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    Pathophysiology of Acute Renal Failure

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    minangsung minangneng
    Acute renal failure can be caused by both non-modifiable and modifiable risk factors. Non-modifiable factors include increased age, family history of kidney disease, obesity, and smoking. Modifiable factors include acute gastroenteritis, medications like NSAIDs, chronic diseases, hospitalization, intensive care, major surgery, bleeding, blood transfusion reactions, and obstructive causes. Acute renal failure occurs through pre-renal failure, initiation and maintenance phases which can lead to tubular necrosis and decreased kidney function if not properly managed. Medical management aims to restore normal chemical balance, prevent complications, treat underlying causes, and may include dialysis. Recovery is possible if damage is not prolonged.

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    Pathophysiology of Acute Renal Failure

    Uploaded by

    minangsung minangneng
    65 views2 pages
    Acute renal failure can be caused by both non-modifiable and modifiable risk factors. Non-modifiable factors include increased age, family history of kidney disease, obesity, and smoking. Modifiable factors include acute gastroenteritis, medications like NSAIDs, chronic diseases, hospitalization, intensive care, major surgery, bleeding, blood transfusion reactions, and obstructive causes. Acute renal failure occurs through pre-renal failure, initiation and maintenance phases which can lead to tubular necrosis and decreased kidney function if not properly managed. Medical management aims to restore normal chemical balance, prevent complications, treat underlying causes, and may include dialysis. Recovery is possible if damage is not prolonged.

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    248449754-Pathophysiology-of-Acute-Renal-Failure

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    Acute renal failure can be caused by both non-modifiable and modifiable risk factors. Non-modifiable factors include increased age, family history of kidney disease, obesity, and smoking. Modifiable factors include acute gastroenteritis, medications like NSAIDs, chronic diseases, hospitalization, intensive care, major surgery, bleeding, blood transfusion reactions, and obstructive causes. Acute renal failure occurs through pre-renal failure, initiation and maintenance phases which can lead to tubular necrosis and decreased kidney function if not properly managed. Medical management aims to restore normal chemical balance, prevent complications, treat underlying causes, and may include dialysis. Recovery is possible if damage is not prolonged.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
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    65 views2 pages

    Pathophysiology of Acute Renal Failure

    Uploaded by

    minangsung minangneng
    Acute renal failure can be caused by both non-modifiable and modifiable risk factors. Non-modifiable factors include increased age, family history of kidney disease, obesity, and smoking. Modifiable factors include acute gastroenteritis, medications like NSAIDs, chronic diseases, hospitalization, intensive care, major surgery, bleeding, blood transfusion reactions, and obstructive causes. Acute renal failure occurs through pre-renal failure, initiation and maintenance phases which can lead to tubular necrosis and decreased kidney function if not properly managed. Medical management aims to restore normal chemical balance, prevent complications, treat underlying causes, and may include dialysis. Recovery is possible if damage is not prolonged.

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    of 2

    ACUTE RENAL FAILURE

    NON-MODIFIABLE RISK FACTORS: MODIFIABLE RISK FACTORS:


     Increased age (72y.o.)
     Family History of kidney disease  Acute Gastroenteritis
     Obesity  Hospitalization: Intensive Care,
     Smoking Major Surgery (TAHBSO)
     Bleeding and blood transfusion
    reaction

     Medications (NSAIDS:Naproxen)
     Use of ACE Inhibitors

     Chronic disease: Diabetes


    Mellitus, kidney disease, heart
    disease, liver disease,
    hypertension
     Obstructive causes such
    as benign prostatic
    hypertrophy and bladder tumor

    Trauma/Injury in Dehydration
    Inhibit COX-1 and
    COX-2 production Muscle

    Rhabdomyolosis Decreased BP
    Decrease renal
    prostaglandin
    production Release of Kidney release
    Myoglobin and Renin
    Hemoglobin
    Angiotensinogen
    Vasoconstriction from liver
    of renal afferent pH is <5.6
    arteriole
    Angiotensin I
    Becomes ACE from Pulmonary and
    ferrihemate Renal Endothelium

    Free hydroxyl Angiotensin II Aldosterone


    radicals
    production
     Vasoconstriction  Na reabsorption
    Vasoconstriction  Hypertension  K excretion
     Na reabsorption  Water retention

    Ischemia Additional Risk


    Factors:
     Hypotension
    Acute Tubular  Blood transfusion
    PRE-RENAL reactions
    Necrosis
    FAILURE  Severe Infection
    (WBC:23.81)
     Dye/Contrast use

    Initiation Injured tubular


    Phase epithelial cells

    Cell death and


    detachment from
    basement membrane

    Decrease renal
    perfusion
    Oliguric Phase
    Tubular necrosis

    Decrease blood
    volume

     Low GFR
     High Creatinine
     High BUN
    Maintenance Renal Injury
    Phase Established
    Oliguric Phase
    (10-20 days)
    Endothelial cells
    necrosis and
    sloughing

    Tubular destruction

    MEDICAL MANAGEMENT:
    Increase tubular
    Objectives: permeability
     Restore normal chemical balance
     Prevent complications
    Low GFR (5-10mL/m)
     Recognition and treatment of
    underlying cause
     BP monitoring  High Creatinine
     High BUN
     I and O monitoring, including
    drainage  Oliguria
     Monitoring of electrolyte levels
     ECG
    Decreased nephron
     ABG and Serum bicarbonate level ability to
    monitoring eliminate waste
     May have blood transfusion
     May initiate dialysis
     Pharmacologic Therapy:  Azotemia
     Cation-exchange resins for  Fluid retention
    hyperkalemia  Electrolyte
    imbalance
     IV dextrose 50%
     Metabolic
     Insulin acidosis
     Calcium replacement
     Albuterol Sulfate nebule
     Avoidance of nephrotoxic
    agents: radiocontrast
    agents, antibiotics with If managed Kidneys have a remarkable
    nephrotoxic potential, heavy
    metal preparations, cancer
    ability to recover Diuretic Phase
    chemotherapeutic agents,
    nonsteroidal anti-
    inflammatory drugs [NSAIDs]
     Diuretic agents Recovery Growth factors
     Nutritional therapy: Phase released
     Weigh patient daily
     Dietary proteins
    Repair and
     High carbohydrate diet regeneration of
     Low salt, potassium, low renal tissue
    phosphorus food
     Restrict potassium intake
    Recover tubular
     Follow up check up within 1-2 function
    weeks

    Recover renal
    function
    If not managed
     Increase Urine
    output
    Prolonged damage  Decreased urea
    to kidney tubules  Decreased
    Creatinine

    End-stage Renal
    Disease

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