Skip to main content
Top
Published in: BMC Nephrology 1/2019

Open Access 01-12-2019 | Amoxicillin | Case report

Idiosyncratic hepatic toxicity in autosomal dominant polycystic kidney disease (ADPKD) patient in combined treatment with tolvaptan and amoxicillin/clavulanic acid: a case report

Authors: Angela Maria Pellegrino, Luigi Annicchiarico Petruzzelli, Eleonora Riccio, Antonio Pisani

Published in: BMC Nephrology | Issue 1/2019

Login to get access

Abstract

Background

Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary disease characterized by the presence of renal cysts. Over time the expanding cysts lead to progressive renal failure. The use of tolvaptan, a V2-receptor antagonist, was recently approved in ADPKD patients. It was demonstrated that tolvaptan get slower decline in Kidney function compared with placebo. Idiosyncratic hepatic toxicity was described in patients receiving tolvaptan, with elevations in aminotransferases levels. We describe the first case reported in the literature in which hepatic toxicity is caused by the association of amoxicillin/clavulanic acid and tolvaptan.

Case presentation

A 41 years old woman with diagnosis of ADPKD had been in treatment with tolvaptan for 16 weeks when an elevation of liver enzyme levels was detected. She had taken autonomously amoxicillin/clavulanic acid (in doses of 825/175 mg twice a day for 7 days) about 5 weeks before.
The timing of the event and the kind of hepatocellular injury could be attributed to the concomitance of medication of tolvaptan and amoxicillin/clavulanic acid.

Conclusion

We highlight the need to careful monitor hepatic enzyme levels in order to recognize early hepatic side effects in ADPKD patients in treatment with tolvaptan and amoxicillin/clavulanic acid.
Literature
1.
go back to reference Chapman AB, Devuyst O, Eckardt KU, Gansevoort RT, Harris T, Horie S, et al. Autosomal-dominant polycystic kidney disease (ADPKD): executive summary from a kidney disease: improving global outcomes (KDIGO) controversies conference. Kidney Int. 2015;88(1):17–27.CrossRef Chapman AB, Devuyst O, Eckardt KU, Gansevoort RT, Harris T, Horie S, et al. Autosomal-dominant polycystic kidney disease (ADPKD): executive summary from a kidney disease: improving global outcomes (KDIGO) controversies conference. Kidney Int. 2015;88(1):17–27.CrossRef
2.
go back to reference Grantham JJ, Mulamalla S, Swenson-Fields KI. Why kidneys fail in autosomal dominant polycystic kidney disease. Nat Rev Nephrol. 2011;7(10):556–66.CrossRef Grantham JJ, Mulamalla S, Swenson-Fields KI. Why kidneys fail in autosomal dominant polycystic kidney disease. Nat Rev Nephrol. 2011;7(10):556–66.CrossRef
3.
go back to reference Grantham JJ, Torres VE, Chapman AB, Guay-Woodford LM, Bae KT, King BF Jr, et al. Volume progression in polycystic kidney disease. New Engl J of Med. 2006;354(20):2122–30.CrossRef Grantham JJ, Torres VE, Chapman AB, Guay-Woodford LM, Bae KT, King BF Jr, et al. Volume progression in polycystic kidney disease. New Engl J of Med. 2006;354(20):2122–30.CrossRef
5.
go back to reference Belibi FA, Reif G, Wallace DP, Yamaguchi T, Olsen L, Li H, et al. Cyclic AMP promotes growth and secretion in human polycystic kidney epithelial cells1. Kidney Int. 2004;66(3):964–73.CrossRef Belibi FA, Reif G, Wallace DP, Yamaguchi T, Olsen L, Li H, et al. Cyclic AMP promotes growth and secretion in human polycystic kidney epithelial cells1. Kidney Int. 2004;66(3):964–73.CrossRef
6.
go back to reference Wang X, Wu Y, et al. Vasopressin directly regulates cyst growth in polycystic kidney disease. J Am SocNephrol. 2008;19(1):102–8. Wang X, Wu Y, et al. Vasopressin directly regulates cyst growth in polycystic kidney disease. J Am SocNephrol. 2008;19(1):102–8.
7.
go back to reference Gattone VH 2nd1, Wang X, et al. Inhibition of renal cystic disease development and progression by a vasopressin V2 receptor antagonist. Nat Med. 2003;9(10):1323–6.CrossRef Gattone VH 2nd1, Wang X, et al. Inhibition of renal cystic disease development and progression by a vasopressin V2 receptor antagonist. Nat Med. 2003;9(10):1323–6.CrossRef
8.
go back to reference Meijer E, Gansevoort RT, et al. Therapeutic potential of vasopressin V2 receptor antagonist in a mouse model for autosomal dominant polycystic kidney disease: optimal timing and dosing of the drug. Nephrol Dial Transplant. 2011;26(8):2445–53.CrossRef Meijer E, Gansevoort RT, et al. Therapeutic potential of vasopressin V2 receptor antagonist in a mouse model for autosomal dominant polycystic kidney disease: optimal timing and dosing of the drug. Nephrol Dial Transplant. 2011;26(8):2445–53.CrossRef
9.
go back to reference Torres VE, Chapman AB, et al. Tolvaptan in patients with autosomal dominant polycystic kidney disease. TEMPO 3:4 trial investigators. N Engl J Med 20. 2012;367(25):2407–18.CrossRef Torres VE, Chapman AB, et al. Tolvaptan in patients with autosomal dominant polycystic kidney disease. TEMPO 3:4 trial investigators. N Engl J Med 20. 2012;367(25):2407–18.CrossRef
11.
go back to reference Gansevoort RT, Mustafa A, et al. Recommendations for the use of tolvaptan in autosomal dominant polycystic kidney disease: a position statement on behalf of the ERA-EDTA working groups on inherited kidney disorders and European renal best practice. Nephrol Dial Trasplant. 2016;31(3):337–48.CrossRef Gansevoort RT, Mustafa A, et al. Recommendations for the use of tolvaptan in autosomal dominant polycystic kidney disease: a position statement on behalf of the ERA-EDTA working groups on inherited kidney disorders and European renal best practice. Nephrol Dial Trasplant. 2016;31(3):337–48.CrossRef
12.
go back to reference Watkins PB1, Lewis JH2, et al. Clinical pattern of Tolvaptan-associated liver injury in subjects with autosomal dominant polycystic kidney disease: analysis of clinical trials database. Drug Saf. 2015;38(11):1103–13.CrossRef Watkins PB1, Lewis JH2, et al. Clinical pattern of Tolvaptan-associated liver injury in subjects with autosomal dominant polycystic kidney disease: analysis of clinical trials database. Drug Saf. 2015;38(11):1103–13.CrossRef
13.
go back to reference Gresser U. Amoxicillin-clavulanic acid therapy may be associated with severe side effects -- review of the literature. Eur J Med Res. 2001;6(4):139–49.PubMed Gresser U. Amoxicillin-clavulanic acid therapy may be associated with severe side effects -- review of the literature. Eur J Med Res. 2001;6(4):139–49.PubMed
14.
go back to reference Watkins PB. Amoxicillin/clavulanic acid/tolvaptan. Reactions. 2017;1655:27–10. Watkins PB. Amoxicillin/clavulanic acid/tolvaptan. Reactions. 2017;1655:27–10.
Metadata
Title
Idiosyncratic hepatic toxicity in autosomal dominant polycystic kidney disease (ADPKD) patient in combined treatment with tolvaptan and amoxicillin/clavulanic acid: a case report
Authors
Angela Maria Pellegrino
Luigi Annicchiarico Petruzzelli
Eleonora Riccio
Antonio Pisani
Publication date
01-12-2019
Publisher
BioMed Central
Published in
BMC Nephrology / Issue 1/2019
Electronic ISSN: 1471-2369
DOI
https://doi.org/10.1186/s12882-019-1612-7

Other articles of this Issue 1/2019

BMC Nephrology 1/2019 Go to the issue
Obesity Clinical Trial Summary

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.

Developed by: Springer Medicine

Highlights from the ACC 2024 Congress

Year in Review: Pediatric cardiology

Watch Dr. Anne Marie Valente present the last year's highlights in pediatric and congenital heart disease in the official ACC.24 Year in Review session.

Year in Review: Pulmonary vascular disease

The last year's highlights in pulmonary vascular disease are presented by Dr. Jane Leopold in this official video from ACC.24.

Year in Review: Valvular heart disease

Watch Prof. William Zoghbi present the last year's highlights in valvular heart disease from the official ACC.24 Year in Review session.

Year in Review: Heart failure and cardiomyopathies

Watch this official video from ACC.24. Dr. Biykem Bozkurt discuss last year's major advances in heart failure and cardiomyopathies.