dr.

Hertanti IL, SpA

Sub divisi Nefrologi IKA FK Unsri
 Gagalginjal akut (GGA) adalah suatu sindroma
yang ditandai dengan penurunan fungsi ginjal
yang mendadak dengan akibat terjadinya
penimbunan hasil metabolit senyawa nitrogen
seperti ureum dan kreatinin.
 ETIOLOGI
GGA pre renal GGA renal GGA paska renal

• Kehilangan darah: • Kerusakan epitel • Obstruksi

trauma, pendarahan tubulus: • Katup uretra
• Kehilangan air dan • Nekrosis tubular posterior,
elektrolit: akut (iskemik, • batu,
gastroenteritis akut nefrotoksik) • bekuan darah,
• Kehilangan plasma: • Kerusakan • tumor,
luka bakar, peritonitis glomerulus:
• kristal (asam
• Hipoalbuminemia • GNA, jengkol, asam urat)
berat pada sindroma • Penyakit vaskular
nefrotik • anomali ginjal
• Dekompensasio (ginjal polikistik)
kordis: infark miokard
• Pada neonatus akibat
sepsis/asfiksia berat
 Etiologi
PRA RENAL
RENAL

RENAL

PASKA
RENAL
DIAGNOSIS

Manifestasi
klinis Laboratorium

Penentuan Laju
Filtrasi Glomerulus
(GFR)
Manifestasi
Komplikasi

• Uremia dengan segala akibat

Bentuk klinis
• Edema/kongesti vaskuler
• GGA non oliguria: • Hipertensi berat
▫ Produksi urine normal • Gangguan elektrolit
▫ Peningkatan ureum dan (hiperkalemia, hiponatremia,
keratin hipokalsemia, hiperfosfatemia).
• GGA oliguria: • Asidosis metabolik
▫ ditandai volume urine • Kejang
< 240 ml/m2/24 jam atau • Infeksi
0,5 - 1 ml/kgBB/jam • Anemia
▫ Pada neonatus • Gangguan pertumbuhan
< 1ml/kgBB/jam • Osteoporosis
• dan lain-lain
 Nilai Normal LFG pada anak
 Klirens kreatinin (CrCl) Umur LFG
(ml/mnt/1.732) Lahir 20.8 ± 1.9
Formula Schwart 1 minggu 46.6 ± 5.2
K x ___Tinggi badan (cm)__ 3 – 5 minggu 60.1 ± 4.6
Kreatinin serum (mg/dl) 6 – 9 minggu 67.5 ± 6.5
3 – 6 bulan 73.8 ± 7.2
 Nilai K: 6 – 12 bulan 93.7 ± 14.0
 BBLR < 1th = 0,33
1 – 2 tahun 99.1 ± 18.7
 Aterm < 1th = 0,45
2 – 5 tahun 126.5 ± 24.0
 1-12 th = 0,55
 P: 13-21th = 0,57 5 – 15 tahun 116.7 ± 20.2
 L: 13-21 th = 0,70
 Kriteria LFG Kriteria Output Urin (OU)

RISK Kenaikan kreatinin serum x 1,5 atau OU < 0,5 ml/kg/jam

penurunan LFG >25% (selama 6 jam)

INJURY Kenaikan kreatinin serum x 2 atau OU < 0,5 ml/kg/jam

penurunan LFG >50% (selama 12 jam)

Kenaikan kreatinin serum x 3 atau

FAILURE penurunan LFG >75%, atau kreatinin OU < 0,3 ml/kg/jam
serum >4 mg/dl (peningkatan akut (selama 24 jam), atau
anuria dalam 12 jam
>0,5 mg/dl)

LOSS Gagal ginjal akut menetap. Hilangnya fungsi ginjal > 4 minggu.

End Stage Renal Disease (ESRD)

ESRD Gagal Ginjal Terimal (GGT)
Penurunan fungsi ginjal > 3 bulan
 TATA LAKSANA

Terapi
Tergantung Terapi
pengganti
penyebab supportif
ginjal

Balans cairan, asam

Pra Pasca basa, elektrolit, Peritoneal
Renal anemia, hipertensi, dialysis
Hemodialysis
renal renal
antikonvulsan, dll
PENYAKIT
GINJAL KRONIK

CHRONIC KIDNEY DISEASES

(CKD)
 GGK adalah suatu keadaan gangguan yang
kompleks, baik klinis, kimiawi maupun
metabolisme tubuh sebagai akibat
menurunnya fungsi ginjal yang kronik dan
progresif dalam hal ini laju filtrasi
glomerulus (LFG)
 Beberapa tahun ini digunakan istilah
Chronic Kidney Diseases (CKD) atau
Penyakit Ginjal Kronik (PGK)
dengan konsep lebih luas tidak hanya melihat
dari LFG saja
1. Kerusakan ginjal selama >3 bulan, yang
didefinisikan sebagai abnormalitas struktur
atau fungsi ginjal dengan atau tanpa
penurunan laju filtrasi glomerulus (LFG), yang
bermanifestasi sebagai salah satu dari gejala:
a) Abnormalitas komposisi urin
b) Abnormalitas pemeriksaan pencitraan
c) Abnormalitas biopsi ginjal

2. LFG < 60 ml/mnt/1,73m2 selama >3 bulan

dengan atau tanpa gejala kerusakan ginjal
Stadium LFG(<60ml/mnt/ Deskripsi
1,73m2)
1 >90 Kerusakan ginjal dengan
LFG normal/meningkat
2 60-89 Kerusakan ginjal dengan
penurunan LFG ringan
3 30-59 Kerusakan ginjal dengan
penurunan LFG sedang
4 15-29 Gagal ginjal
5 <15 (atau dialisis)
ETIOLOGY
 Related
to age at the time renal failure 1st
detected
 < 5 y: anatomic abnormalities (hypoplasia,
dysplasia, obstruction, malformations)
 > 5 y: glomerular diseases, glomerulonephritis,
hemolytic-uremic syndrome, or hereditary
disorders (Alport syndrome, cystic diseases)
 Pathogenesis
Once critical level of renal functional deterioration is reached,
progression to end-stage renal failure is inevitable

 Precise mechanisms unclear

 Factors that may have important roles:
 Ongoing immunologic injury
 Hemodynamically mediated hyperfiltration in
surviving glomeruli
 Dietary protein and phosporous intake
 Persistent proteinuria
 Systemic hypertension
Hyperfiltration Benefical vs harmful

 Once nephrons are lost for any reason, the remaining

nephrons undergo structural and functional
hypertrophy mediated –at least in part-, by increase
in glomerular flow by dilatation of the afferent
arterioles and angiotensisn II-induced constriction of
the efferent arterioles increase the driving force for
glomerular filtration in the surviving nephrons
 Damage of glomeruli due to direct effect of the
elevated hydrostatic pressure on the capillary wall,
increase in passage of proteins across capillary wall
or both
 This leads changes in mesangium and epithelial cells
and development of glomerular sclerosis
“Vicious cycle”
Loss of some nephrons Surviving nephrons
dilatation constriction
afferent efferent
arterioles arterioles
Decreased Increasing ACE
glomerular blood flow glomerular blood flow inhibitor

Hyperfiltration

 hydrostatic  proteinuria
pressure

Decreased Damage
glomeruli
glomerular filtration
rate
Changes in messangium and
epithelial cells

Chronic renal failure Glomerular scleroris

Clinical manifestations
 Underlying diseases
 Non specific symptoms
 Headache
 Fatigue
 Lethargy
 Anorexia
 Vomiting
 Polyuria,polydipsia
 Growth failure
Clinical manifestations

Manifestation Mechanisms
Accumulation of nitrogeneous Decline in glomerular filtration
waste products (azotemia) rate
Acidosis Urinary bicarbonate wasting
Decreased ammonia excretion
Decreased acid ecxretion
Sodium wasting Solute diuresis
Tubular damaged
Functional tubular adaptation for
sodium excretion
Sodium retention Nephrotic syndrome
Congestive heart failure
Anuria
Excessive salt intake
Clinical manifestations
Manifestation Mechanisms
Urinary concentrating Nephron loss
defect Solute diuresis
Increased medullary blood flow
Hyperkalemia Decline in glomerular filtration rate
Acidosis
Excessive potassium intake
Hypoaldosteronism
Renal osteodystrophy Decreased intestinal calcium
absorption
Impaired production of 1.25-dihydroxy-
vit.D
Hypocalcemia and hyperphosphatemia
Secondary hyperparathyroidism
Clinical manifestateions
Manifestation Mechanisms
Growth Protein-calorie deficiendy
retardation Renal osteodystrophy
Acidosis
Anemia
Inhibitors of insulin-like growth factors
Anemia Decreased erythropoietin
Low grade hemolysis
Bleeding
Decreased erythrocyte survival
Inadequate iron intake
Inadequate folic acid intake
Inhibitors of erythropoiesis
Bleeding tendency Thrombocytopenia
Defective platelet function
Clinical manifestateions
Manifestation Mechanisms
Infection Defective granulocyte function
Impaired cellular immune function
Neurologic Uremic factors
Alumunium toxicity
Glucose intolerance Tissue insulin resistance

Pericarditis and Unknown

cardiomyopathy
Hypertridlyceridemia Diminished plasma lipoprotein lipase
activity
Hypertension Sodium and water overload
Excessive renin production
Gastrointestinal Gastric acid hypersecretion
ulceration Gastritis reflux
Decreased motility
Management
Renal osteodystrophy (bone mineral diseases)
Hypocalcemia
Hyperphosphatemia
 Target: maintance PTH level in range of 200-400 pg/ml

 Calcium supplementation
 If Ca remains low after correction of serum phosphorous
 Dose 500-2000 mg/day
 Vitamin D therapy
 If persistent hypocalcemia despite reductin of serum
phosphour level <6 mg and supplement of Ca
 Renal osteodystrophy
 Dose dihydroxyvitamin-D (rocatrol) 0.05-0.2 mg/day
Management
Anemia

 Target:maintance Hb concentration in range

of 11-12 g/dl

 Evaluation inadequate iron and folic acid

intake
 Transfusion of PRC
 If Hb < 6 g/dl
 Erythropoietin therapy
 Pre or post dialysis
Management
Hypertension

 Non farmacologic
 Restriction of salt intake
 Farmacologic
 Diuretices
 ACE inhibitor
 Hypertensive emergencies
 Nifedipine
 Intravenous agents (clonidine)
Management
Dietary intake

 If GFR <50%
 Optimal caloric intake
 Carbohydrate
 Fat
 Restriction of protein
 High biologic value
 Eggs, milk, meat, fish
 Restriction of phosphorous
 Milk
 Phosphate binders
 Restriction of salt intake
 Supplementation of water-soluble vitamen (dialyzable)
Management
Water and electrolyte imbalance

Hypervolemia
 Water restriction (ESRD)

Hyponatremia
Hyperkalemia

Metabolic acidosis
End-stage renal diseases

 Dialysis
 Hemodialysis
 Hemofiltration
 Peritoneal dialysis
 Continuous ambulatory peritoneal dialysis (CAPD)
 Continuous cyclic peritoneal dialysis