Risk factors for development of HRS include hyponatremia, low urine sodium, hyperkalemia, large volume paracentesis (> 5 L removal), drug-induced nephrotoxicity, acute liver failure, decompensated cirrhosis (spontaneous bacterial peritonitis, bleeding esophageal varices), or, as a complication, post-transjugular intrahepatic portosystemic shunts (TIPS).
Presentation varies between type 1 and type 2 HRS. In both types, patients present with low urine output and rising serum creatinine values:
- Type 1 HRS – Progressive, acute renal failure (creatinine > 2.5 mg/dL or 50% reduction in glomerular filtration rate [GFR]) over a 2-week period. Often triggered by infection. Poor prognosis with a 10% 90-day survival rate.
- Type 2 HRS – Moderate and stable reduction in GFR that occurs in patients with relatively preserved hepatic function and diuretic resistance. Can precipitate type 1 HRS. More favorable prognosis than type 1 HRS; median survival 6-8 months.
- Acute kidney injury with increase in serum creatinine of 0.3 mg/dL or more within 48 hrs or an increase of greater than 50% from baseline within 7 days.
- Other definitions include a serum creatinine > 1.5 mg/dL or 24-hour creatinine clearance < 40 mL/min.
- Absence of shock, fluid losses, ongoing bacterial infection, or use of nephrotoxic medications.
- No improvement in renal function despite plasma expansion with intravenous (IV) albumin (1 g/kg of body weight up to 100 g/day for 2 days) and/or diuretic withdrawal.
- Proteinuria < 500 mg/day and no ultrasonographic evidence of uropathy or intrinsic parenchymal disease.