Understanding acute kidney injury in cirrhosis: Current perspective

Table 3 Commonly used kidney biomarkers in patients with cirrhosis

Newer markers	Role in differentiating between ATN and HRS	As a predictor of mortality	Role in diagnosing HRS-AKI	Comments
NGAL[35,36,38,39]	417 mg/g Cr in ATN and 76 ug/g Cr in HRS	uNGAL 110 ng/mL is associated with inpatient mortality[53]	Increased in 1-2 hours after ischaemic renal injury	Can be high in other diseases. Higher synthesis in the presence of sepsis. High in lupus nephritis, IgA nephropathy[41]
KIM-1[47,53]	Differentiate HRS from ATN; Cut-off: 15.4 ng/mL (AUC: 0.63); HRS: 3.1 pg/mL	No data	Early rise predicts AKI; Better marker than creatinine[53]	Not widely available
Cystatin C[42-45,55]	No data	Serum cystatin-C level of > 1.45 mg/L had the highest 90-day mortality (sensitivity and specificity of 66.7% and 68.4%)[44]. Cystatin-MELD score predicts mortality[45]	Predicts development of AKI in one year[55]; Serum cystatin-C > 1.47 mg/dL is an early marker of AKI in cirrhosis[44,45]	Higher reliability than Cr in patients with sarcopenia

AUC: Area under the curve; AKI: Acute kidney injury; ATN: Acute tubular necrosis; HRS: Hepatorenal syndrome; KIM-1: Kidney injury molecule-1; MELD: Model for end stage liver disease; NGAL: Neutrophil-gelatinase-associated lipocalin; RARI: Renal artery resistive index; uNGAL: Urinary neutrophil gelatinase-associated lipocalin.