Professional Documents
Culture Documents
Sindrom Nefritik Vs Sindrom Nefrotik: Preseptor: Dr. Santoso Chandra. SPPD
Sindrom Nefritik Vs Sindrom Nefrotik: Preseptor: Dr. Santoso Chandra. SPPD
VS
SINDROM NEFROTIK
Preseptor :
dr. Santoso Chandra. SpPd
GLOMERULAR DISEASE
Sindrom Nefritik
Azotemia,
Hipertensi,
Edema,
Hematuria (RBC
cast),
proteinuria (< 3
g/hr),
terkadang oliguria.
Sindrom Nefrotik
Proteinuria masif
(> 3.5 gram / 24
jam / 1,73 m2
atau 40-50
mg/kg/hari / +3+4 )
Hipoalbuminemia,
Edema anasarka,
Hiperlipidemia,
Lipiduria.
Sindroma Nefritik
Glomerulonefritis akut (GNA)
Sindroma Nefritik / GNA adalah
sindroma klinik yg ditandai kelainan :
Azotemia,
Hipertensi,
Edema,
Hematuria (RBC cast),
proteinuria (< 3 g/hr),
terkadang oliguria.
3
Etiologi :
1.
2.
3.
Patogenesis
Inflamatory process
Degree of glomerular inflamation the
sverity of renal dysfunction and
associated clinical manifestations.
Poststreptococcal glomerulonephritis
tissue injury or result in inflammatory
reaction.
Patofisiologi
1. Kel. urinalisis: ok. Kerusakan dd.
Kapiler glomerulus selektif
proteinuri < 3 g/hr, hematuria
disertai silinder eritrosit.
2. LFG menurun, disertai reabsorbsi Na.
dan air sehingga terjadi oliguri
,edema, edema paru dan hipertensi.
Gejala klinis:
1.
2.
3.
4.
Laboratorium
Urinalisis
Macroscopic hematuria (tea cola
colored urine)
Microscopic urine reveals RBCs
Proteinuria (< 3gr/hari)
Hematologi
Anemia
Underlying disease :
Imaging
Pulmonary Edema Wageners
Granulomatosis & good pasteur
disease
Echocardiogram pericardia
effusion or endocarditis
USG Renal Kidney Size ( <9 cm
Extensive renal Scarring)
Biopsi
Untuk diagnosis dan membedakan
antara penyebab primer dan
sekunder.
KOMPLIKASI
Fluid retention Edema dan
Hipertensi
Short and long therm renal
replacement therapy Renal
Insufficiency
Resistance to erythropoietin or
decreased production anemia
SINDROM NEFROTIK
Merupakan salah satu gambaran klinik
penyakit glomerulus yang ditandai
dengan :
Proteinuria masif (> 3.5 gram / 24 jam / 1,73
m 2)
atau 40-50 mg/kg/hari
Hipoalbuminemia,
Edema anasarka,
Hiperlipidemia, dan
Lipiduria.
ETIOLOGI
Glomerular disease :
Membranous Nephropathy(40%)
Minimal change disease (15%)
Focal glomerulosclerosis (15%)
Membarnoproliferative GN (7%)
Masangioproliferatif GN (5%)
Immunotactoid and Fibrilary GN
Systemic Causes
Diabetes mellitus, SLE, Amyloidosis, HIVassociated nephropathy
Drugs : Gold, Penicillamine, probenecid, street
heroin, captopril, NSAIDs
Infection : bacterial endocarditis, hepatitis B,
shunt Infection, shypilis, malaria, hepatic
schistosomiasis
Malignancy : multiple myeloma, light chain
deposition disease, hodgkins and other
lymphomas, leukemia, carcinoma of breast, GI
tract.
Patogenesis
Reflects noninflammatory damage
glomerular capillary wall.
Proteinuria from alterations in the
charge or size selectivity of the
glomerular capillary wall.
Patofisiologi
Gejala Klinik
Proteinuria Asymptomatic Edema
Edem (High Intravascular hydrostatic
pressure and tissue hydrostatic
pressure) edem anasarka.
Laboratorium
Urinalisis
Proteinuria (urine dipstick +3 to +4
dan 24 hour urine collection >3.5 g
protein/1.73 m2)
Few cells or cast and
Urinary lipid in sediment
Hematologi
Serum albumin <3 g/dL
Total serum protein <6 g/dL
Hyperlipidemia
BUN dan Kreatinin >> , GFR normal.
Anemia, Elevated erythrocyte
sedimentation Rate (ESR),
Hypocalcemia nad Vit. D deficiency.
Biopsi
Kontroversi Standar procedure
determining the cause of proteinuria.
TERIMA KASIH