Acute Renal Failure Final

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    Acute Renal Failure

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    Acute Renal Failure ( ARF )

    - is a rapid loss of renal function due to

    damage of the kidneys.

    - depending on the duration and severity, a

    wide range of potentially life-threatening

    metabolic complications can occur.

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    - widely accepted criterion for ARF

    50% or greater in serum creatinine above

    baseline

    Urine volume may be normal or changes may

    occur. Possible changes include:

    Oliguria

    Nonoliguria

    anuria

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    When reductions in renal blood flow

    interrupt glomerular pressure; the result is the

    development of acute renal failure.

    Prerenal ARF occurs in 60% to 70% of cases

    - result of impaired blood flow

    that leads to hypoperfusion of

    the kidney and a decrease in

    the GFR.

    Categories of ARF

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    Intrarenal ARF anything that causes direct

    insult to the kidneys.

    - Acute tubular necrosis (ATN) isthe most common type of

    intrarenal ARF.

    Characteristics of ATN:Intratubular Obstruction

    Tubular back leak

    vasoconstriction

    Changes in glomerular permeability

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    Postrenal ATF results from obstruction distal

    to the kidney.

    pressure rises in the kidney

    tubules and eventually, the GRF

    .

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    Causes of ARF

    1. Prerenal Failure- volume depletion

    - impaired cardiac efficiency

    - vasodilation

    2. Intrarenal Failure

    - prolonged renal ischemia

    - nephrotoxic agents- infectious processes

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    3. Postrenal Failure

    - urinary tract obstruction, including:

    Calculi

    Tumors

    Benign prostatic hyperplasia

    Strictures

    Blood clots

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    Phases of ARF

    1. Initiation begins with the initial insultand ends with oliguria develops. This phase

    can last from hours to days and is

    characterized by:

    Renal flow at 25% of normal

    Oxygenation to the tissue at 25% of normal

    Urine output at 30 ml (or less) per hour

    Urine sodium excretion greater than 40 mEq/L.

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    2. Oliguric - this phase usually lasts between8-14 days and is characterized by further

    damage to the renal tubular wall and

    membranes. Other characteristics in the

    oliguric phase include:

    Great reduction in the GFR

    Increased BUN/Creatinine

    Electrolyte abnormalities (hyperkalemia,

    hyperphosphatemia and hypocalcemia)

    Metabolic acidosis

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    3. Diuresis - this phase occurs when thesource of obstruction has been removed but

    the residual scarring and edema of the renal

    tubules remains. This phase usually lasts and

    additional 7-14 days and is characterized by: Increase in GFR

    Urine output as high as 2-4 L/day

    Urine that flows through renal tubules Renal cells that cannot concentrate urine

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    4. Recovery - The recovery phase can lastfrom several months to over a year.. Signals

    the improvement of renal function. At this

    point the GFR has usually returned to 70% to

    80% of normal.

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    Pathophysiology

    decline in renal blood flow (RBF)

    decreased glomerular filtration

    causes tissue ischemia and eventually cell necrosis or

    cell death

    produces oxygen free radicals and other enzymes

    which exacerbate the problem

    sloughing of cells which in turn block renal tubules and

    cause a back leak of glomerular filtrate

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    Assessment

    History

    Changes in the urine output

    - varies from scanty to a normal volume

    - hematuria may be present

    - urine has low specific gravity- inability to concentrate urine early

    manifestation of tubular damage

    - prerenal azotemia: amount of Na in theurine normal urinary sediment

    -intrarenal azotemia: amount of Na inurine with urinary cast and cellular debris

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    BUN level

    - steadily at a rate dependent on the

    degree of catabolism, renal perfusion, protein

    intake

    Creatinine level

    - useful in monitoring kidney function

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    Assess pts for hyperkalemia

    - may lead to dysrhythmias, such as

    ventricular tachycardia and cardiac arrest

    Progressive metabolic acidosis

    - cannot eliminate metabolic load of acid-

    type substances produced by the normal

    metabolic processes

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    There may be an increase in blood phosphate

    concentrations

    Calciums level may be low

    Anemia as a result of reduced erythropoietin

    production, uremic GI lesions, reduced RBC

    lifespan and blood loss from the GI tract

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    Diagnostic studies

    - ultrasonography effective in

    determining existing renal failure and/orobstruction of the urinary collecting system

    - CT or MRI scan may show evidence of

    anatomic changes

    -Creatinine Clearance Test this is

    believed to be the most accurate test to

    determine glomerular filtration rates- blood exam

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    - urinalysis

    - renal biopsy only be done if the result will

    alter the treatment plan