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LES : Soluble immune complexes disease

Remisi & eksaserbasi
NEFROPATI LUPUS
Predisposisi : Genetika
Infeksi virus
Kelainan humoral/hormonal
• Lesi oto imun
• Pembentukan antibodi ganda thd sendi,
paru, otak & ginjal
Etiologi : ?
Klinis :
Gejala bervariasi  kelainan urinalisis tanpa keluhan


Proteinuria persisten hematuria
Sindroma nefritik akut


GAGAL GINJAL KRONIK
• Histopatologis  prognosis
• Imunofluoresen
• Mikroskop elektron
• Reseptor komplemen pada glomeruli
lasifikasi
Disseminated Lupus Erythematosus


Soluble Immune Complex Disease


Kidney Liver


Glomerular Damage Impaired protein Manufacture


 GFR  Peritubular capillary pressure
Hipoproteinemia

BUN/SC   Na reabsorbed


Proteinuria EDEMA

Hematuria

Oliguric  plasma vol

Pulmonary congestan
Hypertension


Hypertensive encephalopathy


Patofisiologi : Sindrom nefritik akut


A. Penampakan klinis :
- sindroma nefritis akut
- sindroma RPGN

B. Histopatologis renal WHO
- Derajat III atau IV

Steroid
- Intravenous (dosis tinggi) 500 mg-1000 mg metil predni-
solon
- Lanjut dgn oral 0,5-1 mg / Kg BB/hari dosis tunggal pagi
hari  2 minggu
- Tapp off s/d > 10 minggu
- Pulse dose metil pred tiap bulan (bila relapse)

Azatioprin (sitostatika oral) + siklofosfamid
( 2 – 2,5 mg/Kg BB) (1,5 – 2 mg/Kg BB)

Dialisis / Transplantasi ginjal

Klinis :
terutama urinalisis  proteinuria faal ginjal
Serologis :
- C3C4
- Fana
- Anti Ds DNA

Prognosis : sulit ditemukan
• 40 – 50 % pada DM type I
5 – 10 % pada DM type II
• Penyebab No. I pd ESRD di luar negeri
Penyebab No. 3 pd ESRD di Indonesia
1. Proteinuria
2. Sembab
3. Hipertensi
4. Azotemia (GGK)
Gambaran Klinis :
Pateogenesis Nefropati Diabetik

Perubahan biokimia pd DM

Hiperfiltrasi perubahan komponen
Glomerulus biokimia glomerulus /
circulating protein

Gangguan selektivitas Glomerulus

Penimbunan Proteinuri
dari circulating (albuminuria)
& glomerular protein


Glomerulosklerosis ? Faktor imun
Faktor genetika
Faktor hemoreologi
& hemostatik
Perubahan patofisiologi sebagai petanda
nefropati diabetik
 Hiperfiltrasi & nefromegali
 Mikroalbuminuria
 Proteinuria
 LFG  dan hipertensi
sistemik
 Nefropati diabetik terminal
 kematian
 Hiperfiltrasi berhubungan
dgn nefropati
 Tanda dini glomerulopati
 Tanda kebocoran
membran basal (kerusak-
an glomerulus)
 Petanda kerusakan lanjut
nefropati
 Petanda stadium lanjut
 Petanda stadium terminal
1. Optimalisasi terapi DM
2. Pembatasan “protein intake” 0,6 – 0,8 gr/Kg BB/hari
dgn nilai biologis tinggi
3. ACE Inh  “hati-hati SC > 2
4. Pengobatan hipertensi sistemik 
5. Simptomatis : edema  diuretika
6. Anticoagulantia dan antitrombotik
7. Terapi pengganti  HD :
- Intermitent
- regular
 Transplantasi ginjal
Lipid, deposit fibrin DM
Dan trombosit Insulinemia, hiperglicemia


 LFG (DM tipe I) Ekspansi sel-sel mesangial Filtrasi
penebalan membran basal protein
glomerulus glomerulus


Glomerulosklerosis proteinuria masif Mikroalbuminuria
(sindroma nefrotik)

Hipertensi
NEFROPATI DIABETIK TERMINAL
Patogenesis nefropati diabetik terminal
1. early renal hypertrophy and glomerular hyperfiltration
(belum bergejala)
2. glomerural lessions without clinically evident disease
(klinis tidak khas)
- nefromegali
- hiperfiltrasi glomerular (hipertensi intra glomerular)
3. Incipient diabetic nephropathy
- Mikroalbuminuria menetap (15-300 mg/hari)
4. Overt diabetik nephropathy
Mikroalbuminuria > 300 ug/m (- 500 ug/hr)
LFG 70 – 130 ml/mn
5. Nefropati diabetik terminal
5 stadium nefropati diabetik
• Kerusakan tubulo interstitial e.c. analgetic >>
• Aspirin, phenacetin, caffein Prostaglandin
Synthetase
Kombinasi Inhibitors
NSAID

local renal
vasodilatory hormon


Ischemia & Necrosis
(Renal papillae)
- Pengguna analgetik lama
- Arthritis, gastritis
- Hipertensi
- UTI
- Colic
- Normal, proteinuria, sterile pyuria
- USG ginjal dpt normal atau mengecil pada kasus yg
lanjut  GGK

linis
ab :
The 1982 criteria for classification of systemic lupus erythematosus
1 Malar rash Fixed erythema, flat or raised, over the malar
eminences
2 Discoid rash Erythematous raised patches with adherent
keratotic scaling and follicular plugging;
atrophic scarring may occur
3 Photosensitivity
4 Oral ulcers Includes oral and nasopharyngeal, observed
by physician
5 Arthritis Nonerosive arthritis involving two or more
peripheral joints, characterized by
tenderness, swelling, or effusion
6 Serositis Pleuritis or pericarditis documented by ECG
or rub or evidence of pericardial effusion
7 Renal disorders Proteinuria greater than 0.5 g/d or greater
than 3+, or cellular casts
8 Neurologic disorder Seizures without other cause or psychosis
without other cause
9 Hematologic disorder Hemolytic anemia or leukopenia (less than
4000/mm3) or lymphopenia (less than
1500/mm3) or thrombocytopenia (less than
100,000/mm3) in the absence of offending
drugs
10 Immunologic disorder Positive LE cell preparation or anti-dsDNA or
anti-Sm antibodies or false-positive VDRL
11 Antinuclear antibodies An abnormal titer of ANAs by
immunofluorescence or an equivalent
assay at any point in time in the absence of
drugs known to induce ANAs
If four of these criteria are present at any time during the course of disease, a diagnosis
of systemic lupus can be made with 98 percent specificity and 97 percent sensitivity.
Source: Criteria published by Tan EM et al: The 1982 revised criteria for the
classification of systemic lupus erythematosus. Arthritis Rheum 25:1271, 1982.
A. Acute Tubular Necrose (ATN)
 ARF (3-5%)

B.Chronic tubulointerstitial nephritis
- Interstitial fibrosis (20-40%)
- Tubular atrophy
- Vesico ureteric reflux, obstruction &
analgetic abuse
ATN  ARF oligo anuric / non oligouric drug induced

CTN  CRF

Urinalisis :
- Normal
- Hematuria
- Leucocyturia

linis
• Sesuai penyakit dasar
- infeksi
- Obstruksi
- Malignancy
- Metabolik  As. urat
- Radiasi

• Steroid 1 – 2 minggu
- Komplikasi HD terutama HD Ix; usia muda
- Sindroma klinik yg ditandai dgn gejala sbg :
Sakit kepala, mual, muntah, lelah, gelisah, mata kabur
s/d gangguan kesadaran  kejang  kematian
- Terjadi saat HD s/d 12 jam setelah HD

- Kontroversiil : disepakati oleh adanya
hubungan dgn peningkatan
cairan di otak secara menda-
dak, cairan bergeser dari plasma
ke otak secara mendadak plasma
hipotonus karena proses hemo-
dialisis (ikut perubahan kadar
urea plasmakotak)
- Teori lain : perubahan pH cairan cerebrospinal
tiologi :
* Intracranial bleeding :
- Subdural
- Subarachnoid
- Intracranial
* Metabolik
- Hyperosoular
- Hypercalcemia
- Hypoglycemia
- Hyponatremia
* Cerebral infark
* Hypotension
- Ultrafiltration
- Cardiac
- Myocardial infarction
- Anaphilaxis
* Aluminium intraxication (Sub acut)
DD :
• Penggunaan dialyzer yg kecil dgn permu-
kaan yang kecil
• Menurunkan blood flow rates
• Lakukan HD Ix 2 – 3 jam saja

A. Disequilibrium ringan :
Gejalanya mual, muntah, gelisah, sakit kepala tak
spesifik. Cukup dgn obat simptomatis kramp otot :
glucose / NaCl hipertonik
B. Disequilibrium berat :
Gejalanya : kejang, kesadaran , koma stop dialisis,
ingat diff. diag.
- Infus larutan manitol 20% 50 cc/jam
- Dapat diberikan bersamaan (Diazepam)