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    SINDROM NEFROTIK

    Lestari Sukmarini, MN

    KMB FIK-UI2009

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    SINDROM NEFROTIK

    PENGERTIANmerupakan salah satu gambaran klinikpenyakit glomerulus yang di tandaidengan: protenuria masif >3,5 gram / 24 jam / 1,73

    m2 hipoalbuminemia, edema anasarka, hiperlipidemia, lipiduria,dan hiperkoagulabilitas.

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    DIAGNOSIS Anamnesis : bengkak seluruh tubuh,buang air

    kecil keruh Pemeriksaan fisis: edema anasarka,asites

    Laboratorium:Proteinuria masif >3,5 gram / 24jam / 1,73 m2, hiperlipidemia,hipoalbuminemia (

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    Patogenesis edema pd SNProteinuria

    albumin plasma Tekanan osmotik koloid plasma

    Pergeseran cairan

    ekstraselCairaninterstisiel

    Edema

    Cairan

    ekstrasel

    CairanintravaskularRenin-angiotensin

    Aldosteron

    Reabsorbsi Na pd tubulus

    Retensi Na &

    H2O

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    INVESTIGASI URINALISA Proteinuria Dipstick test

    24-hour quantitative test Analisa darah Albumin < 2.5 gr/dL Lipid: LDL/VLDL ; HDL BUN/Creatinine

    Biopsi ginjal Imaging studies: renal USG

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    Proteinuria

    Dipstick test: negative, trace

    1+ (closest to 30 mg/dL)

    2+ (closest to 100 mg/dL) 3+ (closest to 300 mg/dL)

    4+ (greater than 2,000 mg/dL)

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    Proteinuria Normal range

    100mg/m2/day (150mg/day), 1 gm/ m2/day >40mg / m2/hour

    Spot urine for albumin/creatinine ratio

    (mg:mg) Normal =

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    Indikasi biopsi ginjal Proteinuria > 1gr/hari Hematuria +

    Hipertensi + Fungsi ginjal

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    Etiologi NS

    Penyakit ginjal primer (75-80%)

    Penyakit sekunder

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    Orth S and Ritz E. N Engl J Med 1998;338:1202-1211

    Relative Frequency of Primary Glomerular Diseases Underlying the Nephrotic Syndrome inChildren and Adults

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    Glomerulopathy lesi minimal Faal ginjal normal, respon kortikosteroid +remisi 90%

    Remisi spontan 60% Glomerulopathy lesi membranosa

    Faal ginjal

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    Orth S and Ritz E. N Engl J Med 1998;338:1202-1211

    Rare Causes of the Nephrotic Syndrome

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    Orth S and Ritz E. N Engl J Med 1998;338:1202-1211

    Major Factors Contributing to the Hypercoagulable State in the Nephrotic Syndrome

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    Symptoms

    Edema: swollen face,ascites, pleuraleffusion, swollengenital.

    Oliguria

    Hematuria anorexia, fatigue,

    irritable, pale Diare Respiratory distress Hipertensi Infeksi Tromboemboli

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    Treatment terapi spesifik untuk kelainan dasar ginjalatau penyakit penyebab (pada SNsekunder),

    mengurangi atau menghilangkanproteinuria, memperbaiki hipoalbuminemi mencegah dan mengatasi penyulit.

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    Patofisiologi Pengobatan

    Kerusakan glomerulus Imunosupresif: mycophenolate mofetil(MMF), siklosporin

    Antikoagulan:heparin/warfarinAnti agregasi trombosit: aspirin

    Kehilangan protein Diit 35 kal/kgBB/hr RP 0.8-1gr/kgBB/hr atau 0.6 gr/kgBB/hr +gram proteinurin

    Hipoalbuminemia dan penurunantekanan onkotik Infus albumin (15%) 300 ml/45 mnt

    Sekresi aldosteron Diuretik spironolakton

    Retensi natrium dan air Diuretik furosemid 40 mg/hr

    Diit rendah garam 1-2 gr/hari

    Sembab yang resisten ultrafiltrasi

    Kontrol infeksi antibiotik

    Kolesterol darah hidroxymethyl glutaryl co-enzyme A(HMG Co-A) reductase

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    Kontrol hipertensi angiotensinconverting enzyme (ACE-1) inhibitors danAngiotensin Receptor antagonist

    sirkulasi, tekanan darah, tekananglomerulus

    kebocoran protein, memperlambatprogressive scarring glomeruli.

    Non farmakologi lain: bedrest, diet rendahkolesterol

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    Complications atherosclerosis "hardening of thearteries

    adverse reaction to steroids and

    immunisuppressant: osteoporosis, cataractdevelopment, increased risk of infection,and diabetes.

    Kidney function: insufficiency CKD

    Growth Delays in children Infection

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    Prognosis Umur & gender: anak, wanita > baik. komplikasi,

    tipe histopatologis ginjal Kematian: GGK, infeksi sekunder,

    gagal sirkulasi.

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    PENGKAJIAN KEPERAWATANRiwayat kesehatan : ISPA, infeksi kulit, infeksi saluran kemih,

    hepatitis, obat nefrotoksik, riwayat keluarga dengan penyakit

    polikistik, keganasan, nefritis herediter.Sirkulasi : hipertensi, disritmia kardia, distensi vena jugular, edemageneral (termasuk area periorbital, sakrum), pallor.

    Eliminasi : perubahan pola urin, perubahan warna urin seperti merah,keruh, pekat, oliguri.

    Makanan/cairan : penambahan berat badan (edema), dehidrasi, mual,

    muntah, adanya penggunaan diuretik, perubahan turgor kulit, edema.Nyeri : pada area kostovertebral/pinggangPernafasan : dispnea, takipnea, adanya batuk produktif (edema paru)Pemeriksaan diagnostik :Pemeriksaan sedimen urin : urin 24 jam untuk pemeriksaan bersihan

    kreatinin dan protein total untuk memperhitungkan fungsi ginjal

    residual dan ekskresi protein urin. cast sel darah merah membantumengarahkan bahwa hematuria dari glomerulus.Biopsi ginjal kelainan histologi yang terjadi.Darah : Hb menurun karena anemia, BUN-creatinin meningkat, protein

    albumin serum menurun.

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    Pemeriksaan lain yang penting adalah : ureum serum,albumin, kolesterol, elektrolit dan jugapemeriksaan serologis seperti: autoantibodi,complement C3 C4, imunoglobulin.

    Urin: jumlah urin

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    Nursing diagnosis alteration in fluid volume: excess; risk for infection; alteration in nutrition: less than body

    requirements, potential alteration in comfort; knowledge deficit; and

    potential disturbance in self-concept: bodyimage.

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    NURSING

    MANAGEMENT Monitor I & Opossibly limit fluids balance (-) Weigh dailyevaluating amount of edema, abdominal

    circumference Making patient comfortable

    Maintaining good nutrition DietHigh protein, high CHO for protein sparing, low fat,salt restrictions

    Preventing infections: universal precautions, limit invasiveprocedure,

    Bedrest

    Activity may increase as edema decreases Measures to prevent skin breakdown. Monitor lab Monitor side effect of medications

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    Lifestyle and homeremedies

    Limit salt intake to help minimize fluidretention and swelling and to reduce bloodpressure

    Modify diet to decrease cholesterol andtriglyceride levels

    Take vitamin D supplements Report signs of relaps Infection prevention Check regularly to doctor or dietitian

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    Diet

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    References:

    Black, JM. & Matassarin-Jacobs, E. (1997). Medical surgicalnursing: Clinical management for continuity of care. (5thed.).WB Saunders Company, Philadelphia.

    Goldman, L. & Bennett, JC. (2001). Pocket companion to ceciltextbook of medicine(21st ed.). WB Saunders Company,Philadelphia.

    Reeves, CJ., Roux, G., Lochart, R. (2001). Keperawatanmedikal bedah (Ed. Setyono, J.). Penerbit Salemba Medika,Jakarta.

    Sukandar, E. (1997). Nefrologi klinik. (2nd ed.). Penerbit ITB,Bandung.

    Wilson, DD. (1998). Nurses guide to understanding

    laboratory and diagnostic test. Lippincott William&Wilkins,Philadelphia. http://www.nephrologychannel.com/nephrotic/diagnosis.sht

    ml http://nephroticsyndrome.com

    http://www.nephrologychannel.com/nephrotic/diagnosis.shtmlhttp://www.nephrologychannel.com/nephrotic/diagnosis.shtmlhttp://www.nephrologychannel.com/nephrotic/diagnosis.shtmlhttp://www.nephrologychannel.com/nephrotic/diagnosis.shtml
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    THANK YOU ..