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GLOMERULAR DISEASE Sindrom Nefritik (GNA) ±Azotemia, ±Hipertensi, ±Edema, ±Hematuria(RBC cast), ±proteinuria (< 3 g/hr) ± terkadang oliguria Sindrom Nefrotik ±Proteinuria masif (> 3.5gram / 24 jam / 1,73 m2 atau 40-50 mg/kg/hari /+ 3 - + 4 ) ±Hipoalbuminemia, ±Edemaanasarka, ±Hiperlipidemia, ±Lipiduria. Etiologi : 1. Glomerulopati (GP) idiopatik /primera. GP akut proliferatif b.GP mesangioproliferatif (IgA)(penyakit Burger) c. GP membranoproliferatif. 2. Infeksi : a.post-infection streptococcus B haemolitik b. Non Streptococcal :endokarditis bakterialis(nefritis Lohlein)sepsis, pneumococcal pneumonia, thypoid fever, etc. c. parasit : malaria, toxoplasmosis, etc. d. Viral : hepatitisB, mumps, measles, varicella, etc. 3. Sistemik :Lupus Nephritis, Vaskulitis, Good pasteur syndrome. Patogenesis Inflamatory process ±Degree of glomerular inflamationthe sverity of renal dysfunction and associated clinicalmanifestations. ±Poststreptococcal glomerulonephritistissueinjury or result in inflammatory reaction. Patofisiologi

Glomerular Disease

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Page 1: Glomerular Disease

GLOMERULAR DISEASE

Sindrom Nefritik (GNA) ±Azotemia,±Hipertensi,±Edema,±Hematuria(RBC cast),±proteinuria (< 3 g/hr)± terkadang oliguria

Sindrom Nefrotik±Proteinuria masif (> 3.5gram / 24 jam / 1,73 m2 atau 40-50 mg/kg/hari /+ 3 - + 4 )±Hipoalbuminemia,±Edema anasarka,±Hiperlipidemia,±Lipiduria.

Etiologi :1. Glomerulopati(GP) idiopatik /primera. GP akut proliferatif b.GP mesangioproliferatif (IgA)(penyakit Burger)c. GP membranoproliferatif.2 . I n f e k s i :a.post-infection streptococcus B haemolitikb. Non Streptococcal :endokarditis bakterialis(nefritis Lohlein)sepsis, pneumococcal pneumonia, thypoid fever, etc.c. parasit : malaria, toxoplasmosis, etc.d. Viral : hepatitisB, mumps, measles, varicella, etc.3. Sistemik :Lupus Nephritis, Vaskulitis, Good pasteur syndrome.

PatogenesisInflamatory process�±Degree of glomerular inflamation the sverity of  renal dysfunction and associatedclinicalmanifestations.±Poststreptococcal glomerulonephritis tissueinjury or result in inflammatory reaction.

Patofisiologi1. Kel. urinalisis: ok. Kerusakan dd. Kapilerglomerulus selektif proteinuri <3 g/hr,hematuria disertai silinder eritrosit.2. LFG menurun, disertai reabsorbsi Na. dan airsehingga terjadi oliguri ,edema, edema parudan hipertensi.

Page 2: Glomerular Disease

Gejala klinis:1 . h i p e r t e n s i(malignant in some cases).2 . E d e m a3. O l i g u r i a4. Phys i ca l examina t i on :a. SLE MalarR ash, Oral ulcersb. Henoch-schonlein purpura andcryoglobulinemia palpable purpura

Laboratorium-UrinalisisMacroscopic hematuria(� tea cola colored urine) �Microscopic urine reveals RBCs Proteinuria(<3gr/hari)

Hematologi±Anemia±Underlying disease :�Trombocytopenia or leukopenia (SLE)B� lood culturesfever & murmurStreptozyme &ASOsore throat etc

BiopsiUntuk diagnosis dan membedakan antara� penyebab primer dan sekunder.

KOMPLIKASI�Fluid retention Edema dan HipertensiShort and long therm renal replacementtherapyRenal InsufficiencyResistance to erythropoietin or decreasedproduction anemia

SINDROM NEFROTIK

ETIOLOGI

Glomerular disease :�Membranous Nephropathy(40%)�Minimal change disease (15%)Focal glomerulosclerosis (15%) �Membarno proliferative GN (7%)Masangioproliferatif GN(5%)Immunotactoid and Fibrilary GN

PatogenesisReflects noninflammatory damage glomerular capillary wall.Proteinuriafrom alterations in the charge or size selectivity of the glomerular capillary wall.

Page 3: Glomerular Disease

Gejala KlinikProteinuria A symptomatic Edema Edem(High Intravascular hydrostatic pressureand tissue hydrostatic pressure)edemanasarka.

Hematologi�Serum albumin <3g /dL �Total serum protein <6g /dL�HyperlipidemiaBUN dan Kreatinin >>, GFR normal.Anemia, Elevated erythrocyte sedimentationRate(ESR), Hypocalcemia nad Vit. Ddeficiency.