GAGAL GINJAL

KRONIK
Arif Santoso, S.Farm, Apt
Stage Deskripsi GFR
( ml/min/1,73 m2) Action

Treatment of comorbid
1 Kerusakan ginjal ≥90 conditions,
dengan slowing progression,
GFR Normal CVD risk reduction

2 Kerusakan ginjal 60 – 89 Estimating progression

dengan
GFR ↓ Ringan

3 Kerusakan ginjal 30 – 59 Evaluating and treating

dengan complications
GFR ↓ Sedang

4 Kerusakan ginjal 15 – 29 Preparation for kidney

dengan replacement therapy
GFR ↓ Berat

5 Gagal Ginjal tahap akhir <15 atau dialisis Replacement (if uremia present)
(ESRD) or kidney transplant
 Patofisiologi
• Gangguan fungsi renal progressif  Irreversibel
dan berkembang menjadi ESRD

• 3 hal utama yang menyebabkan :

(a) Penurunan massa nephron
(b) Peningkatan tekanan pada kapiler glomerulus
(c) Proteinuria

• Penyebab lainnya : Hipertensi, Diabetes Mellitus,

Hiperlipidemia
Manifestasi klinik
• Gejala CKD muncul  stage 3 (moderate) – 5

• Tanda & gejala yang terjadi :

• Uremia (lemah, mual muntah, selera makan turun)
• Edema (perifer, pulmo)
• Proteinuria (foaming urin)
Tes Laboratorium
• Serum Creatinin
• Blood Urea Nitrogen (BUN)
• Bikarbonat  asidosis metabolik
• Hemoglobin
• Kadar Fe
• Elektrolit (Na, K, Ca, PO4)
Tujuan terapi :

• Menghambat progress CKD dengan

meminimalkan perkembangan komplikasi

• Meningkatkan harapan hidup pasien

 Anemia

Kardiovaskuler Komplikasi Hiperparatiroid

GGK sekunder

Fluid- elektrolit
imbalance : Metabolik
asidosis, hiperkalemia
 ANEMIA
• Penyebab :
1. Penurunan produksi hormon eritropoetin
2. Umur eritrosit > pendek
( 120 hari  60 hari ESRD)

• Jenis2 Anemia :
• Normositik-Normokromik (defisiensi eritropoetin)
• Mikrositik (defisiensi Fe)
• Makrositik (defisiensi Folat/B12)
Con’t ...
• Tujuan terapi :
meningkatkan pasokan Oksigen  mencegah gangguan
kardiovaskuler, sesak, lesu

• Prinsip terapi :
Target Hb  maintain : 11 - 12 g/dl
Fe status  Transferrin Saturation (Tsat) > 20%
Serum ferritin > 100ng/ml

Tsat = (Serum Iron/ TIBC) x 100

TIBC : Total Iron Binding Capacity

 Tata laksana terapi

1. Non farmakologi :
a. Dietary intake iron 1 – 2 mg/day (not significant)
b. Transfusi darah (situasi tertentu, resiko tinggi)

2. Farmakologi :
a. Erytropoetic Stimulating Agents (ESA)
• Pemberian sc memiliki t 1/2 > panjang
• Contoh : epoetin alfa, darbepoetin alfa (t 1/2 >>)
b. Suplemen Fe (po : 200mg/day, iv  stage 4/dialisis)
Hiperparatiroid sekunder
Tata laksana trapi
a. Hiperfosfatemia :
- phosphat binding agents (CaCO3, Antacid)
• 100 - 300 mg elemental calcium intravenously over
5 to 10 minutes
• 1 g of calcium chloride (27% elemental calcium) or
2 - 3 gram of calcium gluconate (9% elemental
calcium)

b. Hipocalcemia : Ca supplements
c. Hiperparatiroidsm : Calcitriol, analog vitamin D
Kardiovaskuler
• Pre-HD  BP < 140/90 mmHg
• P0st-HD  BP < 130/80 mmHg

• Antihypertension agents  compelling indication

• Diuretics  early CKD

• 1st choice  loop diuretics
• Thiazide and sparing-diuretics ineffective if
GFR reduced (< 30 ml/min)
Metabolic Acidosis
• normal kidney function secret approximately 1
mEq/kg per day of hydrogen ions, which are
generated from the metabolism of dietary
proteins

• Goal theraphy : normalize Blood pH and

maintain bicarbonat

• Contoh terapi : Natrium Bicarbonat

Hiperkalemia
• The kidneys normally excrete 90% to 95% of the
daily potassium dietary load. N : 4,5 – 5,5 mEq/L

• Treatment unnecessary  K : < 6,5 mEq/L and

no changes in ECG

• The majority of patients can be managed with a

dietary K restriction of 50 to 80 mEq/day and a
reduction in dialysate potassium concentrations

• Glucose + Insulin  shifting K intrasel

Natrium and water Retention
• In persons with normal kidney function, sodium is
maintained at 120 - 150 mEq/day.

• The fractional excretion of sodium (FeNa)

is approximately 1% - 3%  30% (nocturia)

FeNa (%) = UNa x SrCr x 100%

Ucr x Sna

Prerenal low  aktivasi RAA krn perfusi drh rndh

ATN high  reabsorbsi oleh t.proximal rendah
Con’t ...
• Excretion decreases despite an increase in sodium
excretion by remaining nephrons.

• Volume overload with pulmonary edema can result,

but the most common manifestation of increased
intravascular volume is systemic hypertension

• Tx : Fluid restriction  Urine output

Diuretics  increased dose or
(combination if resistant)