Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 16-11: Cirrhosis + Key Features Download Section PDF Listen +++ ++ Characterized by Azotemia (increase in serum creatinine level > 0.3 mg/dL [26.5 mcmol/L]) within 48 hours or by ≥ 50% from baseline within the previous 7 days days or a urine volume < 0.5 mL/kg/hr for hours in the absence of Current or recent nephrotoxic drug use Macroscopic signs of structural kidney injury Shock and failure of kidney function to improve following 2 days of diuretic withdrawal and volume expansion with albumin, 1 g/kg up to a maximum of 100 g/day Macroscopic signs of structural kidney injury Shock Failure of kidney function to improve following 2 days of diuretic withdrawal and volume expansion with albumin, 1 g/kg up to a maximum of 100 g/day Diagnosed when other causes of acute kidney injury (AKI) (including prerenal azotemia and acute tubular necrosis) have been excluded in the setting of end-stage liver disease + Clinical Findings Download Section PDF Listen +++ ++ Often precipitated by an acute decrease in cardiac output Pathogenesis involves intense renal vasoconstriction Histologically, the kidneys are normal Acute kidney injury-hepatorenal syndrome (formerly type 1 HRS): serum creatinine doubles to a level > 2.5 mg/dL (208.25 mcmol/L) or the creatinine clearance halves to < 20 mL/min (0.34 mL/s/1.73 m2 body surface area [BSA]) in less than 2 weeks Chronic kidney disease- (or nonacute kidney injury-) hepatorenal syndrome (formerly type 2 HRS): chronic and slowly progressive + Diagnosis Download Section PDF Listen +++ ++ Azotemia, hyponatremia, oliguria, low urinary sodium concentration are typical features Urinary neutrophil gelatinase-associated lipocalin levels (normal, 20 ng/mL) and other biomarkers may help distinguish hepatorenal syndrome (105 ng/mL) from CKD (50 ng/mL) and other causes of AKI (325 ng/mL) + Treatment Download Section PDF Listen +++ ++ In addition to discontinuation of diuretics, clinical improvement and an increase in short-term survival may follow intravenous infusion of albumin in combination with one of the following vasoconstrictor regimens for 7–14 days: Oral midodrine plus subcutaneous or intravenous octreotide Intravenous terlipressin (orphan drug in United States, not yet FDA approved) Intravenous norepinephrine Oral midodrine, 7.5 mg three times daily, added to diuretics, to increase blood pressure has also been reported to convert refractory ascites to diuretic-sensitive ascites Survival benefit has occurred with the molecular adsorbent recirculating system, a modified dialysis method that selectively removes albumin-bound substances Improvement may also follow TIPS placement Liver transplantation is treatment of choice, but many patients die before a donor liver can be obtained Survival after 1 year is reported to be predicted by the combination of a serum bilirubin level < 3 mg/dL (< 50 mcmol/L) and a platelet count > 75,000/mcL (> 75 × 109/L) Type 1 hepatorenal syndrome is often irreversible in patients with a systemic infection Continuous venovenous hemofiltration and hemodialysis are of uncertain value