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
RENA
L

REN
AL

PASKA
RENAL

REN
AL

DIAGNOSIS

Manifestasi
Komplikasi
Bentuk klinis

GGA non oliguria:

Produksi urine normal
Peningkatan ureum dan
keratin
GGA oliguria:
ditandai volume urine
< 240 ml/m2/24 jam atau
0,5 - 1 ml/kgBB/jam
Pada neonatus
< 1ml/kgBB/jam

Uremia dengan segala akibat

Edema/kongesti vaskuler
Hipertensi berat
Gangguan elektrolit
(hiperkalemia, hiponatremia,
hipokalsemia, hiperfosfatemia).
Asidosis metabolik
Kejang
Infeksi
Anemia
Gangguan pertumbuhan
Osteoporosis
dan lain-lain

Nilai Normal LFG pada anak

Klirens kreatinin (CrCl)

Umur

LFG

(ml/mnt/1.732)

Lahir

20.8 1.9

1 minggu

46.6 5.2

3 5 minggu

60.1 4.6

6 9 minggu

67.5 6.5

3 6 bulan

73.8 7.2

6 12 bulan

93.7 14.0

1 2 tahun

99.1 18.7

2 5 tahun

126.5 24.0

5 15 tahun

116.7 20.2

Formula Schwart
K x ___Tinggi badan (cm)__
Kreatinin serum (mg/dl)

Nilai K:

BBLR < 1th

= 0,33
Aterm < 1th = 0,45
1-12 th = 0,55
P: 13-21th = 0,57
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

penurunan LFG >50%

FAILURE

Kenaikan kreatinin serum x 3 atau

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

LOSS

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

ESRD

End Stage Renal Disease (ESRD)

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

OU < 0,5 ml/kg/jam

(selama 12 jam)

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
m
nt/ 1,73m2)
1
>90
2

60-89

30-59

4
5

15-29
<15

(atau

Deskripsi
Kerusakan ginjal
dengan LFG
normal/meningkat
Kerusakan ginjal
dengan penurunan
LFG ringan
Kerusakan ginjal
dengan penurunan
LFG sedang
Gagal ginjal

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

Decreased

Surviving nephrons
dilatation
afferent
arterioles

glomerular blood flow

constriction
efferent
arterioles

Increasing

ACE
inhibitor

glomerular blood flow

Hyperfiltration
hydrostatic
pressure

Decreased
glomerular filtration
rate

proteinuria
Damage
glomeruli

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

rate
waste products (azotemia)
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
defect

Nephron loss
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-dihydroxyvit.D
Hypocalcemia and hyperphosphatemia
Secondary hyperparathyroidism

Clinical manifestateions
Manifestation

Mechanisms

Growth
retardation

Protein-calorie deficiendy
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
cardiomyopathy

Unknown

Hypertridlyceridemia

Diminished plasma lipoprotein lipase

activity

Hypertension

Sodium and water overload

Excessive renin production

Gastrointestinal
ulceration

Gastric acid hypersecretion

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