dr.

Hertanti IL, SpA

Sub divis Nefrologi IKA FK Unsri
 Gagal ginjal 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
 Etiologi
PRA REN
RENA AL
L

REN
AL

PASKA
RENAL
DIAGNOSIS
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
6 9 minggu 67.5 6.5
Kreatinin serum (mg/dl)
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
1-12 th = 0,55 2 5 tahun 126.5 24.0
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
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
Stadiu LFG(<60ml/m Deskripsi
m nt/ 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
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