Teaching Pearls:

• Pathophysiology
  • Involves excessive splanchnic vasodilation due to production of nitric oxide, causing increased decreased flow to the renal circulation.
  • MAP = CO x SVR
    • In patients with HRS, SVR is decreased due to the splanchnic vasodilation. Hence treatment is geared towards improving SVP and MAP.
• Diagnosis of Exclusion
  • Normal urinary sediment
  • No nephrotoxic meds
  • No hypotension
  • Urine studies similar to pre-renal AKI
    • UNa low, elevated FENa or FEUrea
  • Cannot distinguish between HRS and and pre-renal AKI
• Requires fluid challenge with albumin to distinguish between HRS and pre-renal AKI
  • 1g/kg albumin (max 100g) daily x 2 days
  • If renal function improves, suggestive of pre-renal AKI
  • If renal function continues to worsen, suggestive of HRS
• Types
  • Type I
    • Two-fold increase in Cr to Cr>2.5 within two weeks
    • Very poor prognosis
  • Type II
    • Less severe disease, associated with diuretic resistance
• Treatment of Choice
  • Liver Transplantation
  • Medical Management
    • If in ICU
      • Treat with norepinephrine and albumin
    • If non-ICU
      • Treat with midodrine, octreotide, and albumin