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Noradrenaline for reverting hepatorenal syndrome: a prospective, observational, single-center study

Authors Gupta K, Rani P, Rohatgi A, Verma M, Handa S, Dalal K, Jain A

Received 12 October 2017

Accepted for publication 14 February 2018

Published 18 September 2018 Volume 2018:11 Pages 317—324


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 3

Editor who approved publication: Prof. Dr. Everson L.A. Artifon

Kamesh Gupta,1 Pooja Rani,1 Anurag Rohatgi,1 Mukesh Verma,1 Shivani Handa,2 Keemi Dalal,1 Anand Jain1

1Department of Internal Medicine, Lady Hardinge Medical College, New Delhi, India; 2Department of Gastroenterology, Liver Associates of Texas, Houston, TX, USA

Objective: To evaluate the effectiveness of noradrenaline for the treatment of hepatorenal syndrome (HRS).
Background: HRS represents the development of renal failure in cirrhotic patients. The standard treatment for HRS is terlipressin, which, as opposed to noradrenaline, is more expensive and less accessible in most tertiary care centers.
Patients and methods: Thirty consecutive patients with HRS type 1 received noradrenaline (1–4.0 mg/hour) and albumin for 14 days. The parameters recorded were: serum creatinine levels, creatinine clearance, mean arterial pressure (MAP), urine output, and serum sodium levels evaluated at baseline and on treatment days 1, 3, 7, and 14.
Results: Most patients achieved serum creatinine levels <1.5 mg/dL and were considered responders (22/30, 73%), whereas eight patients (27%) were nonresponders. At baseline, responders and nonresponders differed only regarding initial bilirubin levels and international normalized ratio values. Treatment duration was 7.5±3.2 days. Responders experienced a significant (p<0.05) decrease in serum creatinine levels (from 3.26±0.48 to 1.28±0.14 mg/dL), as well as a significant increase (p<0.05) in creatinine clearance (from 21±4.1 to 67.7±12.1 mL/min), urine output (from 583±41.1 to 1163±105 mL/day), MAP (from 79.2±2.94 to 93.9±2.34 mmHg), and serum sodium levels (from 125±2.01 to 132.3±1.39 mEq/L). In nonresponders, the MAP increased, but serum creatinine levels also increased, reflecting a decrease in creatinine clearance and urine output, with no significant change in serum sodium levels over the duration of the treatment.
Conclusion: In most patients, noradrenaline treatment induced systemic vasoconstriction resulting in HRS reversal, with acceptable safety, in agreement with previously reported outcomes of terlipressin treatment.

Keywords: hepatorenal syndrome, vasoconstrictor drug, noradrenaline, CKD, hypovolemia

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