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    Acute Kidney Injury: Ahmad Fariz Malvi Zamzam Zein

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    Fatwa Dea Ramdani Octaviyasmin
    The document discusses acute kidney injury (AKI), summarizing its main causes and types. It describes AKI as being either prerenal, renal, or postrenal in origin. Prerenal AKI is the most common type and is caused by decreased renal perfusion due to factors like decreased blood volume, cardiac issues, vasodilation, or certain drugs. Renal AKI involves direct damage to the kidneys, such as from toxins, ischemia, or diseases of the glomeruli, vessels or tubules. Postrenal AKI is less than 5% of cases and occurs when the urinary tract is blocked.

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    Acute Kidney Injury: Ahmad Fariz Malvi Zamzam Zein

    Uploaded by

    Fatwa Dea Ramdani Octaviyasmin
    41 views30 pages
    The document discusses acute kidney injury (AKI), summarizing its main causes and types. It describes AKI as being either prerenal, renal, or postrenal in origin. Prerenal AKI is the most common type and is caused by decreased renal perfusion due to factors like decreased blood volume, cardiac issues, vasodilation, or certain drugs. Renal AKI involves direct damage to the kidneys, such as from toxins, ischemia, or diseases of the glomeruli, vessels or tubules. Postrenal AKI is less than 5% of cases and occurs when the urinary tract is blocked.

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    FK UGJ

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    Aki

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    The document discusses acute kidney injury (AKI), summarizing its main causes and types. It describes AKI as being either prerenal, renal, or postrenal in origin. Prerenal AKI is the most common type and is caused by decreased renal perfusion due to factors like decreased blood volume, cardiac issues, vasodilation, or certain drugs. Renal AKI involves direct damage to the kidneys, such as from toxins, ischemia, or diseases of the glomeruli, vessels or tubules. Postrenal AKI is less than 5% of cases and occurs when the urinary tract is blocked.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    41 views30 pages

    Acute Kidney Injury: Ahmad Fariz Malvi Zamzam Zein

    Uploaded by

    Fatwa Dea Ramdani Octaviyasmin
    The document discusses acute kidney injury (AKI), summarizing its main causes and types. It describes AKI as being either prerenal, renal, or postrenal in origin. Prerenal AKI is the most common type and is caused by decreased renal perfusion due to factors like decreased blood volume, cardiac issues, vasodilation, or certain drugs. Renal AKI involves direct damage to the kidneys, such as from toxins, ischemia, or diseases of the glomeruli, vessels or tubules. Postrenal AKI is less than 5% of cases and occurs when the urinary tract is blocked.

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    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
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    of 30

    Acute Kidney

    Injury
    AHMAD FARIZ MALVI ZAMZAM ZEIN
    Etiologi

     Prerenal
     Renal
     Postrenal
    Pre renal AKI
     Most common cause of AKI

     Response to renal hypoperfusion

     Integrity of renal parenchyma retained

     Restoration of normal renal perfusion results in prompt


    recovery of renal function

     Severe and sustained renal hypoperfusion – causes


    Ischemic ATN
    Pre renal AKI
     Decreased Intravascular Volume

     Decreased Cardiac Output

     Peripheral Vasodilatation

     Severe Renal Vasoconstriction

     Mechanical Occlusion of Renal Arteries

     Drugs that impair autoregulation and gfr


    Decreased Intravascular
    Volume
     Hemorrhage : traumatic, surgical, gastrointestinal,
    postpartum

     GI loss : vomiting, diarrhoea, nasogastric suction

     Renal loss : drug induced / osmotic diuresis


    diabetes insipidus, adrenal insufficiency

     Skin & Mucous membrane loss : burns, hyperthermia

     Third space loss : pancreatitis, crush injury, nephrotic


    syn
    Decreased Cardiac
    Output
     Myocardial infarction
     Cardiac arrhythmias
     Ischemic heart disease
     Cardiomyopathy
     Valvular heart disease
     Severe cor pulmonale
     Pulmonary hypertension
     Pulmonary embolism
     Anti hypertensives
    Peripheral Vasodilatation

     Sepsis

     Hypoxia

     Hypercapnea

     Adrenal cortical insufficiency


    Severe Renal
    Vasoconstriction
     Severe liver disease – hepatorenal syndrome

     Sepsis

     NSAID intake

     Cyclosporine

     Tacrolimus
    Mechanical Occlusion of
    Renal arteries

     Thrombotic occlusion

     Emboli

     Post procedure – trauma – angiography


    Drugs

     Angiotensin converting enzyme inhibitors in


    renal artery stenosis or severe renal hypoperfusion

     Inhibition of prostaglandin synthesis by NSAIDs in


    cases with renal hypoperfusion
    Post renal AKI

     < 5 % cases of AKI

     Ureteric Obstruction

     Bladder Neck Obstruction ( most common )

     Urethral Obstruction
    Ureteric Obstruction
     Intrinsic : Extrinsic :
     Intraluminal :  Retroperitoneal / Pelvic
     Nephrolithiasis Malignancy
     Sloughed renal papillae  Retroperitoneal fibrosis
     Blood clots  Retroperitoneal adenopathy
     Fungal balls  Endometriosis
     Intramural :  Abdominal Aorta Aneurysm
     Post operative edema -
     Surgical Ligation
    ureteric surgery
     BK virus–ureteric fibrosis -renal
    allograft
    Bladder Outlet
    Obstruction
     Intraluminal : Calculi
    Blood clots
    Sloughed Papillae

     Intramural : Bladder Carcinoma


    Bladder Infection with mural edema
    Neurogenic Bladder
    Drugs ( Tricyclic antidepressants )

     Extramural : Benign Prostatic Hypertrophy


    Carcinoma Prostate
    Urethral Obstruction

     Phimosis

     Stricture

     Tumor

     Congenital valves
    Intrinsic AKI

     Diseases involving large renal vessels

     Diseases of glomeruli and renal microvasculature

     Diseases involving renal tubules with ATN

     Acute diseases of tubulointerstitium


    Diseases involving renal
    vessels

     Renal Arteries : Thrombosis


    Atheroembolism
    Thromboembolism
    Takayasu Arteritis
    Dissection

     Renal Veins : Thrombosis


    Compression
    Diseases involving renal
    tubules with ATN
     Ischemia caused by renal hypoperfusion

     Exogenous Toxins : antibiotics


    anticancer agents
    radiocontrast agents
    poisons

     Endogenous Toxins : myoglobin


    hemoglobin
    myeloma light chains
    uric acid
    Gejala dan tanda

     Bervariasi, tergantung kelainan yang mendasari


    atau ada tidaknya faktor risiko
     Tidak spesifik: anoreksia, lemas, mual dan muntah,
    gatal-gatal, penunrunan produksi urin dan warna
    urin yang kegelapan
     overload: sesak nafas, edema perifer, rhonki,
    distensi vena jugularis
     Pada pemeriksaan fisik dapat ditemukan
    asteriksis, mioklonus, pericardial friction rub,
     Asimtomatik  hanya hasil laboratorium ~ AKI
    Pemeriksaan penunjang

     Berat jenis plasma


     Darah lengkap (Hb, Ht, leukosit, trombosit) 
    hemokonsentrasi, sepsis
     Elektrolit
     Analisa gas darah;
     Asam urat serum, LDH  pada sindrom lisis tumor
     Kreatin kinase  rabdomiolisis
     Eosinofilia  nefritis interstisial
     Pemeriksaan pencitraan  obstruksi
     Biopsi ginjal  nefritis interstisial
    Penatalaksanaan

     Mengenali dini kondisi AKI (perubahan produksi


    urin umumnya terjadi sebelum peningkatan
    kreatinin)
     Mengenali sindrom uremik
     Ketepatan waktu memulai terapi pengganti ginjal
     Pencegahan kerusakan lebih lanjut
     Perawatan suportif
     Koreksi kelainan yang mendasarinya
    Penatalaksanaan

     Memperbaiki atau mengembalikan kondisi yang


    mendasarinya,
     Mempertahankan dan menjaga hemodinamik, status
    volume,
     Sesuaikan dosis dan frekuensi obat-obatan
     Hindari paparan zat nefrotoksik
     Terapi kondisi yang menyertai: infeksi/sepsis dengan
    antibiotik, distress nafas dengan ventilasi mekanik,
    pemberian nutrisi enteral/ parenteral, insulin intensif untuk
    hiperglikemia.
    Indikasi RRT

     Komplikasi uremik: disfungsi platelet dan perdarahan, pericarditis


    atau pleuritis, neuropati, asteriksis, mioklonus, wristdrop atau
    footdrop, ensefalopati, kejang.
     Gangguan asam basa: asidosis metabolik
     Gangguan elektrolit: hiperkalemia
     Kelebihan cairan yang refrakter dengan pemberian diuretik
    Indikasi proaktif: ancaman gangguan asam basa dan elektrolit,
    oligoanuria, prognosis fungsi ginjal yang kurang baik, sepsis atau
    SIRS
    Terima kasih

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