/I micro
Slow correction = (135-125) x 40 x 0.6 = 240 mEq/L
Maintanance = 2 -4 mEq/L = 80 160 mEq/L
Total = 320 400 mEq
With IVFD D5% NaCl 0.9% = 320/154 x 1000 = 2077 cc 155 gtt/I micro,
finished in 18 hours
Hipocalemia correction
1.7 mEq/L with 0.75 mEq/kgBB, 30 mEq KCl in 90 cc D5%, finished in 3 hours =
40 gtt/I micro
Planning :
Electrolit test repetition post correction, full blood, and AGD
Dipstick result
Uro/Bil/Ket/Blood/Pro/Nit/Leu/Glu/Sg/pH
-/+/-/-/+/-/+/-/1.005/6.5
August 13th 2014

S limp (+), nausea and vomit (-), Fever (-)

O Alert : Compos Mentis , Temp: 36,7oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-)
Dyspnoe (-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.
HR: 88 bpm, reguler; murmur (-)
RR: 26 x/i, regular, rales (-)
Abdomen
Soupel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 88 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
140/100 mmhg
Genital
Male; within normal limit.
A Chronic Kidney Disease Stage IV
P O2 1-2 L/I
IVFD D5% 5 gtt/I mikro
Spironolakton 2x25 mg
Diet 1995 kkal + protein 32 gram
Planning :
Electrolit and AGDA repetition test ( if correction of hipocalemia and hiponatremia
finished).
Water Balance
Input :Diet = 1.500 cc
Output : OUP = 900 cc
B=I-O
IVFD = 30 cc
BAB = 0
= 434 cc
Total = 1.524 cc
IWL = 190 cc
K6JB = HS + BC
Total = 1.090 cc
= 1010 cc
August, 14th 2014
S limp (+), nausea and vomit (-),Fever (-)
O Alert : Compos Mentis , Temp: 36,8 oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-)
Dyspnoe (-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.

A
P

S
O

A
P

HR: 98 bpm, reguler; murmur (-)

RR: 24 x/i, regular, rales (-)
Abdomen
Soupel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 98 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
130/90 mmhg
Genital
Male; within normal limit.
Chronic Kidney Disease Stage IV
Management:
O2 - 1 L/I nasal kanul
IVFD D5% 5 gtt/I micro
Spironolakton 2x25 mg
Diet pediasure milk + Diet 1995 kkal + 32 g protein
Water Balance
Input : Diet = 600 cc
Output : OUP = 600 cc B = I - O
IVFD = 150 cc
BAB = 0
= -40cc
Total = 750 cc
IWL = 190 cc K6JB = HS + BC
Total = 790 cc
= 335 cc
August, 15th 2014
limp (+), nausea and vomit (-),Fever (-)
Alert : Compos Mentis , Temp: 37 oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-)
Dyspnoe (-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.
HR: 110 bpm, reguler; murmur (-)
RR: 26 x/i, regular, rales (-)
Abdomen
Soupel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 110 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
130/90 mmhg
Genital
Male; within normal limit.
Chronic Kidney Disease Stage IV
Management
O2 - 1 L/I nasal kanul
IVFD D5% 5 gtt/I micro
Spironolakton 2x25 mg
Diet pediasure milk + Diet 1995 kkal + 32 g protein

Planning
USG Doppler of kidney and bladder
Electrolit correction result
Ca/Na/K/Cl = 7.7/121/1.8/93 mEq/L
Full blood count result
Hb/Ht/RBC/WBC/Plt = 6.7/18.9/2.31x106/9.5x103/431x103
Water Balance
Input : Diet = 600 cc
IVFD = 150 cc
Total = 750 cc

Output : OUP = 600 cc B = I - O

BAB = 0
= -40cc
IWL = 190 cc K6JB = HS + BC
Total = 790 cc
= 335 cc
th
August, 16 2014
S limp (+), nausea and vomit (-),Fever (-)
O Alert : Compos Mentis , Temp: 37 oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-)
Dyspnoe (-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.
HR: 110 bpm, reguler; murmur (-)
RR: 26 x/i, regular, rales (-)
Abdomen
Soupel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 110 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
130/90 mmhg
Genital
Male; within normal limit.
A Chronic Kidney Disease Stage IV
P Management
O2 - 1 L/I nasal kanul
IVFD D5% 5 gtt/I micro
Spironolakton 2x25 mg
Diet 1995 kkal + 32 g protein
Planning
USG Doppler of kidney and bladder
Tranfussion PRC 3 cc/kgbb in 24 hours
Water Balance

Input : Diet = 100 cc

IVFD = 0 cc
Total = 100 cc

S
O

A
P

S
O

Output : OUP = 300 cc

B=I-O
BAB = 0
= 400 cc
IWL = 200 cc K6JB = HS + BC
Total = 500 cc
= 875 cc
th
August, 17 2014
limp (+), nausea and vomit (-),Fever (-)
Alert : Compos Mentis , Temp: 37 oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-)
Dyspnoe (-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.
HR: 110 bpm, reguler; murmur (-)
RR: 20 x/i, regular, rales (-)
Abdomen
Soupel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 110 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
120/80 mmhg
Genital
Male; within normal limit.
Chronic Kidney Disease Stage IV
Management
IVFD D5% 5 gtt/I
Spironolakton 2x25 mg
Diet 1995 kkal + 32 g protein
Planning
USG Doppler of kidney and bladder
Tranfussion PRC 3 cc/kgbb in 24 hours
August, 18th 2014
limp (+), nausea and vomit (-),Fever (-)
Alert : Compos Mentis , Temp: 37 oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-)
Dyspnoe (-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.
HR: 110 bpm, reguler; murmur (-)

RR: 26 x/i, regular, rales (-)

Abdomen
Soupel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 110 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
120/80 mmhg
Genital
Male; within normal limit.
A Chronic Kidney Disease Stage IV
P Management
IVFD D5% 5 gtt/I mikro
Spironolakton 2x25 mg
Diet 1995 kkal + 32 g protein
Planning
USG Doppler of kidney and bladder
Tranfussion PRC 3 cc/kgbb in 24 hours
Repeat electrolit and AGDA
Water Balance
Input : Diet = 900 cc
Output : OUP = 70 cc
B=I-O
IVFD = 300 cc
BAB = 200 cc
= 200 cc
Total = 1200 cc
IWL = 100 cc K6JB = HS + BC
Total = 1.000 cc
= 475 + 200 cc
= 675 cc
Dipstik
Uro/Bil/Ket/Blo/Pro/Nit/Leu/Glu/SG/pH
-/+1/-/-/+2/+3/-/-/1.010/7.0
August, 19th 2014
S limp (+), nausea and vomit (-),Fever (-)
O Alert : Compos Mentis , Temp: 36,8 oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-)
Dyspnoe (-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.
HR: 120 bpm, reguler; murmur (-)
RR: 20 x/i, regular, rales (-)
Abdomen
Soupel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 120 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
120/80 mmhg
Genital
Male; within normal limit.

A Chronic Kidney Disease Stage IV

P Management
IVFD D5% 5 gtt/I
Spironolakton 2x25 mg
Diet 1900 kkal + 32 g protein
Planning
Tranfussion PRC 3 cc/kgbb in 24 hours
Water Balance
Input : Diet = 1300 cc
Output : OUP = 400 cc B = I - O
IVFD = 50 cc
BAB = 0
= - 250 cc
Total = 350 cc
IWL = 200 cc K6JB = HS + BC
Total = 600 cc
= 725 cc
August, 20th 2014
S limp (+), nausea and vomit (-),Fever (-)
O Alert : Compos Mentis , Temp: 37.5,8 oC. Anemic (+). Icteric (-). Edema (-). Cyanosis (-)
Dyspnoe (-)
Body weight: 40 kg, Body length: 165 cm
Head
Right Eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+).
Left eye: Pupil diameter 3 mm. Inferior palpebra conjunctiva pale (+).
Icteric sclera (-). Light reflex (+)..
Neck
Lymph node enlargement (-)
Thorax
Simetris fusiformis. Retraction (-) epigastrial; intercostals, suprasternal.
HR: 100 bpm, reguler; murmur (-)
RR: 20 x/i, regular, rales (-)
Abdomen
Soupel, Rapid turgor.
normoperistaltic. Liver, spleen and renal
unpalpable.
Extremities Pulse 100 x/i, regular, adequate p/v, warm, CRT < 3. Blood Pressure
120/80 mmhg
Genital
Male; within normal limit.
A Chronic Kidney Disease Stage IV
P Management
IVFD D5% 5 gtt/I
Spironolakton 2x25 mg
Diet 1900 kkal + 32 g protein
Water Balance
Input : Diet = 900 cc
Output : OUP = 70 cc
B=I-O
IVFD = 300 cc
BAB = 200 cc
= 200 cc
Total = 1200 cc
IWL = 100 cc K6JB = HS + BC
Total = 1.000 cc
= 475 + 200 cc
= 675 cc
Dipstik

Uro/Bil/Ket/Blo/Pro/Nit/Leu/Glu/SG/pH
-/+/-/-/+/-/+/-/1.005/6.5

Discussion
Chronic kidney disease, is a slow progressive decline of kidney function. Its usually a
result of a complication from another serious medical condition. Unlike acute renal failure,
which happens quickly and suddenly, chronic kidney disease happens gradually over period of
weeks, months, or years as the kidney slowly stop working, leading to end-stage renal disease
(ESRD).
The kidneys play three mayor roles :
Removing waste product from the body, keeping toxin from building up in the
bloodstream
Producing hormones that control other body functions, such as regulating blood
pressure producting red blood cells
Regulating the levels of the minerals or electrolytes (e.g., sodium, calcium, and
potassium) and fluid in the body
The most common causes of chronic kidney disease in North America are diabetes
mellitus (type 1 or type 2 diabetes ) and high blood pressure. The most common cause of end
stage renal failure worldwide is IgA nephropathy (an inflammatory disease of kidneys).
Other common causes of chronic renal failure include :
Recurring pyelonephritis (kidney infection)
Polycystic kidney disease (multiple cysts in the kidneys)
Autoimmune disorders such as systemic lupus erythemastosus
Hardening of the arteries, which can damage blood vessels in the kidneys
Urinary tract blockages and reflux, due to frequent infections, stones, or an
anatomical abnormality that happened at birth
Excessive use of medications that are metabolized through the kidney
Chronic kidney disease can be present for many years before you notice any symptoms.
Patients with chronic kidney disease (CKD) stage 1-3 (glomerular fiktration rate >30
mL/min/1.73 m2) are frequently asymptomatic ; in termsof possible negative symptoms related
simply to the loss of glomerular filtration rate (GFR), they do not experience clinically evident
disturbances in water or electrolyte balance or endocrine/metabolic derangements.

Generally, these disturbances become clinically manifest with CKD stages 4-5 (GFR < 30
mL/min/1.73 m2 ). Patients with tubulointerstitial disease, cystic diseases, nephrotic syndrome,
and other conditions associated with positive symptoms (eg, polyuria, hematuria, edema) are
more likely to develop sign of disease at earlier stages. In patients we found GFR 23,24
mL/min/1.73 m2. It shows chronic kidney disease stage 4.

0.70 x 160 cm
4.97mg/dL

= 23.24 mmL/min/1.73 m2
Anemia, which in CKD develops primary as a result of decreased renal synthesis of
erythropoietin, manifests as fatigue, reduced exercise capacity, impaired cognitive and immune
function, and reduced quality of life. Anemia is also associated with the development of
cardiovascular disease, the new onset of heart failure, the development of more severe heart
failure, and increased cardiovascular mortality. In patients we found of laboratorium result with
Hb 7.20 g%. It shows anemia.
Typical physical findings in persons with uremia are those associated with fluid retention,
anemia, and acidemia. Severe malnutrition can contribute to muscle wasting, while electrolyte
abnormalities may cause muscle cramping, cardiac arrhythmias, and mental status changes.
Other manifestations of uremia in end stage renal disease (ESRD), many of which are more
likely in patients who are inadequately dialyzed, include the following :
Pericarditis : can be complicated by cardiac tamponade, possibly resulting in death
Encephalopathy : can progress to coma and death
Peripheral neuropathy
Restless leg syndrome
Gastrointestinal symptoms : Anorexia, nausea, vomiting, diarrhea
Skin manifestation : Dry skin, pruritus, ecchymosis
Fatigue, increased somnolence, failure to thrive
Malnutrition
Erectile disfunction, decreased libido, amenorrhea

Platelet disfunction with tendency to bleed

Treat these pathologic manifestations of chronic kidney disease (CKD) as follows :
Anemia : When the hemoglobin level is below 10 g/dL, treat wit erithropoiesi-simulating
agents (ESAs) such as epoetin alfa or darbepoetin alfa
Hyperphosphatemia : Treat with dietary phosphate binders and dietary phosphate restriction
Volume overload : Treat with loop diuretic or ultrafiltration
Metabolic acidosis : Treat with oral alkali supplementation
Uremic manifestation : Treat wih long term renal replacement therapy (hemodialysis,
peritoneal dialysis, or renal transplantation)
Cardivascular complication : Treat as appropriate
Growth failure in children : Treat with growth hormone
Correction Hiponatremia
fast Correction = (120-98) x 40 x 0.6 = 501.6 mEq (finished in 6 hours. With NaCl 3% =
501.6/513 =977cc = 160 gtt/I micro
Slow correction = (135-125) x 40 x 0.6 = 240 mEq/L
Maintanance = 2 -4 mEq/L = 80 160 mEq/L
Total = 320 400 mEq
With IVFD D5% NaCl 0.9% = 320/154 x 1000 = 2077 cc 155 gtt/I micro, finished in
18 hours
Correction Hipokalemia 30 mEq in 90 cc D5%, finish in 3 hours = 40 gtt/I mikro
1.7 mEq/L with 0.75 mEq/kgBB, 30 mEq KCl in 90 cc D5%, finished in 3 hours = 40 gtt/I
micro
Hyponatremia is decrease in serum Na concentration < 136 mEq/L caused by an excess of
water relative to solute. Common causes include diuretic use, diarrhea, heart failure, and renal
disease. Clinical manifestation are primarily neurologic (due to an osmotic shift of water into
brain cells causing edema), especially in acute hyponatremia, and include headache, confusion,
and stupor, seizures and coma may occur. Symptoms of hyponatremia include nausea and
vomiting, headache, short-term memory loss, confusion, lethargy, loss of appetite, restlessness
and irritability, muscle weakness, spasms or crumps, seizure, and decreased consciousness or
coma. Diagnosis is by measuring serum Na. Serum and urine electrolytes and osmolality help
determine the cause. Treatment involves restricting water intake and promoting its loss, replacing
any Na deficit, and correcting the underlying cause.

Principal Causes of Hyponatremia

Mechanism
Hypovolemic
hyponatremia
Decreased TBW

Category

Examples

GI losses*

Diarrhea

and Na, with a

Vomiting

relatively greater
decrease in Na
3rd-space losses*

Burns
Pancreatitis
Peritonitis
Rhabdomyolysis

Renal losses

Small-bowel obstruction
Diuretics
Mineralocorticoid deficiency
Osmotic diuresis (glucose,
urea, mannitol )
Salt-losing nephropathies (eg,
interstitial nephritis,
medullary cystic disease,
partial urinary tract
obstruction, polycystic
kidney disease)

Euvolemic
hyponatremia
Increased TBW

Drugs

Diuretics, barbiturates,

with near-normal

carbamazepine ,

total body Na

chlorpropamide , clofibrate ,
opioids, tolbutamide ,
vincristine
Possibly cyclophosphamide ,
Disorders

NSAIDs, oxytocin
Adrenal insufficiency as in
Addison disease
Hypothyroidism
Syndrome of inappropriate

Increased intake of

ADH secretion
Primary polydipsia

fluids
States that increase

Emotional stress

nonosmotic release

Pain

of ADH

Postoperative states

Extrarenal disorders

Cirrhosis

Hypervolemic
hyponatremia
Increased
total
body Na with a

Heart failure

relatively greater
increase in TBW
Renal disorders

Acute kidney dysfunction

Chronic kidney disease

Nephrotic syndrome
*GI and 3rd-space losses cause hyponatremia if replacement fluids
are hypotonic compared with losses.
TBW = total body water.

In patients, natrium concentration is 98 mEq/L. It is severe hyponatremia (serum Na < 109

mEq/L). Treatment is more controversial when neurologic symptoms (eg, confusion, lethargy,
seizure, coma) are present. The debate primary concern the pace and degree of hyponatremia
correction. Hypertonic (3%) saline (containing 513 mEq Na/L) may be used, but only with
frequent (q 2 to 4 h) electrolyte determination. For patients with seizures or coma, 100 mL/h
may be administrated over 4 to 6 h in amounts sufficient to raise the serum Na 4 to 6 mEq/L.
This amount (in mEq) may be calculated using the Na deficit formula as
(Desired Change in Na) x TBW , where TBW is 0.6 x body weight in kg in men and 0.5 x
body weight in kg in women.

Hiponatremia correction in patients :

Fast Correction = (120-98) x 40 x 0.6 = 501.6 mEq (finished in 6 hours. With NaCl 3% =
501.6/513 =977cc = 160 gtt/I micro
Slow correction = (135-125) x 40 x 0.6 = 240 mEq/L
Maintanance = 2 -4 mEq/L = 80 160 mEq/L
Total = 320 400 mEq
With IVFD D5% NaCl 0.9% = 320/154 x 1000 = 2077 cc 155 gtt/I micro, finished in
18 hours
Kalium concentration in patient is 1.7 mEq/L. The normal potassium level is 3.5-5.0
mEq/L. Low potassium is defined as a potassium level below 3.5 mEq/L. Low potassium levels
(hypokalemia), can cause weakness as cellular processes are impaired. Low potassium can occur

for many reasons. Use of water pills (diuretics), diarrhea, and chronic laxative abuse are the most
common causes of flow potassium levels .14
Other causes of hypokalemia include : 14
Kidney losses
Certain kidney disorder such as renal tubular acidosis (for example, chronic kidney failure and
acute kidney disease)
Magnesium deficiency
Leukemia
Cushings disease (and other adrenal disorder)
Loss of potassium through stomach and intestines
Vomiting
Enemas or excessive laxative use
Diarrhea
After ileostomy operation
Effect of medicine
Water pills (diuretics)
Medicined used for asthma or emphysema (beta-adrenergic agonist type of drugs such as
bronchodilators, steroids, or theophylline)
Aminoglycosides ( a type of antibiotic used for treating certain serious infections)
Shifting of potassium into and out of cells can lower the concentration of potassium
measured in the blood
Use of insulin
Certain metabolic states (such as alkalosis)
Decreased food intake or malnutrition
Anorexia
Bulimia
Bariatric surgery
Alcoholism
Hypocalemia correction:
< 2.5 mEq/L : 0.75 mEq/kg body weight with ratio D5% 1 : 3 and finished in 3 h.
2.5 3 mEq/ L : 0.5 mEq /kg body weight with ratio D5% 1 : 3, and finished in 2 h.
3.5 mEq/L : 0.25 mEq/kg body weight with ratio D5% 1 : 3, and finished in 1 h.
In patients potassium concentration is 1.7 mEq/L with calculated potassium correction :
1.7 mEq/L with 0.75 mEq/kgBB, 30 mEq KCl in 90 cc D5%, finished in 3 hours = 40 gtt/I micro

Conclusions
A boy age 15 years suffering from stage chronic kidney disease stage 4 with GFR 23.24
mL/min/1.73 m2.

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