Glomerulonephritis and its

Management
B Dj
INTRODUCTION
Glomerular disease, or glomerulonephritis, is
an inflammation of the glomeruli of the
kidney.
Glomeruli are structures composed of blood
vessels, and are the first part of the kidney's
filtering process. These structures are
surrounded by tubules and tissues called the
tubulointerstitial tissue.

In glomerulonephritis, inflammation of some or
all of the glomeruli reduces their ability to filter a
number of substances out of the bloodstream.
The result is that blood, protein, and lipids (fat
structures) tend to be excreted into the urine.
Eventually, damage to the glomeruli leads to
increasing impairment, and as less urine is
produced, more metabolic waste is left to build up
in the blood. This may lead to renal failure.

Ginjal
Retroperitoneal
Bentuk
Hilus
Otopsi: 11,5 x 6 (l) x 3,5 (t)
120 170 gr = 0,4 % BB
Anak ginjal, Fascia Gerota
Rusuk 11 - 12
Struktur Ginjal
Korteks : Nefron
Medulla: tubuli
Proses: darah sisa metabolisme filtrasi
reabsorbsi sekresi Urine
Vaskularisasi:
Tak ada anastomose dg arteri lain
Lokasi ginjal di dalam tubuh
T 12 dan L 3, L: 5-7cm P: 11-13 cm tebal 2,5 cm
Ginjal kiri
Ginjal kanan
Ureter kanan
Intestine besar
Hati
Paru paru
vena cava
superior
Jantung
Aorta
Spleen
Intestine kecil
Ureter kiri
Kandung kemih
Potongan melintang dari Ginjal
Renal Vein
Renal Artery
Renal Pelvis
Ureter
Renal Medulla
Papilla
Renal Cortex
Cabang dari
vena pada ginjal

Cabang dari
artery Ginjal
Nephron
Struktur tulang
Pengaktivan
Vitamin D
Merangsang absorbsi ca di usus

Keseimbangan
Calcium

Pembentukan
Darah
Erythropoietin
Synthesis
merangsang produksi SDM oleh sumsum tulang
Aktivitas jantung
Keseimbangan
Potassium
N: 3,5-5,5 meq/l
Mengatur PH darah
Mengatur konsentrasi
Bicarbonate
Tekanan darah
Keseimbangan cairan
Membuang
Sodium

Membuang
sisa sisa metabolisme
Membuang
Urea, Creatinine etc.
Fungsi dari ginjal
0,1 l air di dalam
feses
0,9 l Keringat &
pernapasan

1,5 l Urine
2,5 l pembuangan
Keseimbangan cairan
pemasukan dan
Pembuangan air
harus seimbang.
Tugas ini
dilakukan oleh
ginjal
0,3 l air dari
metabolisme
0,9 l air dari
makanan
padat
1,3 l Minuman
2,5 l Intake
+

Healthy Kidney Renal Replacement Physical Basis Diseased Kidney
Filtrasi and Reabsorpsi
1500 l
darah per
hari
masuk ke
arteri arteri
ginjal
180 l
filtrasi per hari
di glomerulus
60 l
urine per hari di
tubulus proximal
20 l
urine per hari
di awal tubulus
distal
10 l
urine per hari
di akhir tubulus
distal
1,5 l
urine per hari
di akhir duktus
collecting
Pembuangan
akhirl:
1,5 l urine
Although a biopsy of the kidney is generally
used for definitive diagnosis of glomerular
disease, there are certain factors and patterns
of clinical findings that can help physicians
narrow down the possibilities.
One factor is the patient's age, while the other
is the characteristics of the urine sediment,
which can be broken down into three general
histologic (microscopic appearance) patterns:
focal nephritic, diffuse nephritic, and
nephrotic.

Focal glomerulonephritis
In this type of glomerular disease, less
than one-half of the glomeruli show
inflammatory lesions.
Urinalysis usually shows the presence
of red blood cells, many of which are
malformed, occasional red cell casts
(cells encased in a small waxy
structure), and a mild level of protein.


Patients with this type of glomerulonephritis do not
usually show symptoms of more severe kidney
disease, such as :
high levels of protein in the urine,
edema (water retention that causes swelling in the extremities),
high blood pressure, or
kidney dysfunction.
In fact, they may not have any symptoms and their
condition may go unnoticed until blood and protein in
the urine are found during routine examinations.

Diffuse glomerulonephritis
This type of glomerular disease affects
most of the glomeruli. Urinalysis usually
shows high levels of protein, and
symptoms and signs such as edema,
hypertension, and kidney dysfucntion
may be observed.
Nephrotic syndrome
This form of glomerular disease is characterized
by large amounts of protein and fats (or lipids) in
the urine, but few red blood cells or casts. It is
harder to differentiate nephrotic syndrome from
other kidney diseases, because the symptoms and
clinical findings can also be caused by a number of
other conditions, including diabetes mellitus.

SINDROMA NEFROTIK
Bambang Djarwoto,
Suhardi D.A.

Sub Bagian Ginjal-Hipertensi
Bagian/SMF Penyakit Dalam FK-UGM/
RS Dr. Sardjito Yogyakarta
TIK
Mampu:
1. Definisi - Etiologi
2. Patofisiologi
3. Perubahan metabolik
4. Gambaran klinis
5. Laboratorium
6. Komplikasi
7. Pengobatan dasar
8. Terapi Diit/Interaksi Gizi
SINDROMA NEFROTIK
DEFINISI: Kumpulan gejala terdiri
^Proteinuria berat > 3,5 g/hari
^Hipoalbuminemia < 3 g%
^Udema
^Hiperlipidemia

ETIOLOGI:
^Primer glomerulo nefritis 80%
^Sekunder akibat penyakit lain 20%
1
PENYEBAB NEFROTIK SINDROME
4DEWASA:
80% Glomerulonefritis primer (terutama
Glomerulonefritis membranosa)
20% glomerulonefritis sekunder (SLE, DM,
Amiloidosis)
4ANAK-ANAK:
70% GN Tipe minimal
15% GN focal and segmental
10% GN sekunder
2
TIK
Mampu:
1. Definisi - Etiologi
2. Patofisiologi
3. Perubahan metabolik
4. Gambaran klinis
5. Laboratorium
6. Komplikasi
7. Pengobatan dasar
8. Terapi Diit/Interaksi Gizi
GAMBARAN KLINIS
NKELUHAN:
Udema/sembab bila albumin < 1,5 g
sembab di kelopak mata, dada, perut, punggung, tungkai,
genital, ascites, pleural effusi
Otot skelet atrophi
Diare

NPEMERIKSAAN FISIK:
Bengkak, ascites, pleura effusi
Anemia ringan
Parotis kadang membesar
Hipertensi:
Tidak ada hipertensi
Ringan berat
3
LABORATORIUM
URINE:
- Proteinuria masif (3,5 - 30 g/hari)
- Sedimen: silinder hialin, lemak
- Cenderung: oliguria
DARAH:
- Albumin (<2,5 g%)
- Kolesterol
- Trigliseride
- Fibrinogen
- Urea, kreatinin: normal atau
- Volume darah efektif 10-20%
- Faktor koagulasi tertentu
4
PROTEINURIA > 3,5 G/HARI
eK (BM kecil) < 100.000:
- Albumin (BM 69.000)
- Transferin (BM 90.000)
eS (BM sedang) 100.000 - 150.000:
- IgG (BM 150.000)
eB (BM besar) > 150.000:
- 2 makroglobulin (BM 840.000)
- Betalipoprotein (BM 250.000)
- Fibrinogen (BM 341.000)
5
Disebut proteinuria selektif apabila:
Proteinuria hanya berisi protein dengan BM
kecil: Albumin & transferin
Disebut proteinuria non selektif apabila:
Proteinuria berisi protein dengan BM sedang
atau BM besar dan BM kecil : IgG, 2
makroglobulin & betalipoprotein, albumin,
transferin
PROTEINURIA > 3,5 G/HARI
6
HIPERLIPIDEMIA
KOLESTEROL : 400-600-1000 mg%
TRIGLISERIDE : 500-1000-2000 mg%

Hubungan antara kadar albumin serum dengan kolesterol total
250
500
750
1000
1
2
3
4
KOLESTEROL TOTAL
A
L
B
U
M
I
N

Semakin rendah kadar albumin darah, semakin tinggi kadar kolesterol
7
KOMPLIKASI NEFROTIK SINDROME
GAGAL GINJAL AKUT
TROMBOSIS VASKULER
INFEKSI
MALNUTRISI (PROTEIN-KALORI)
8
KOMPLIKASI GGA PADA NEFROTIK
SINDROME
Penyebab GGA:
Diuresis berlebihan sehingga volume efektif
plasma ---> hipotensi/syok hipovolemik
Obat-obat NSAID: Indometacin, Ibuprofen
9
KOMPLIKASI TROMBOSIS VASKULER
PADA NEFROTIK SINDROME
Organ yang terkena:
Trombosis vena renalis
Trombosis vena perifer
Trombosis arteri:
coroner
mesenteric
femoral
cerebral
10
Penyebab:
- Faktor koagulasi
- Faktor 8
- Fibrinogen
KOMPLIKASI INFEKSI PADA NEFROTIK
SINDROME
Sering terjadi:
Cellulitis
Peritonitis
Pneumonia:
Pneumococe
- IgG (dibuang lewat urine)

- Protein kalori malnutrisi
11
KOMPLIKASI PROTEIN KALORI MALNUTRISI
PADA NEFROTIK SINDROME
Penyebab:
Perfusi usus menurun
Odema alat visceral:
hepar, saluran cerna
Ascites dengan distended

Kebocoran ginjal malnutrisi
Makan
Absorbsi
12
PENGOBATAN
PENGOBATAN CAUSA

PENGOBATAN SIMTOMATIK
13
PENGOBATAN GNK DENGAN NEFROTIK SINDROME
CAUSA: Imunosuppresi (Prednison, endoxan, cyclosporin)
SIMTOMATIK:
Udema: * Diet rendah natrium
* Pengaturan jumlah minum
* Diuresis
* Dialisis
Hipertensi: Obat-obat anti hipertensi
Hiperlipidemia: obat-obat anti lemak
Hipoalbumin: Diet protein 1-2 g/KgBB
Infus albumin (keadaan tertentu)
Proteinuria: Obat-obat pengurang proteinuria
ACE inhibitor, AIIRA
Trombosis: Warfarin
14
REMISI
+LENGKAP:
Proteinuria minimal
Albumin darah
Kolestrol < 300 mg
Diuresis lancar
Sembab menghilang
+PARSIAL:
Proteinuria tetap ada namun < 3,5 g/hari
Albumin darah
Kolesterol < 350 mg
Diuresis kurang lancar
Sembab masih ada
+RESISTEN:
Tak ada perbaikan laboratoris dan klinis
15
EFEK SAMPING PREDNISON
- Infeksi
- Neuro psykiatri
- Muscular myopati
- Komplikasi tulang
- Komplikasi ocular
- Komplikasi gastro intestinal
- Komplikasi kardio vascular
- Hipertensi
- Komplikasi kulit
- Komplikasi endokrin: DM/Obese
- Retardasi pertumbuhan
16
PERANAN PENGOBATAN STEROID & IMUNOSUPRESI LAIN
PADA NEFROTIK SINDROMA
LESI


1. G Tipe minim


2. GN Mesangial


3. GN Foc. Sklero


4. GN Membran


5. GN Mes. Prolif
LM


Normal


Prolif Difus


Foc. & Seg. Skle


Dinding Kap.
Tebal BM bentuk
spike
Perub. Mes.
Difus prolif +
IFM


IgM


IgM, IgG, C3
Deposit di Mes.

Foc. & Seg, IgM
C3

IgG, Granul sebar
difus di BM

IgM, IgG, C3
kresent +
EM


Deposit -, foot
proses fusion

Deposit di Mes.


Foot proses fusi
Sklero, hyalin

Deposit sub
Epithelial

Deposit +
RESPON
PENGOB

Steroid ++
sitotoksik +

Steroid
Sitotoksik ?

Steroid +
Sitotoksik -

Steroid
Sitotoksisk +

Steroid -
sitotoksik -
FYS


95%


80%


45-
50%

70%


45%
FYS: 5 years survival
17
Intervensi Gizi
Tujuan:
mengganti kehilangan protein.
Memperbaiki kadar albumin.
Mengurangi edema.
PROGNOSIS SINDROMA NEFROTIK
Umur waktu menderita
Jenis penyakit penyebab
Kelainan histologi pada ginjal
Ada tidaknya hipertensi
Berat ringannya proteinuria
Contoh:
NS pada anak prognosisnya umumnya baik
NS pada dewasa prognosisnya kurang baik
- GN tipe membranosa progresif lambat
- GN nefritis fokal bervariasi
- GN proliferatif difus jelek
18