Chapter 22 Renal failure

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    Chapter 22

    RENALFAILURE

    FERNANDEZ, ROWENA S.

    BSP 4A

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    The Urinary Structure

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    Pathophysiology

    Renal system is uniquely susceptible to

    toxic injury.

    In humans, the kidneys receive 20% to25% of the cardiac output despite

    weighing only 150g each.

    Kidney is metabolically active, containing

    several enzyme systems capable of

    bioactivating a non-toxic substance into a

    toxic compound.

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    ACUTE RENAL FAILURE

    occurs when kidney function declinerapidly and the kidney are no longer ableto filter waste products from the blood.

    Manifests as an abrupt decline inglomerular filtration rate occurring over aperiod of days or weeks.

    This results in an accumulation of water,nitrogenous waste products and othertoxins.

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    Classification

    of

    ACUTE RENAL FAILURE

    Prerenal failure

    Intrinsic renal failure

    Post renal failure

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    Pre-renal failure

    Characterized by inadequate bloodcirculation to the kidney w/c leaves themunable to clean the body properly.

    Causes: dehydration, heart failure, sepsis,(severe infection), and severe blood loss.

    Signs: volume depletion, dizziness, drymucous membrane, tachycardia,orthostatic hypotension, and weight loss.

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    Mechanisms that lead to hypotenion

    and decrease renal perfusion:

    1. toxin-induced cardiotoxicity resulting in

    a lowered cardiac output.

    2. toxin-induced vasodilation3. toxin-induced vasoconstriction

    4. toxin-induced loss of effective circulatory

    volume

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    Substances decreased glomerular

    perfusion via intrarenal vascular

    effects:

    ACE inhibitor

    Cyclosporine

    Radiocontrast agents

    NSAIDs

    Mannitol

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    Intrinsic renal failure

    Involves damage within both kidneys.

    Causes: vascular disease, disease of tubules

    and interstitium, and acute tubular necrosis.

    Signs and symptoms: fever, rash, flank pain, and

    oliguria (decreased urine output), peripheraledema, lethargy, dyspnea.

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    Substances cause Glomerulonephritis:

    Heroin abuse

    Hydrocarbons

    Hydralazine

    Halogenated alkanes

    D-penicillamine

    Methimazole

    Captopril

    Thiopronine

    Gold Mercurous and Mercuric salts

    Silicon

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    Substances that cause Direct tubular

    toxicity:

    Aminoglycosides, Polymyxin, Uranium

    Cisplatin, Arsenic, Bismuth

    Mithramycin, Chromium, Mycotoxins

    Ifosfamide, mercurous and mercuric salts

    Streptozotocin, Perchloroethylene, Hydrocarbons

    Amphotericin B, Cadmium, Fluorinated Anesthetics

    Diethylene glycol, Diquat, Paraquat

    Toluene

    Carbon tetrachloride

    Radiocontrast agent

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    Substances that cause Insterstitial

    nephritis:

    Allopurinol

    B-lactam antibiotics

    CimetidineNSAIDs

    Rifampin

    sulfonamides

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    Postrenal failure

    Caused by an acute obstruction that affects the

    normal flow of urine out of both kidneys.

    Causes: renal injury, retroperitoneal fibrosis,

    bladder obstruction.

    Signs and symptoms: distended bladder,edema, complain of hesitancy, decreased

    urinary flow and abdominal pain.

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    Substances that cause Obstractive

    Uropathy due to Tubular

    precipitation:

    Ethylene glycol metabolites

    Acyclovir

    Methotrexate

    Sulfonamides

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    Laboratory Studies

    Microscopic Examination

    Blood Urea Nitrogen (BUN)

    Serum Creatinine

    Urinalysis

    Cystoscopy

    Voiding Cystourethrography

    Intravenous Urography

    Renal Ultrasoound

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    Poisoned patient with prerenal failure:

    Urinary sodium (UNa+) level less than

    20 mEq/L

    Urinary osmolality (UOsm) greater than500 mOsm/kg

    Urine:plasma creatinine ration (U/PCr)

    greater than 40

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    Definitive treatment:

    PRERENAL FAILURE

    Increased chronotropy and inotropy,vasopressor support, fluid resuscitation,

    and blood transfusion

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    INTRINSIC RENAL FAILURE

    Causative agent should be discontinued.

    Life-threatening complications:

    Pulmonary edema managed with oxygen,diuretics, and preload and afterload reducers.

    Hyperkalemia treatment may include calcium,

    insulin and glucose, sodium bicarbonate,

    sodium polysterene sulfonate, furosemide, andalbuterol.

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    POSTRENAL FAILURE

    Treated by relieving the obstruction.Can be accomplished by Foley catheter

    insertion or urologic consultation for

    nephrostomy tube placement.

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    Emergent hemodialysis

    Reserved for severe volume overload and life

    threatening metabolic disturbances.

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    Disposition/Need for Consultants:

    Patients with acute renal failure should be

    admitted to hospital.

    Discharge patients with mild renalinsufficiency and no underlying medical

    conditions.

    Nephrology consultation in patients with

    hyperkalemia, pulmonary or

    cadrdiovascular compromise, need for

    emergent hemodialysis or renal biopsy for

    definitive diagnosis.