Neutrophil gelatinase-associated lipocalin and cystatin C in cirrhosis and portal hypertension: Relations to organ extraction and dysfunction

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Background and Aims:

Early detection of renal dysfunction in cirrhosis is important, and several renal biomarkers have been put forward. Neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C are markers of renal dysfunction, but relations to splanchnic and systemic hemodynamics and kinetics are sparsely studied in cirrhosis.

Background and Aims:

In patients with cirrhosis and portal hypertension, we studied plasma levels and renal, hepatic, and peripheral extraction of NGAL and cystatin C and relations to patients characteristics, liver dysfunction, and hemodynamics.


Forty-five cirrhotic patients (Child class A/B/C:15/15/15) and 15 controls were evaluated with a full clinical, biochemical, and hemodynamic assessment. Urine and regional plasma concentrations of NGAL and cystatin C were measured.


There was no significant difference in circulating or hepatic NGAL or cystatin C between all patients and controls but a trend towards increased levels with increasing Child class. In addition, there was a significant renal but no hepatic or systemic extraction of both NGAL and cystatin C (P < 0.001).


Plasma NGAL correlated with glomerular filtration rate (r = −0.56, P < 0.0001), and hepatic venous pressure gradient (r = 0.34, P = 0.02) and urinary NGAL correlated with heart rate (r = 0.58, P= 0.007), blood pressure (r = −0.46, P < 0.05), cardiac output (r = 0.45, P < 0.05), and systemic vascular resistance (SVR) (r = −0.48, p < 0.05). Plasma cystatin C correlated with hepatic venous pressure gradient (r = 0.45, P < 0.005), blood pressure (−0.40, P < 0.01), and glomerular filtration rate (r = 0.98, P < 0.000).


Extractions of NGAL and cystatin C levels seem largely unaffected by the severity of liver disease in cirrhosis with a renal extraction. These biomarkers therefore have the potential of being both valuable in diagnosing renal failure and reflecting the degree of portal hypertension and systemic haemodynamic changes.

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