R1 Acute Kidney Failure

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jknell
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203997
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R1 Acute Kidney Failure
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2013-03-09 12:34:23
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Renal II
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Renal II
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  1. Acute Kidney Injury Definition
    • -abrupt loss of renal function secondary to a decrease in glomerular filtration rate
    • -often reversible
  2. Why is it important to detect and treat AKI?
    • 1. Clinical findings associated with loss of kidney function
    • -water and electrolyte metabolism
    • -regulation of acid-base
    • -excretion of nitrogen waste products (Urea, Cr)
    • -production of hormones (Epo, 1,25 Vit D)

    • 2. Associated with higher morbidity and mortality
    • -more organs failing lead to higher mortality
    • -mortality hasn't changed even with new techniques

    3. Adequate management leads to reduced morbidity and mortality

    4. Patients who recover of AKI may develop CKD and ESRD

    5. Associated with increased cardiovascular and all cause morbidity and mortality
  3. Staging AKI
    • -Stages I-III
    • -based on Cr, urine output
  4. Types of AKI
    • 1. Prerenal
    • 2. Post Renal
    • 3. Intrinsic
    • -Acute glomerulonephritis
    • -Acute interstitial nephritis
    • -Acute tubular necrosis

    • Most commonly:
    • -prerenal
    • -ischemic acute tubular injury
    • -nephrotoxic acute tubular injuyr
  5. Prerenal AKI
    Caused by transient renal hypoperfusion

    • Due to:
    • -hypotension
    • -decreased cardiac output
    • -decreased effective arterial blood volume
  6. Postrenal AKI
    -due to obstruction of the urinary tract
  7. Intrinsic AKI
    • 1. Acute glomerulonephritis
    • -inflammation and damage to the glomerular membrane

    • 2. Acute interstitial nephritis
    • -allergic reaction
    • -may be caused by drugs

    • 3. Acute tubular necrosis
    • ->50% of AKI
    • -Caused by:
    • -nephrotoxic agents
  8. Reduction in Renal Blood Flow
    • 1. True intravascular depletion
    • -hemorrhage
    • -diarrhea
    • -dehydration
    • -overdiuresis

    • 2. Redistribution of intravascular fluid/low effective arterial volume
    • -CHF
    • -edema
    • -advanced liver disease
    • -nephrotic syndrome
    • -pancreatitis
    • -sepsis

    • 3. 1 or 2 associated with agents capable of modifying renal vascular resistances
    • -conditions of 2 treated with NSAIDs or ACEIs/ARBs
  9. Drugs that can modify renal vascular resistance
    • -NSAIDs
    • -diuretics
    • -ACEIs
    • -ARBs
    • -Antibiotics
    • -contrast agents
  10. Prerenal Azotemia and NSAIDs
    • Normal Dehydration:
    • -decreased volume activates RAAS
    • -AII has both vasoconstrictive and vasodilatory effects (via PGs)
    • -leads to normal or slightly increased renal resistance

    • Dehydration + NSAIDS:
    • -decreased volume activates RAAS
    • -vasoconstriction occurs as normal
    • -NSAIDs block the synthesis of PGs and resultant vasodilation
    • -huge increase in renal resistance --> decreased GFR and AKI
  11. Prerenal Azotemia and ACEIs/ARBs
    • Normal:
    • -AII increases efferent resistance more than afferent resistance
    • -renal function is maintained because PGC increases (resulting in increased GFR)

    • With ACEI or ARB:
    • -block the effects of AII
    • -PGC drops and GFR drop
  12. Continuum of Prerenal AKI
    • -If prerenal injury is treated you can restore normal function
    • -If injury persists pt can progress from prerenal to intrinsic renal
    • -treatment is significantly affected by whether the injury is prerenal or intrinsic
  13. Why is kidney at increased risk of injury?
    -The proximal tubule is active at transporting many things and can retain many things making it vulnerable to DRUGS

    -the kidney is in a chronic state of hypoxemia (countercurrent exchange system puts veins and arteries in close proximity and O2 can jump between them without perfusing the kidney), at increased risk for ISCHEMIA
  14. Acute Tubular Necrosis: Mechanisms of GFR Reduction
    • -most common cause of AKI
    • -pts will stop making urine

    1. Intratubular obstruction due to sloughed cell, cell debris or casts

    2. Backleak of filtrate across the tubular epithelium

    • 3. Tubuloglomerular feedback reduces GFR
    • -Macula densa of distal tubule is in contact with it's own glomerulus, regulates GFR based on NaCl and flow

    **All three probably contribute
  15. Cellular Effects of Ischemia in AKI


    • Proximal tubule cells have polarity:
    • -normally Na/K ATPase is on basolateral side
    • -during ischemia PT cells lose their polarity and Na/K ATPase moves to the apical side --> puts ions right back where they were reabsorbed from

    • **Increasing GFR in these situations can make the patients worse!
    • -cells already at maximal work load, increasing the load can increase the injury

    Endothelial cells can increase function if injected into injured kidneys
  16. ARF Secondary to Aminoglycosides
    • -frequent cause of ARF (up to 10% of AG users)
    • -usually non-oliguric
    • -occurs 7-10 days after started using meds
    • -accumulate in renal cortex (can stay for months)

    • -Aminoglycosides bind brush border and are internalized where they affect mitochondrial function

    • -Aminoglycosides are ALWAYS nephrotoxic
    • -biomarkers are elevated before severe injury starts
    • -may only need to stop treatment when GFR changes

    • Increased Risk Factors for Aminoglycosides:
    • 1. Conditions of volume depletion
    • -increased aminoglycoside reabsorption in the proximal tubule leads to increased accumulation
    • -dehydration

    • 2. Higher doses
    • -amount, longer treatment

    • 3. Combined with other nephrotoxic drugs
    • -NSAIDs
    • -diuretics
    • -cisplatin
    • -contrast
  17. Contrast and AKI
    • Contrast may cause AKI in three ways:
    • 1. Vasoconstriction
    • 2. Oxidative Stress
    • 3. Direct Tubular Injury

    • Risk Factors for contrast-induced AKI:
    • -diabetes
    • -renal insufficiency
    • -intravascular volume depletion
    • -CHF-volume contrast used
    • -intra-arterial contrast (higher dose)

    • Prevention:
    • 1. ID risk
    • 2. IV fluids (most helpful)
    • 3. Alternative imaging if possible
    • 4. N-Acetylcysteine (given IV can lead to allergic reaction but may also decrease Cr)

    • Presentation:
    • -patients stop making urine for a couple of days
    • -then recover function (distinguish from atheroembolism AKI)
  18. Angiogram and AKI
    • -angiogram may dislodge atherothrombotic emboli (cholesterol emboli)
    • -these clots may produce characteristic skin lesions
    • -may also produce renal clots

    • Presentation:
    • -patients look very similar to constrast induced AKI
    • -BUT don't recover after a few days
    • -patients stop making urine then progress quickly to renal failure
    • -due to an inflammatory response against the cholesterol emboli
  19. Rhabdomyolysis and AKI
    • -results from crush injuries
    • -myoglobin from muscles release into systemic circulation

    • Mechanisms of injury:
    • 1. Myoglobin is a potent antioxidant that damages tubular cells directly
    • 2. Muscle injury also leads to fluid sequestration (third spacing)
    • 3. Injury to cells liberates cytokines which may also injure the kidneys

    • Presentation:
    • 1. hyperkalemia
    • 2. hyperphosphatemia
    • 3. hypocalcemia (Ca precipitates at site of injury)
    • 4. Urine + for Hb but NOT RBCs (due to myoglobin pigment)

    • Prevention and Treatment:
    • 1. Be aggressive with fluid
    • 2. May eventually need to dialyze (these patients can become hyperkalemic very fast)
  20. Clinical History Suggestive of Postrenal Failure
    • -urinary frequency, urgency, dysuria, dribbling, recurrent stones, UTIs
    • -sudden aneuria
    • -history of known tumor, retroperitoneal or pelvic disease
    • -previous abdominal radiation
    • -history of vaginal bleeding, abnormal menstruation, subtotal hysterectomy

    **must affect both kidneys
  21. How to Diagnose AKI
    • -if volume resuscitation fixes the AKI the problem is probably prerenal
    • -if volume resuscitation doesn't fix the AKI look for casts to distinguish what type of intrarenal AKI
  22. Renal Casts
    • C: tubular cells included in casts --> tubular injury
    • B: RBCs in casts --> AGN

    ***GU bleeds will cause RBCs in the urine but NO CASTS
  23. Urinary Indices in AKI
    • Prerenal:
    • -should be able to concentrate urine normally
    • -Urine osm > 500
    • -Specific Gravity > 1.020
    • -Uosm/Posm > 1.3
    • -FENa (%) <1
    • -Urinary Na < 20

    • Acute Tubular Necrosis:
    • -kidney cannot concentrate urine (low osmolality and specific gravity)
    • -Uosm < 350
    • -Specific Gravity < 1.010
    • -Uosm/Posm < 1.1
    • -FENa > 1
    • -Urinary Na > 40

    **can help distinguish if patient is still prerenal or if they have progressed to ATN

    FENa = (U/P)Na/(U/P)Cr x 100

  24. Clinical Presentation of ARF
    -can vary from patient to patient

    • 1. symptomatic elevation in BUN and serum Cr
    • 2. Alteration in urine flow rate (oliguria or anuria)
    • 3. Clinical features of precipitating cause of ARF
    • 4. Clinical complications of uermia
    • 5. Biochemical complications of uremia
  25. Natural History
    • 1. Prerenal/Obstructive ARF
    • -rapidly reversible if caught early enough

    • 2. ATN
    • -requires 1-2 weeks before tubular cells regenerate and function is restored
    • -OLIGURIC PHASE: 1-2 weeks
    • -POLIURIC PHASE: high daily urine output, decrease in BUN and Cr (until Cr returns close to baseline)
    • -most left with minimal residual findings
  26. Biochemical complications of ARF
    • -salt and water retention
    • -hyponatremia
    • -hyperkalemia
    • -metabolic acidosis
    • -hypocalcemia
    • -hyperphosphatemia
    • -hypermagnesemia
    • -hyperuricemia
  27. Indications for Acute Dialysis
    • 1. Hyperkalemia
    • 2. Acidosis
    • 3. Uremic Syndrome (with symptoms!!!)
    • 4. Fluid Overload
  28. Treatment of AKI
    • Prerenal Azotemia (secondary to intravascular depletion)
    • -0.9% NaCl administration

    • For low effective arterial volume (CHF, nephrotic syndrome, cirrhosis)
    • -manage underlying cause
    • -stope ACEI/ARBs/NSAIDs

    • Obstruction
    • -relieve obstruction or place nephrostomy tubes

    • ATN:
    • -no specific treatment
    • -dialysis if indicated
    • -adequate nutrition (protein, PO4, K restriction)
    • -restore normal volume status
    • -avoid nephrotoxic agents
    • -remove all unnecessary catheters (infection is #1 cause of death!!!!)
    • -administer calcium and phosphate binders

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