18. Acute Kidney Injury - Cox

• prerenal - response to severe volume depletion and hypotension (shock)

  • intact nephron
• intrinsic due to inflammation, infection or ischemia

  • nephron structural and functional damage
• postrenal - acute obstruction urinary flow

  • increase intra-tubular pressure --> decrease GFR
• AKI

  • decrease urine output
  • increase creatinine levels
• oliguria - indicates bilateral injury
• non-oliguria - is either - intrinsic or post renal injury

  • usually bilateral - so unaffected kidney can compensate
• AKI - prerenal

  • bilateral can affect renal perfusion --> decrease GFR = oliguria
  • caused by impaired perfusion
• Acute Tubular injury - 2 type

  • due to inflammation
  • due to ischemia or toxicity
• renal is vulnerable to toxin by reabsorption
• renal - ischemic risk

  • active transport require high O2 and ATP
• 3 stages of intrinsic renal injury

  • initiation phase - ischemia initiate cell injury
  • maintenance phase - stabilization of GFR
  • recovery - regeneration of tubular epithelial cell
• Pathophysiology of ATI

  • direct tubular injury or impaired blood flow (vasoconstriction)
  • reduce GFR
  • leading to oliguria
• ischemia can cause structural alternation in epithelial cell

  • loss of cell polarity early event leading to redistribution of membrane protein
• ischemia

  • cause decrease reabsorption by PCT leading to increase to DCT
  • macular densa will cause afferent vasoconstriction = decrease GFR
• Ischemia

  • loss of cell adhesion = sloughing = cast formation (muddy brown cast)
  • tubular obstruction leading to decrease GFR
• acute tubular necrosis (ischemia) - is no good adhesion which cause them to slough off

  • formation of muddy brown cast
• toxin affect mostly PCT
• toxin - cause cast nephropathy

  • leading to obstruction --> inflammation + decrease GFR
• obstructive nephropathy

  • thin renal parenchyma
  • interstitial scarring
  • atrophy of tubules
• Rhabdomyolysis (RM) injury to skeletal muscle fibers

  • myoglobin into kidney tubules
  • PCT - myoglobin break down leading to excess iron
  • TAL - myoglobin combines with Tamm Horsfall protein
  • forming obstructing tubular casts
• Cast for ATI is made of - cast material (light chain, bile, myoglobin) + tamm Horsfall
• Bladder outlet obstruction cause Post-renal AKI