Article Text


General Liver I
PTU-018 Cystatin C and protein: creatinine ratio; potential predictors of early acute kidney injury, renal replacement therapy and in-hospital death in patients with cirrhosis
  1. A Slack1,
  2. J Wendon1,
  3. M J McPhail1,
  4. R Sherwood2,
  5. R Musto2,
  6. M Heneghan1
  1. 1Institute of Liver Studies, King's College Hospital, London, UK
  2. 2Clinical Biochemistry, King's College Hospital, London, UK


Introduction Acute kidney injury (AKI) is common, but difficult to predict in patients with cirrhosis as lower baseline serum creatinine can mask significant chronic kidney dysfunction. Cystatin C is a biomarker of glomerular filtration rate (GFR), which may overcome this weakness. Quantifying proteinuria using the widely available protein:creatinine ratio (PCR) may better the degree of structural glomerular damage.

Methods 34 patients with cirrhosis and mean (SD) age 51 (14) years and, median (range) Child-Pugh Turcotte (CPT) score 11 (9–11) were prospectively assessed for 10 days or until AKI, developed. Baseline iohexol clearance was performed to calculate GFR and urine underwent PCR analysis. Daily urine and serum samples were collected for determination of novel serum and urine biomarkers of kidney injury, including Cystatin C. Biomarkers were assessed by area under the receiver operating curve (AUROC) for predicting AKI stage 1, renal replacement therapy (RRT) and death.

Results 16 (47%) patients developed AKI defined by an increase of >26.4 umol/l from baseline serum creatinine (median 73 range (37–120 umol/l)). Estimated GFR overestimated GFR with median eGFR 95 (47–181) ml/min/1.73 m2 compared to a median iohexol derived GFR of 55 (20–115) mL/min/1.73 m2, p<0.0001. Median PCR was 55 (36–189) compared to 17 (13–29) in the AKI and Non-AKI groups, p<0.0005. Liver disease severity scores were not significantly different between AKI groups for both CTP (p=0.86) or model for end-stage liver disease (MELD, p=0.14). Plasma cystatin C at 48 h prior to AKI predicted its subsequent development with an AUROC of 0.82 (sensitivity 86%, specificity 75%, p=0.004, cut off 1.18 mg/l). A random urine PCR of >30 predicted AKI during that hospital admission with an AUROC of 0.72 (sensitivity, 77%, specificity 63%, p=0.001). Plasma cystatin C at 48 h prior to AKI predicted death with an AUROC of 0.88 (sensitivity 100%, specificity 76%, p≤0.0001, cut off 1.18 mg/l). PCR >49 predicted the need for RRT with an AUROC of 0.85 (sensitivity 73%, specificity 86%, p≤0.0001).

Conclusion Estimated GFR using serum creatinine based equations overestimates GFR, therefore an accurate assessment requires a gold standard measure, like iohexol, in patients with advanced liver disease. Cystatin C and the widely available urine PCR measurement can be used to assess the risk of AKI. They both demonstrate potential for predicting AKI 48 h prior to onset, the need for RRT and hospital survival.

Competing interests None declared.

Reference 1. Slack A, Yeoman A, Wendon J. Renal dysfunction in chronic liver disease. Crit Care 2010;14:214.

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