Abstract

Background:Therapeutic abdominal paracentesis is associated with the occurrence of paracentesis induced circulatory dysfunction (PICD), manifested by a marked increase of plasma renin activity. Previous studies were performed either before model for end-stage liver disease (MELD) allocation or done in patients with low MELD scores. The aim of study was to characterize the change of plasma renin activity - aldosterone concentration and investigate the clinical importance of PICD after non-large volume paracentesis with differences in the MELD cirrhotic ascites.

Methods:Cirrhotic patients with tense ascites were divided in two groups by MELD calculation: MELD ≤ 15 and MELD > 15. Changes in plasma renin, aldosterone and other laboratory tests were assessed before and 6 days after modest volume paracentesis (less than 5 liters). PICD was defined as an increase in plasma renin activity on the sixth day after paracentesis of more than 50% of baseline value to a level > 4 ng/mL/hr. After paracentesis, complications were also assessed within 90 days of follow up periods. Factors associated with death were determined using Cox proportional hazards models.

Results: Sixteen patients with MELD ≤ 15 and 14 patients with MELD greater than 15, the high meld group, were included in this study.  A significant increase in the median change of plasma renin but not plasma aldosterone between the groups of MELD > 15 and MELD ≤ 15 were  54.7 % (10.8 – 1800) vs 17.6% (0 – 536.4) (p=0.01) and 15.2% (3.3 – 59.1) vs 11.6% (0 – 200) (p=0.55) respectively. Notably, 35.7% of patients, all of whom were in the high MELD group, had PICD events with the Kaplan–Meier survival analysis demonstrating a short median survival of 28 days. High MELD patients had more acute kidney injury consequence (28.6% vs 0%; p=0.04) and a significantly increased 90 days mortality as compared to low MELD patients (71.4% vs 6.3%, p < 0.01). Multivariate Cox regression analysis indicated that only high MELD but not PICD can predict mortality with 10.73 times higher risk of death after paracentesis than low MELD patients (adjusted hazard ratio 10.73, 95% CI 1.24-92.98, p=0.03).

Conclusion:Non–large volume paracentesis in high MELD cirrhotic patients causes a significant increase in plasma renin activity. PICD occurred only in high MELD patients and was associated with an increasing risk of acute kidney injury and mortality. An elevated MELD score in advanced cirrhotic patients should be considered as an increased risk for development of circulatory dysfunction, more complications and a short survival even after non-large volume paracentesis without albumin replacement.

Keywords: ascites, Model of End-Stage Liver Disease, paracentesis induced circulatory dysfunction, renin