BAB I

PENDAHULUAN

Chronic kidney disease (CKD) is a common condition in which there is a loss of kidney function
over time. It is associated with an increased risk of cardiovascular disease and chronic renal failure.
Kidney disease is the ninth leading cause of death in the United State. It was historically termedis a
term that encompasses all degrees of decreased renal function, from damagedat risk through mild,
moderate, and severe chronic kidney failure. CKD is a worldwide public health problem. In the United
States, there is a rising incidence and prevalence of kidney failure, with poor outcomes and high cost.
The Kidney Disease Outcomes Quality Initiative (KDOQI) defines CKD as either kidney damage
or a decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for 3 or more months.
Whatever the underlying etiology, once the loss of nephrons and reduction of functional renal mass
reaches a certain point, the remaining nephrons begin a process of irreversible sclerosis that leads to a
progressive decline in the GFR.
 BAB II
DASAR TEORI

1. DEFINITION
The Kidney Disease Outcomes Quality Initiative (KDOQI) defines CKD as either kidney
damage or a decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for 3 or more
months. Whatever the underlying etiology, once the loss of nephrons and reduction of functional renal
mass reaches a certain point, the remaining nephrons begin a process of irreversible sclerosis that
leads to a progressive decline in the GFR.

2. PATHOPHYSIOLOGY
A normal kidney contains approximately 1 million nephrons, each of which contributes to the
total glomerular filtration rate (GFR). In the face of renal injury (regardless of the etiology), the
kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, as the
remaining healthy nephrons manifest hyperfiltration and compensatory hypertrophy. This nephron
adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances
such as urea and creatinine start to show measurable increases only after total GFR has decreased to
50%.
The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons
noted, has been hypothesized to represent a major cause of progressive renal dysfunction. The
increased glomerular capillary pressure may damage the capillaries, leading initially to secondary
focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. This
hypothesis is supported by studies of five-sixths nephrectomized rats, which develop lesions identical
to those observed in humans with chronic kidney disease (CKD)
Haker et al found a strong association between episodes of acute kidney injury (AKI) and
cumulative risk for the development of advanced CKD in multiple hospitalized patients with diabetes
mellitus.[7] Any AKI versus no AKI was a risk factor for stage 4 CKD, and each additional AKI
episode doubled that risk.[7]
Findings from the Atherosclerosis Risk in Communities (ARIC) Study, a prospective
observational cohort, suggest that inflammation and hemostasis are antecedent pathways for CKD.
[8] This study used data from 1787 cases of CKD that developed between 1987 and 2004.
3. HISTORY
Patients with chronic kidney disease (CKD) stages 1-3 (glomerular filtration rate [GFR] >30
mL/min/1.73 m) are frequently asymptomatic; in terms of possible negative symptoms related
simply to the loss of glomerular filtration rate (GFR).
Generally, these disturbances become clinically manifest with CKD stages 4-5 (GFR < 30
mL/min/1.73 m). Patients conditions associated with positive symptoms (eg, polyuria, hematuria,
edema) are more likely to develop signs of disease at earlier stages. Uremic manifestations in patients
with CKD stage 5 are believed to be primarily secondary to an accumulation of multiple toxins, the
full spectrum and identity of which is generally not known. Metabolic acidosis in stage 5 may
manifest as protein-energy malnutrition, loss of lean body mass, and muscle weakness. Altered salt
and water handling by the kidney in CKD can cause peripheral edema and, not uncommonly,
pulmonary edema and hypertension.
Anemia, which in CKD develops primarily 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. 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 manifestations: Dry skin, pruritus, ecchymosis
Fatigue, increased somnolence, failure to thrive
Malnutrition
Erectile dysfunction, decreased libido, amenorrhea
Platelet dysfunction with tendency to bleed

4. PHYSICAL EXAMINATION AND APPROACH CONSIDERATION

A careful physical examination is imperative. It may reveal findings characteristic of the
condition that is underlying chronic kidney disease (CKD). However, the lack of findings on physical
examination does not exclude kidney disease. In fact, CKD is frequently clinically silent, so screening
of patients without signs or symptoms at routine health visits is important.
a. Screening for depression
Forty-five percent of adult patients with CKD have depressive symptoms may emphasize
somatic symptoms - specifically, sleep disturbance, fatigue, and anorexia - that can coexist with
chronic disease symptoms.
b. Laboratory
Testing in patients with chronic kidney disease (CKD) typically includes a complete
blood count (CBC), basic metabolic panel, and urinalysis, with calculation of renal function.
Normochromic normocytic anemia is commonly seen in CKD. Other underlying causes
of anemia should be ruled out.
The blood urea nitrogen (BUN) and serum creatinine levels will be elevated in patients
with CKD.
Hyperkalemia or low bicarbonate levels may be present.
patients may have hypoalbuminemia as a result of urinary protein loss or malnutrition.
A lipid profile should be performed in all patients with CKD because of their risk of
cardiovascular disease.
Serum phosphate, 25-hydroxyvitamin D, alkaline phosphatase, and intact parathyroid
hormone (PTH) levels are obtained to look for evidence of renal bone disease..
serum cystatin-C levels is gaining a greater role in the estimation of kidney function.
[37] Cystatin-C is a small protein that is expressed in all nucleated cells, produced at a
constant rate, and freely filtered by the glomerulus; it is not secreted but is instead
reabsorbed by tubular epithelial cells and catabolized, so it does not return to the
bloodstream. These properties make it a valuable endogenous marker of renal function.
[38]
c. Urinalysis
In adult patients who are not at elevated risk for chronic kidney disease (CKD), screening
with total protein can be done with a standard urine dipstick, according to guidelines from the
National Kidney Foundations Kidney Disease Outcomes Quality Initiative (KDOQI). If the
dipstick test is positive (1+ or greater), patients should undergo testing for confirmation of
proteinuria.[39] In children, teenagers, and young adults in particular, a first morning urine
specimen is preferable to a random specimen, as so-called orthostatic proteinuria (considered
benign) can be excluded.
Although 24-hour urine collection for total protein and creatinine clearance (CrCl) can be
performed, spot urine collection for total proteinto-creatinine (P/C) ratio allows reliable
 approximation (extrapolation) of total 24-hour urinary protein excretion. Patients with a P/C ratio
above 200 mg/mg should undergo a full diagnostic evaluation.[39] A value of greater than 300-
350 mg/mg is within the nephrotic range. However, a total P/C ratio is acceptable if the albumin-
to-creatinine ratio is high (>500 to 1000 mg/g).[39]
For screening patients at elevated risk, the KDOQI recommends using an albumin-
specific dipstick; this is because albuminuria is a more sensitive marker than total protein for
CKD from diabetes, hypertension, and glomerular diseases. A positive dipstick test should be
followed by calculation of the albumin-to-creatinine ratio, with a ratio greater than 30 mg/mg
followed by a full diagnostic evaluation.[39]
The urine sediment finding of red blood cells (RBCs) and RBC casts suggests
proliferative glomerulonephritis. Pyuria and/or white blood cell casts suggest interstitial nephritis
(particularly if eosinophiluria is present) or urinary tract infection.
d. Renal Function Formulas
The Cockcroft-Gault formula for estimating creatinine clearance (CrCl) should be used
routinely as a simple means to provide a reliable approximation of residual renal function in all
patients with chronic kidney disease (CKD). The formulas are as follows:
CrCl (male) = ([140-age] weight in kg)/(serum creatinine 72)
CrCl (female) = CrCl (male) 0.85

e. Imaging
Ultrasonography
Renal ultrasonography is useful to screen for hydronephrosis, which may not be
observed in early obstruction, or involvement of the retroperitoneum with fibrosis, tumor, or
diffuse adenopathy. Small, echogenic kidneys are observed in advanced renal failure.
 Retrograde pyelogram
May be indicated if a high index of clinical suspicion for obstruction exists despite a
negative finding on renal ultrasonography. Intravenous pyelography is not commonly
performed, because of the potential for renal toxicity from the intravenous contrast; however,
this procedure is often used to diagnose renal stones.
Computed tomography (CT) scanning
Can better define renal masses and cysts usually noted on ultrasonography. Also, CT
scanning is the most sensitive test for identifying renal stones. Intravenous (IV) contrast
enhanced CT scans should be avoided in patients with renal impairment to avoid acute renal
failure; this risk significantly increases in patients with moderate to severe CKD. Dehydration
also markedly increases this risk.
Magnetic resonance imaging (MRI)
Very useful in patients who would otherwise undergo a CT scan but who cannot
receive IV contrast. Magnetic resonance angiography (MRA) is becoming more useful for the
diagnosis of renal artery stenosis, although renal arteriography remains the criterion standard.
However, MRI contrast is problematic in patients with existing chronic kidney disease (CKD)
because they have a low, but potentially fatal, risk of developing nephrogenic systemic
fibrosis.
Renal radionuclide scan
Can be used to screen for renal artery stenosis when performed with captopril
administration; it also quantitates differential renal contribution to total glomerular filtration
rate (GFR). However, radionuclide scans are unreliable in patients with a GFR of less than 30
mL/min/1.73 m.
Renal Biopsy
This procedure is generally indicated when renal impairment and/or proteinuria
approaching the nephrotic range are present and the diagnosis is unclear after an appropriate
workup. Biopsies are also indicated to guide management in already-diagnosed conditions,
such as lupus, in which the prognosis is highly dependent on the degree of kidney
involvement. Biopsy is not usually indicated when renal ultrasonography reveals small,
echogenic kidneys on ultrasonography, because this finding represents severe scarring and
chronic, irreversible injury.
The most common complication of this procedure is bleeding, which can be life-
threatening in a minority of cases. Surgical open renal biopsy can be considered when the risk
 of renal bleeding is felt to be great, occasionally with solitary kidneys, or when percutaneous
biopsy is technically difficult to perform. Renal histology in chronic kidney disease (CKD)
reveals findings compatible with the underlying primary renal diagnosis. In some cases, a
biopsy may show nonspecific changes, with the exact diagnosis remaining in doubt.
5. TREATMENT
Early diagnosis and treatment of the underlying cause and/or the institution of secondary
preventive measures are imperative in patients with chronic kidney disease (CKD). Early referral to a
nephrologist is of extreme importance. The medical care of patients with CKD should focus on the
following:
1. Delaying or halting the progression of CKD
Aggressive blood pressure control to target values per current guidelines
The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure (JNC VII) and the National Kidney Foundations Kidney Disease
Outcomes Quality Initiative (KDOQI) suggest a target blood pressure of less than 130/80 mm
Hg.

Treatment of hyperlipidemia to target levels per current guidelines

Aggressive glycemic control per the American Diabetes Association (ADA)
recommendations (target hemoglobin A1c [HbA1C] < 7%)
Avoidance of nephrotoxins, including intravenous (IV) radiocontrast media, nonsteroidal
anti-inflammatory agents (NSAIDs), and aminoglycosides
Use of renin-angiotensin system (RAS) blockers among patients with diabetic kidney disease
(DKD) and proteinuria
 Use of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin-receptor
blockers (ARBs) in patients with proteinuria
2. Treating the pathologic manifestations of CKD
Anemia: With erythropoietin treatment, the goal is a hemoglobin level of 10-12 g/dL,
as normalization of hemoglobin in patients with CKD stages 4-5 has been associated
with an increased risk of adverse outcomes
Hypocalcemia: Treat with calcium supplements with or without calcitriol
Hyperparathyroidism: Treat with calcitriol, vitamin D analogues, or calcimimetics
Volume overload: Treat with loop diuretics or ultrafiltration
Metabolic acidosis: Treat with oral alkali supplementation . Experts recommend alkali therapy
to maintain the serum bicarbonate concentration above 22 mEq/L
Uremic manifestations: Treat with long-term renal replacement therapy (hemodialysis,
peritoneal dialysis, or renal transplantation)
Cardiovascular complications: Treat as appropriate
3. Timely planning for long-term renal replacement therapy . Indications for renal replacement
therapy in patients with chronic kidney disease (CKD) include the following:
Severe metabolic acidosis
Hyperkalemia
Pericarditis
Encephalopathy
Intractable volume overload
Failure to thrive and malnutrition
Peripheral neuropathy
Intractable gastrointestinal symptoms
Consider the following:
Early patient education regarding natural disease progression, different dialytic
modalities, renal transplantation, and option to refuse or discontinue chronic dialysis
Timely placement of permanent vascular access (arrange for surgical creation of
primary arteriovenous fistula, if possible, and preferably at least 6 mo in advance of
the anticipated date of dialysis for patients in whom transplantation is not imminent)
Timely elective peritoneal dialysis catheter insertion
Timely referral for renal transplantation
 4. Patients with CKD acutely presenting with indications for dialytic therapy should be
transferred to a hospital center where acute dialysis can be performed.

CALCIUM SALTS binding of phosphate, typically with calcium, to reduce

Calcium acetate hyperphosphatemia

Calcium carbonate
VITAMIN D ANALOGUES recommended in patients with CKD stages 3-5 who are not
Calcitriol on dialysis and in whom the serum parathyroid hormone
Doxercalciferol (PTH) level is elevated or has been persistently rising.
Paricalcitol Vitamin D increases the absorption of calcium in the
intestines and helps to prevent secretion of calcium in the
kidneys. By increasing calcium levels in serum, it helps to
decrease phosphate and PTH levels, as well as bone
resorption
IRON SALTS Iron salts are nutritionally essential inorganic substances
Ferrous sulfate used to treat anemia.
Iron dextran complex
Iron sucrose

6. DIET
a. Protein restriction
Protein restriction early in chronic kidney disease (CKD) as a means to delay a
decline in the glomerular filtration rate (GFR) is controversial; however, as the patient
approaches CKD stage 5, this strategy is recommended in adults (but not in children) to
delay the onset of uremic symptoms.
b. Salt restriction
Reduction in salt intake may slow the progression of diabetic CKD, at least in part by
lowering blood pressure. The dietary sodium recommendation for the general population in
public health guidelines is less than 5-6 g daily.

7. PROGNOSIS
 Patients with chronic kidney disease (CKD) generally experience progressive loss of kidney
function and are at risk for end-stage renal disease (ESRD). The rate of progression depends on age,
the underlying diagnosis, the success of implementation of secondary preventive measures, and the
individual patient. Timely initiation of chronic renal replacement therapy is imperative to prevent the
uremic complications of CKD that can lead to significant morbidity and death.
Hospitalization
Unadjusted rates of hospitalization in the CKD population, reflecting its total disease burden, are
3-5 times higher than those of patients without CKD.[25]
Dialysis
In the United States, hemodialysis and peritoneal dialysis patients average 2 hospital admissions
per year; patients who have a renal transplant average 1 hospital admission per year. Additionally,
patients with ESRD who undergo renal transplantation survive longer than those on long-term
dialysis.[27]
Hemodialysis performed 6 times per week significantly increased the risk of vascular access
complications compared with a conventional 3-day regimen in one study.[28, 29] Of 125 patients who
received hemodialysis 6 days per week, 48 experienced the composite primary endpoint event of
vascular repair, loss, or related hospitalization, compared with only 29 of the 120 patients undergoing
conventional treatment. Results indicated that overall risk for a first access event was 76% higher
with daily hemodialysis than with the conventional regimen.[28, 29]
Mortality
The mortality rates associated with CKD are striking. Mortality in patients with CKD in 2009
was 56% greater than that in patients without CKD.[25] For patients with stages 4-5 CKD, the
adjusted mortality rate is 76% greater.
The highest mortality rate is within the first 6 months of initiating dialysis. Mortality then tends to
improve over the next 6 months, before increasing gradually over the next 4 years. The 5-year
survival rate for a patient undergoing long-term dialysis in the United States is approximately 35%,
and approximately 25% in patients with diabetes.
The most common cause of sudden death in patients with ESRD is hyperkalemia, which often
follows missed dialysis or dietary indiscretion. The most common cause of death overall in the
dialysis population is cardiovascular disease; cardiovascular mortality is 10-20 times higher in
dialysis patients than in the general population.[31]
Sexual and reproductive issues
 Puberty is often delayed among males and females with significant CKD. Female patients with
advanced CKD commonly develop menstrual irregularities. Women with ESRD are typically
amenorrheic and infertile.
8. PATIENT EDUCATION
Patients with chronic kidney disease (CKD) should be educated about the following:
Importance of avoiding factors leading to increased progression
Natural disease progression
Prescribed medications (highlighting their potential benefits and adverse effects)
Avoidance of nephrotoxins
Diet
Renal replacement modalities, including peritoneal dialysis, hemodialysis, and
transplantation
Timely placement of vascular access for hemodialysis

BAB III
 LAPORAN KASUS

1. IDENTITAS PASIEN
a. Nama : Tn. R
b. Usia : 66 tahun
c. Jenis Kelamin : laki-laki
d. Agama : Islam
e. Alamat : Tunirejo 3/7
f. Pekerjaan : Petani
g. No. CM : 05.23.50
h. Ruang : ICU
i. Masuk : 13 September 2013
j. Keluar : 15 September 2013

2. RIWAYAT PENYAKIT
a. ANAMNESA
Keluhan Utama : sesak
Riwayat penyakit sekarang : pasien mengeluh sesak sejak 3 hari yang lalu.
Sebelumnya pasien mengeluh demam sejak 5 hari yang lalu. Keluarga pasien
menyebutkan bahwa sebelumnya pasien pergi ke Kalimantan 2 minggu yang lalu.
Sebelum dibawa ke rumah sakit, pasien muntah darah satu kali sebanyak
setengah gelas belimbing. Riwayat batuk lama (-).
Anamnesa sistematik
- Keadaan umum : sesak
- Kulit : ikterik (-), pucat (-)
- Kepala : mesosephal
- Mata : kabur (-)
- Telinga : discharge (-), kurang pendengaran (-)
- Hidung : sekret (-), nafas cuping hidung (-)
- Mulut : sianosis (-)
- Tenggorokan : nyeri dan sulit menelan (-), serak (-)
- Leher : simetris, pembesaran KGB (-)
- Thorax : dyspneu (+), batuk (-)
- Jantung : nyeri dada (+), palpitasi (+)
- Saluran cerna : mual (-), muntah (-), nyeri ulu hati (-),
- Muskuloskeletal : nyeri pinggang (-)
- Ekstremitas : oedem ekstremitas (+)
Riwayat penyakit dahulu : pasien tidak pernah sakit serupa
- Riwayat hipertensi (+) tidak terkontrol
- Riwayat asma (-)
- Riwayat diabetes mellitus (-)
- Riwayat TB (-)
- Riwayat merokok (+)
Riwayat penyakit keluarga : tidak ada keluarga yang sakit serupa
Riwayat social ekonomi : pasien menggunakan Jamkesmas sebagai biaya
pengobatan. Kesan : kurang

b. PEMERIKSAAN FISIK
 Keadaan umum : gelisah dan dyspneu
Kesadaran : Compos mentis
Status Gizi : baik
Vital Sign :
- TD : 157/95 mmHg
- HR : 107 x / menit
- RR : 34 x / menit
- T : 38,9 C
Pemeriksaan sistematik
- Kepala : mesosephal
- Mata : sklera ikterik (-), konjungtiva anemis (+/+)
- Telinga : discharge (-)
- Hidung : sekret (-), nafas cuping hidung (-)
- Mulut : sianosis (-)
- Tenggorokan : nyeri telan (-)
- Leher : simetris, pembesaran KGB (-)
- Ekstremitas : oedem ekstremitas superior (-) dan inferior (-)
Pemeriksaan Thorak
- Paru : suara dasar vesicular (+) N, suara tambahan (-)
- Jantung
- Inspeksi : ictus cordis tidak tampak
- Palpasi : Ictus cordis teraba di ICS VI linea mid clavicula
sinistra, thrill (-).
- Perkusi : pekak
- Batas atas : ICS II linea sternalis sinistra
- Pinggang jantung : ICS III linea parasternalis sinistra
- Batas kanan bawah : ICS VI linea parasternalis dextra
- Batas kiri bawah : ICS VII 2 cm lateral linea mid clavicula
sinistra
Pemeriksaan abdomen
- Inspeksi : datar, sikatrik (-), striae(-), caput medusa (-).
- Auskultasi : peristaltic (+) N
- Perkusi : tympani, shifting dullness (-), area troube(+) tympani
- Hepar : pekak (+), liver span dextra 11 cm, liver span sinistra 6
cm
- Palpasi
1. Superfisial : supel, massa (-)
2. dalam : nyeri tekan (-), hepar, lien dan ginjal tidak teraba

- Ekstremitas

Ekstremitas superior Inferior

Oedem -/- +/+
Akral dingin -/- -/-
Reflek fisiologis +/+ +/+
Ikterik -/- -/-

c. PEMERIKSAAN PENUNJANG
Laboratorium tanggal 13 september 2013
 Hb 7,9 g/dl
Ht 24 %
Leukocyte 1200
Platelet 67.000
SGOT 24
SGPT 22

EKG

tanggal 13 september 2013

3. ABNORMALITAS DATA

ANAMNESA PEMERIKSAAN FISIK PENUNJANG

- Dyspneu - Dyspneu dengan RR 32 - Laboratorium : Anemia
- Oedem ekstremitas kali per menit
inferior - Hipertensi

4. DAFTAR MASALAH
Chronic Kidney Failure

5. INITIAL PLAN

ASSESMENT Akut dan kronik

IP diagnosis - Laboratorium : Ht, factor koagulasi, BGA
- Radiologi : foto Thorax
- EKG
- ekokardiografi
IP terapi - Supply oksigen : target saturasi > 88 %
- Meningkatkan fungsi ventrikel kanan : diuretic, digitalis dan
walfarin
- Menurunkan vasokonstriksi paru : CCB, Beta selektif
agonis dan Theophyline
- Invasif : phlebotomy
IP monitoring Monitoring kadar O2 dan kondisi klinis
IP edukasi Menyampaikan bahwa pengobatan ini sangat penting dan vital.
 Menjelaskan prognosis.

6. FOLLOW UP

13/9/13 UGD 13/9/13 ICU 14/9/13 ICU 15/9/13 ICU

Kesadaran E4M6V5 E4M6V5 E4M6V5 E3M5V5
Keadaan Gelisah Gelisah Somnolen Somnolen
Umum Sesak Sesak Sesak
Tanda vital
TD 157/95 140/89 128/73 86/43
HR 107 120 112 119
RR 34 34 32 23
S 38,9 37 36,8 36
SpO2 100 100 100 86
Laborat
Hb 7,9
Leukosit 1200
Trombosit 67.000
Ht 24
SGOT 24
SGPT 22
Ureum 364 342
Creatinin 13,9 10,27
GDS 51 71 94
Natrium 118,6
Kalium 5,35
Kalsium 7,34
Magnesium 1,9
Clorida 88,9
Protein 6,8
Albumin 2,5
Globulin 4,3
diagnosa Febris 5 hari CKD gr V CKD gr V CKD gr V
dengan anemia CCT 4,5 Anemia Anemia
Ensefalopati Ensefalopati uremic
uremic
Terapi - O2 8-10 l/mt -Inf D5% 2 flash - RL 12 tpm Terapi lanjut
- RL 30 tts/mt -Bicnat drip 250 - Inj Cefotaxim
- Inj. Cefotaxim mg D5% plus 2x1 gr
2x1 gr 100 cc bicnat, 12 - Inj Furosemid
- Inj. Ranitidine tts/mnt 2x1
6x1A - Inj Ranitidine
- Inj vit K 3x1 6x1
- Paracetamol drip - Bicnat 3x50
1 gr - Asam folat 1x1
- Pasang NGT,
DC
- Usaha transfuse
PRC 2 kolf
 Tanggal 15/9/13

07.00 08.00 09.00 10.00 11.00 12.00 13.00 14.00 15.00 16.00 17.00 18.00 19.00
TD 86/43 101/ 92/57 91/47 77/51 103/ 63/21 93/52 100/ 80/27 60/23 60/40 127/52
51 57 45
HR 119 120 130 124 117 126 111 124 107 117 92 54 65

sp 86 98 80 90 100 94 96 100 100 87 100 98 76

O2
RR 23 26 22 36 28 29 26 20 27 23 16 22 23
s 36 55,8 36 36
ventil
ator

BAB IV
KESIMPULAN

In chronic kidney disease (CKD), doses and dosing intervals of drugs that are excreted or
metabolized renally should be adjusted according to the residual glomerular filtration rate (GFR). Some
drugs are contraindicated in moderate to severe renal impairment because of potentially serious effects
from drug or metabolite accumulation. Routine consultation of the appropriate references should be
undertaken when prescribing any new drug to a patient with CKD.
For patients undergoing dialysis, it is extremely important to carefully check dosing guides or
monitor levels when possible. These modalities differ in their clearance of drugs. Hospitalized patients
undergoing other types of continuous renal replacement therapy also require close monitoring. An
experienced clinical pharmacist can be invaluable in assisting to design individualized dosing regimens.
Treatments for the pathologic manifestations of CKD include the following:
Hyperphosphatemia: Dietary phosphate binders and dietary phosphate restriction
Hypocalcemia: Calcium supplements and possibly calcitriol
Hyperparathyroidism: Calcitriol or vitamin D analogues

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15 2011;305(23):2432-9. [Medline]. [Full Text].

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and their associations with albuminuria. Hum Mol Genet. Jul 15 2012;21(14):3293-
8. [Medline]. [Full Text].

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15. Su SL, Lu KC, Lin YF, Hsu YJ, Lee PY, Yang HY, et al. Gene polymorphisms of angiotensin-
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