1

PEMERIKSAAN

Prof.Dr.Prihatini dr SpPK(K)
LABORATORIUM KLINIK
PENYAKIT GINJAL

PRIHATINI
BAGIAN PATOLOGI KLINIK FKUWKS 2015-2016
BUKU ACUAN 2

Prof.Dr.Prihatini dr SpPK(K)
FISBACH A MANUAL OF LABORATORY DIAGNOSTIC TESTS
MCPHEE SJ.,LINGAPPA.VR.,PATHOPHYSIOLOGY OF
DISEASE
MARSHALL,WJ.,BANGERT,SK.,CLINICAL CHEMISTRY
SCHRIER,rw.,MANUAL OF NEPHROLOGY
AMES,URODYNAMICS
PENDAHULUAN 3

Prof.Dr.Prihatini dr SpPK(K)
GINJAL:
25 % CARDIAC OUTPUT GINJAL
NEFRON: KAPILER GLOMERULUS+ TUBULUS 1 JUTA
KAPSUL BOWMAN S: ARTERIOL AFFERENT & EFFERENT
TUBULUS RENALIS:TUBULUS PROKSIMAL BERBELIT 80 %
ELEKETROLIT & AIR KEMBALI,LOOP DARI HENLE, DISTAL
TUBULUS BERBELIT & DUKTUS PENGUMPUL
FUNGSI GINJAL 4
Urine formation

Prof.Dr.Prihatini dr SpPK(K)
Fluid & electrolyte balance
Regulation of acidbase balance
Excretion of the waste products of protein
metabolism
Excretion of drugs & toxins
Secretion of hormones:
1. Renin
2. Erythropoietin
3. 1,25-Dihydroxy vitamin D3
4. Prostaglandins
Hormon dihasilkan ginjal : 5

vitamin D (calcitriol or 1,25 dihydroxy-vitamin D):

Prof.Dr.Prihatini dr SpPK(K)
mengatur absorpsi Ca & P dari makanan,membentuk tulang agar
kuat

Erythropoietin (EPO), merangsanag sumsum tulang

menghasilkan eritrosit .

Renin, mengatur volume darah & tekanan darah

FISIOLOGI GINJAL 6

Prof.Dr.Prihatini dr SpPK(K)
GFR 120 mL/men
ssd filtrasi :Na+, K+,glucose diresorbsi tubulus
proksimalis
Air diresorbsi secara osmotik,
Sekresi ke tubulus :organik anion, kation;
kreatinin, histamine,obat & toksin
Normal:isotonik filtrat 30 mL/men => loop Henle
Pengendali resorbsi air: vasopressin(ADH)
Fixed acid ( as sulfat& fosfat)
FISIOLOGI GINJAL 7

Prof.Dr.Prihatini dr SpPK(K)
1. duktus pengumpul dikendalikan hormon
tubulus proksimalis fungsi & komposisi
cairan tubulus
2. duktus pengumpul,daerah akhir tubulus
renalis menyisakan 1-2 mL/men GFR
dikeluarkan ke ureter
FISIOLOGI GINJAL 8

Prof.Dr.Prihatini dr SpPK(K)
1. Mengatur tekanan darah
2. Mengatur metabolisme kalsium
3. Mengatur Erythropoiesis
4. Mengatur fungsi ginjal
Pengatur aliran darah &pengangkutan di 9
medulla renalis

Prof.Dr.Prihatini dr SpPK(K)
1. Medula vasodilator
2. Medula vasokonstruktor
3. Menghambat pengangkutan di cabang
medulla tebal
4. Mengembalikan tubuloglomerular
Medula vasodilator 10

Prof.Dr.Prihatini dr SpPK(K)
Nitric oxide
Prostaglandin E2
Adenosine
Dopamine
urodilatin
Medula vasokonstruktor 11

Prof.Dr.Prihatini dr SpPK(K)
Endothelin
Angiotensin II
vasopressin
Menghambat pengangkutan 12

di cabang medulla tebal

Prof.Dr.Prihatini dr SpPK(K)
Prostaglandin E2
Adenosine
Dopamine
Platelet activating factor
Cytochrome P450 dependent
arachidonate metabolites
 Penyebab utama penyakit ginjal 13

Prof.Dr.Prihatini dr SpPK(K)
Pre-renal:
Volumemenurun ss:GI, renal, keringat >,
perdarahan
Gagal jantung
Sirosis hepatis(HRS)
Hipotensi
Nonsteroid anti-inflamasi bilateral renal artery
stenosis
 Penyebab utama penyakit ginjal 14

Intrarenal disease

Prof.Dr.Prihatini dr SpPK(K)
Peny vaskuler:
akut;vaskulitis,hipertensi maligna, scleroderma,thromboembolic
disease
Kronik:nefrosklerosis
Peny.glomerulus:glomerulonephritis,sindrom nefrotik
Penytubulus: akut: ATN,MM,hiperkalsemia,UA nefropati;
kronik:PKD,MSK(medullary sponge kidney)
Peny intertisial:
Akut:pyelonephritis,interstitial nephritis(drug induced);
kronik:pyelonephritis,analgesic abuse
 Penyebab utama penyakit ginjal 15

Postrenal:

Prof.Dr.Prihatini dr SpPK(K)
Obstructive uropathy
Prostatic disease
Maligna
Calculi
Congenital abnormalities
 Pemeriksaan fungsi ginjal 16

(kimia klinik )

Prof.Dr.Prihatini dr SpPK(K)
GLOMERULAR FILTRATION RATE(GFR)
PLASMA KREATININ
PLASMA UREA
CYSTATIN C
GLOMERULAR FILTRATION 17

RATE(GFR)

Prof.Dr.Prihatini dr SpPK(K)
CLEARANCE = U x V mL /men
P
U= konsentrasi kreatinin (mol/L)
V= urine flow rate(mL/men atau L/24h)1.44)
P= konsentrasi plasma kreatinin (mol/L)
Normal= 120 mL/men
CC > GFR sesungguhnya
 Penafsiran CC/GFR 18
Normal 120 mL/men,1,73 m2

Prof.Dr.Prihatini dr SpPK(K)
MENINGKAT:
CO (cardiac output)
Hamil
Luka bakar
Keracunan CO
Meningkat CC kreatinin urine:
Gigantisme
Akromegali
DM
Hipotiroidisme
Penafsiran CC/GFR 19
MENURUN RENAL BLOOD FLOW

Prof.Dr.Prihatini dr SpPK(K)
Gangguan fungsi ginjal:peny ginjal intrinsik,
glomerulonephritis, pyelonephritis, sindrom
nefrotik,ATD,amyloidosis,nefritis interstitial
Renjatan,dehidrasi
COPD
Gagal jantung (Congestive heart failure)
 Penafsiran CC/GFR 20
MENURUN CC URINE

Prof.Dr.Prihatini dr SpPK(K)
HYPERTIROIDISM
Anemia
Muscular dystrophy
Polymyositis
Inflamatory muscle disease
Advance renal disease,renal stenosis
leukemia
 Faktor pengganggu CC urine 21

Prof.Dr.Prihatini dr SpPK(K)
Latihan : meningkat CC dan kreatinin urine
Hamil: CC
obat
CC perkiraan berlebihan pd gangguan ginjal berat
Diet daging berlebih
Proteinuria & gagal ginjal metode CC tak dpt dipercaya untuk
GFR
Estimated GFR 22

Prof.Dr.Prihatini dr SpPK(K)
eGFR = 186,3 x (sCr) -1,154
x umur -0,203

eGFR= estimate GFR berdasarkan

pemeriksaan creatinine clearance
sCr = kadar serum kreatinin (mol/L)
Umur= dalam tahun
Penyebab abn plasma urea thd 23
rasio kreatinin

Prof.Dr.Prihatini dr SpPK(K)
MENINGKAT MENURUN
Asupan protein tinggi Asupan protein rendah
Perdarahan GI Dialisis

Hyperkatabolik
Peny hati parah

Dehidrasi
Stasis urine
Pemborosan otot
amputasi
CYSTATIN C 24

Peptide dgn bm rendah dihasilkan sel berinti

Prof.Dr.Prihatini dr SpPK(K)
Tidak tdp di plasma sb di saring glomerulus
Indikator lebih peka dari kreatinine
Meningkat pd maligna & R/steroid
Tidak jelas peran dlm menilai gangguan ginjal
Penilaian gabungan glomerular

Prof.Dr.Prihatini dr SpPK(K)
25

Protein uria > 300 mg/L( dgn carik celup)

Mikroalbumin tak dpt ditemukan dgn carik celup
Haematuria: KERUSAKAN GLOMERULUS
SILINDER ERITROSIT : disfungsi glomerulus
 Awal klinik &laborat.dasar gej.nefrologi26
sindrom
Akut/gagal ginjal progresif
Akut nefritis
Gagal ginjal kronik
Sindrom nefrotik
Petanda penting diagnosis
Anuria,oligouria,GFR
Hematuria,silinder
eri,azotemia,oliguria,edema,h circulatory congestion
ipertensi
Azotemia>3 bl,gejala & tanda
uremia lama;gejala & tanda
renal osteodystrophy;ginjal
mengecil bilateral,silinder
broad
Proteinuria> 3,5 g/1,73m2 per
24 jam; hipoalbuminemia;
hyperlipidemia,lipiduria
Gejala umum tidak punya
nilai diagnostik
Prof.Dr.Prihatini dr SpPK(K)
Hipertensi,hematuria,protein
-uria,pyuria,silinder,edema
Proteinuria,pyuria,
hematuria,proteinuria,
,silinder,oliguria,polyuria;
nocturia,hipertensi,edema,ga
ngguan elketrolit
Silinder
edema
Patofisiologi sindrom nefrotik 27

Prof.Dr.Prihatini dr SpPK(K)
 Awal klinik &laborat.dasar gej.nefrologi 28

sindrom Petanda penting diagnosis Gejala umum tidak punya

Prof.Dr.Prihatini dr SpPK(K)
nilai diagnostik
Tanpa gejala urin abnormal Hematuria;proteinuria;steril
pyuria,silinder
ISK Bakteri 105 Hematuria,azotemia
koloni/mLpenyebab infeksi ringan,proteinuria
lain,pyuria,silinder ringan,demam
lekosit,frekuensi,darurat;
Buli-buli lunak,nyeri
pinggang
Gangguan renal tubulus Gangguan elektrolit, Hematuria,azotemia
polyuria, nokturia, ringan,proteinuria ringan,
lama;tanda &gejala renal
osteodystrophy,ginjal
membesara,gangguan
 Awal klinik &laborat.dasar gej.nefrologi 29
sindrom Petanda penting diagnosis Gejala umum tidak punya
nilai diagnostik

Prof.Dr.Prihatini dr SpPK(K)
hipertensi Sistolik/diastolic Proteinuria,silinder,
hipertensi azotemia

nefrolitiasis Riwayat batu Hematuria,pyuria,sering,

liwat/keluar,tampak di darurat
xray;kolik renal
Obtruksi saluran kemih Azotemia,oliguria,anuria, Hematuria,pyuria,dysuria,
Polyuria,nocturia,retensi enuresis
urine, pancaran urine
lambat,prostat>,ginjal>;ny
eri pinggang,buli-buli
penuh ssd kencing
30

Prof.Dr.Prihatini dr SpPK(K)
Gagal ginjal akut
Penyebab utama ARF/GGA 31

GANGGUAN CONTOH

Prof.Dr.Prihatini dr SpPK(K)
HIPOVOLEMIA Volume hilang melalui
GI,kulit,ginjal,perdarahan,skuestrasi
ESF(luka bakar,pankreatitis,peritonitis)
Gagal kardiovaskuler Kegagalan cardiac output
(MI,tamponade),vascular
pooling(anafilaksis,sepsis,obat)
Obstruksi ekstrarenal Oklusi uretral:
vesika,pelvik,prostat,retroperitoneal
neoplasma,kecelakaan
pembedahan,pengobatan,batu,pus
bekuan darah.
Obstruksi intrarenal Kristal(UA,axalic acid,sulfonamide,mtx)
 Penyebab utama ARF/GGA 32
GANGGUAN CONTOH

Prof.Dr.Prihatini dr SpPK(K)
Robek(rupture) buli-buli Trauma
Peny vaskuler Vaskulitis,maligna
HT,TTP,scleroderma,penyum-
batan arteri/vena
Glomerulonefritis Immune complex dis.,GBM
disease
Intertitial nephritis Drugs,hiperkalsemia,infeksi,idio
pati
Posischemic Hipovelemia& gagal
kardiovaskuler
 Penyebab utama ARF/GGA 33
GANGGUAN CONTOH

Prof.Dr.Prihatini dr SpPK(K)
Pigment induced hemolysis,(reaksi
transfuse,malaria),rhadomyolisis(trau
ma,koma,heat stroke,latihan
berat,kekurangan K &fosfat)
Rangsangan racun Antibiotik;bahan
kontras,anestesi,logam berat,bahan
organik,
Berkaitan kehamilan(pregnant related) Septic abortion,perdarahan
uterus,eklampsia
acute renal failure 34

Prof.Dr.Prihatini dr SpPK(K)
Most community acquired acute renal
failure (70%) is prerenal
Most hospital acquired acute renal failure
(60%) is due to ischemia or nephrotoxic
tubular epithelial injury (acute tubular
necrosis).
Mortality rate 50-70%
urine output ARF 35

Prof.Dr.Prihatini dr SpPK(K)
Oliguria
= daily urine output < 400 mL
When present in acute renal failure, associated with
a mortality rate of 75% (versus 25% mortality rate in
non-oliguric patients)
Mostdeaths are associated with the underlying disease
process and infectious complications
Anuria
No urine production
Uh-oh, probably time for dialysis
Most commom cause ARF 36

Prof.Dr.Prihatini dr SpPK(K)
Prerenal
Acute tubular necrosis (ATN)
Acute on chronic renal failure (usually due to ATN
or prerenal)
Obstructive uropathy
Glomerulonephritis/Vasculitis
Acute Interstitial nephritis
Atheroemboli
Assessing the patient with 37

acute renal failure

Prof.Dr.Prihatini dr SpPK(K)
History:
Cancer?

Recent Infections?
Blood in urine?
Change in urine output?
Flank Pain?
Recent bleeding?
Dehydration? Diarrhea? Nausea? Vomiting?
Blurred vision? Elevated BP at home? Elevated
Continued. 38

Prof.Dr.Prihatini dr SpPK(K)
Family History:
Cancers?
Polycystic kidney disease?

Meds:
Any non-compliance with diabetic or
hypertensive meds?
Any recent antibiotic use?
Any NSAID use?
 Physical examination ARF 39

Vital Signs:

Prof.Dr.Prihatini dr SpPK(K)
Elevated BP: Concern for malignant hypertension
Low BP: Concern for hypotension/hypoperfusion (acute tubular necrosis)
Neuro:
Confusion: hypercalcemia, uremia, malignant hypertension, infection,
malignancy
HEENT:
Dry mucus membranes: Concern for dehydration (pre-renal)
Abd:
Ascites: Concern for liver disease (hepatorenal syndrome), or nephrotic
syndrome
Ext:
Edema: Concern for nephrotic syndrome
Skin:
Tight skin, sclerodactyly Sclerodermal renal crisis
Malar rash - Lupus
Assessing the patient with acute renal 40
failure Laboratory analysis

Prof.Dr.Prihatini dr SpPK(K)
Fractional excretion of sodium:

(UrineNa+ x PlasmaCreatinine)
FENa= ______________________ x 100
(PlasmaNa+ x UrineCreatinine)

FENa < 1% Prerenal

FENa > 2% Epithelial tubular injury (acute tubular
necrosis), obstructive uropathy
If patient receiving diuretics, can check FE of urea.
 Urinalysis 41
Hematuria

Prof.Dr.Prihatini dr SpPK(K)
Non-glomerular:
Urinary sediment: intact red blood cells
Causes:
Infection
Cancer
Obstructive Uropathy
Rhabdomyolysis
myoglobinuria; Hematuria with no RBCs
Glomerular:
Urine sediment: dysmorphic red blood cells, red cell casts
Causes:
Glomerulonephritis
Vasculitis
Atheroembolic disease
TTP/HUS (thombotic microangiopathy)
Urinalysis cont 42

Protein

Prof.Dr.Prihatini dr SpPK(K)

Need microscopic urinalysis to see microabluminemia

Can check 24-hour urine protein collection
Nephrotic syndrome - 3.5 g protein in 24 hours
Albuminuria
Glomerulonephritis
Atheroembolic disease
(TTP/HUS) Thrombotic microangiopathy
Nephrotic syndrome
Tubular proteinuria
Tubular epithelial injury (acute tubular necrosis)
Interstitial nephritis
43

Prof.Dr.Prihatini dr SpPK(K)
Indication hemodialysis 44
Refractory fluid overload

Prof.Dr.Prihatini dr SpPK(K)
Hyperkalemia (plasma potassium concentration >6.5 meq/L)
or rapidly rising potassium levels
Metabolic acidosis (pH less than 7.1)
Azotemia (BUN greater than 80 to 100 mg/dL [29 to 36
mmol/L])
Signs of uremia, such as pericarditis, neuropathy, or an
otherwise unexplained decline in mental status
Severe dysnatremias (sodium concentration greater than
155 meq/L or less than 120 meq/L)
Hyperthermia
Overdose with a dialyzable drug/toxin
 45
PMH:

Prof.Dr.Prihatini dr SpPK(K)
Alzheimers Dementia
Osteoarthritis
Allergies: PCN
Meds:
Aricept
Ibuprofen prn
46

Prof.Dr.Prihatini dr SpPK(K)
Gagal ginjal
kronik
 47

Prof.Dr.Prihatini dr SpPK(K)
Patofisiologi GGK
 pankreatitis kolitis
trombositopat
i 48

Prof.Dr.Prihatini dr SpPK(K)
perikarditis Mekannisme tak
diketahui poliuria

koma
Anemia berat Fungsi keseimbangan air
ensefalopa
ti
Eritropoietin (-) asidosi
Retensi s
toksin Homeostasis gagal
Fungsi endokrin(-) endogenus
Gagal ginjal Kronik Retensi fosfat

hipertensi Gagal pengubah vit hipokalsium

D
Retensi
sodium hiperparatiroid
Edema paru
Resorpsi tulang
Edema perifer
Chronic renal failure 49
= a GFR of < 60 for 3 months or more.

Prof.Dr.Prihatini dr SpPK(K)
Most common causes:
Diabetes Mellitus
Hypertension
Management:
Blood pressure control!
Diabetic control!
Smoking cessation
Dietary protein restriction
Phosphorus lowering drugs/ Calcium replacement
Most patients have some degree of hyperparathyroidism
Erythropoietin replacement
Start when Hgb < 10 g/dL
Bicarbonate therapy for acidosis
Dialysis?
50

Prof.Dr.Prihatini dr SpPK(K)
 51

Prof.Dr.Prihatini dr SpPK(K)
Contoh kasus
PELAJARI DISKUSI DENGAN TEMAN
KELOMPOK BELAJAR
A 52-year-old man with a history of AIDS, hypertension,
52
diabetes mellitus, and alcohol abuse was found

Prof.Dr.Prihatini dr SpPK(K)
unconscious in his home by his roommate. In the
emergency department, he was hypotensive (103/60
mm Hg), febrile (temperature 101F), and unresponsive.
Computed tomography scan of the abdomen
showed cholecystitis and gallstones. Laboratory data
are listed.
 53
The patient was diagnosed with acute renal failure.

Prof.Dr.Prihatini dr SpPK(K)
He was administered intravenous fluids; BUN
fell to 68 mg/dL and creatinine fell to 2.2 mg/dL.
The patients blood culture report was positive for E.
coli. He was treated with tobramycin and cefepime.
The patient continued to deteriorate and died 5 days
after admission. Cause of death was multiorgan failure
secondary to AIDS, sepsis, and alcoholic cirrhosis.
Questions

1. What is the significance of the patients elevated 54

CK? Explain why the physician ordered a CK-MB

Prof.Dr.Prihatini dr SpPK(K)
and troponin level. What can you conclude about
the patients cardiac status?
2. What is the cause of his acute renal failure?
3. What is the significance of the patients large
urine hemoglobin?
 Questions
4. How would you interpret this patients liver 55
Function tests considering his clinical history?

Prof.Dr.Prihatini dr SpPK(K)
Drugs of Abuse Negative Urinalysis
Serum ethanol 84 mg/dL Hemoglobin Positive
WBC 4 HPF (04)
RBC 2 HPF (04)
CK 3,308 U/L (24204) BUN 71 mg/dL (821)
CK-MB 15 ng/mL (07.5) Creatinine 4.1 mg/dL (0.91.5)
Troponin T <0.01 ng/mL (00.4) Alkaline phosphatase 443 U/L (45122)
pH 7.50 Aspartate aminotransferase 305 U/L (945)
pCO2 27 mm Hg Alanine aminotransferase 78 U/L (863)
Total CO2 15 mmol/L Gamma glutamyl transpeptidase 724 U/L (1150)
Total bilirubin 2.7 mg/dL (0.21.0)
Direct bilirubin 2.4 mg/dL (00.2)
Laboratorium: 56

Prof.Dr.Prihatini dr SpPK(K)
WBC: 19.2 BUN: 32
Hgb.: 11 Cr.: 1.8
Hct: 32.8 Glucose: 79
Platelets: 202
Sodium: 132 Urine dipstick:
Protein: none
Potassium: 5.6
Ketones: trace
Chloride: 103
Blood: none
Bicarbonate: 18
Leuk est: none
Question 1 57

Prof.Dr.Prihatini dr SpPK(K)
What further information would be helpful in
evaluating this patient?
What are some possible diagnoses in this patient?
What further studies would you like to do?
What might you see in urinary sediment?
Question 1 58

Prof.Dr.Prihatini dr SpPK(K)
Urine sodium = 40 mg/dL
Urine creatinine = 140 mg/dL
Renalultrasound: no sign of
hydronephrosis
 59

Prof.Dr.Prihatini dr SpPK(K)
What kind of renal failure do you think this patient
has?
How would you treat this patient?
 60

Prof.Dr.Prihatini dr SpPK(K)
Gambaran sedimen
61

Prof.Dr.Prihatini dr SpPK(K)
62

Prof.Dr.Prihatini dr SpPK(K)
64

Prof.Dr.Prihatini dr SpPK(K)
68

Prof.Dr.Prihatini dr SpPK(K)
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Prof.Dr.Prihatini dr SpPK(K)
70

Prof.Dr.Prihatini dr SpPK(K)
71

Prof.Dr.Prihatini dr SpPK(K)
72

Prof.Dr.Prihatini dr SpPK(K)
73

Prof.Dr.Prihatini dr SpPK(K)
Soal 1 76

Prof.Dr.Prihatini dr SpPK(K)
Wanita 18 tahun sering kencing .nyeri kencing(dysuria)
selama 4 bulan
Apa yang anda tanyakan pada pqsien selqnjutnya ?
Macam iSK pada pasien ?
Pemeriksaan laboratorium yang dilakukan apa saja?
Bagaimana anda mengobati berapa lama ?
Soal 2 77

Prof.Dr.Prihatini dr SpPK(K)
Laki-laki
28 tahun pernah berhubungan
dengan PSK 1 minggu yang lalu .Setelah
kembali dirumah berasa panas kalau
kencing. Dan mengeluarkan secret kuning
di celananya Pemeriksaan mikroskopik
lekosit esterase 4 + dan dikerjakan cat
Gram .
78

Prof.Dr.Prihatini dr SpPK(K)
pengobatan 79

Prof.Dr.Prihatini dr SpPK(K)
Antibiotic pilihan dan lamanya ditentukan jenis
ISK
Penyebab terbesar untuk ISK adalah re E. Coli,
Staph. Saprophyticus, Proteus mirabilis,
Enterococci & Gram-negatives
Dont use moxifloxacin for UTI!
Penyaring Chlamydia dianjurkan pada semua
wanita usia 25 tahun dan infeksi tanpa gejala dan
beresiko PID /infertile cukup tinggi
80

Prof.Dr.Prihatini dr SpPK(K)
SELAMAT BELAJAR