Indian Journal of Medical Biochemistry

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VOLUME 23 , ISSUE 3 ( September-December, 2019 ) > List of Articles

RESEARCH ARTICLE

Pancreatic Enzymes in End-stage Renal Disease Patients on Maintenance Hemodialysis

Taoufiq Aatif, Rachid Akka

Keywords : Amylase, End-stage renal disease, Hemodialysis, Lipase, Pancreatic enzymes

Citation Information : Aatif T, Akka R. Pancreatic Enzymes in End-stage Renal Disease Patients on Maintenance Hemodialysis. Indian J Med Biochem 2019; 23 (3):343-346.

DOI: 10.5005/jp-journals-10054-0119

License: CC BY-NC 4.0

Published Online: 01-06-2018

Copyright Statement:  Copyright © 2019; The Author(s).


Abstract

Background: Elevated serum levels of pancreatic enzymes are frequently observed in end-stage renal disease (ESRD) in the absence of pancreatic diseases. Aim: Evaluate the prevalence of elevated pancreatic enzymes in patients on maintenance hemodialysis (HD) and compare it with healthy controls. Materials and methods: Serum amylase (SA) and serum lipase (SL) levels were evaluated in 20 patients on maintenance HD (group I) and compared with levels in 25 healthy controls (group II). Results: In group I, hyperamylasemia and/or hyperlipasemia were found in 14 (70%) patients. Abnormal levels of both SA and SL simultaneously were noted in 7 (35%); however, hyperamylasemia and hyperlipasemia only were noted, respectively, in 11 (55%) and in 10 (50%) patients. There was a significant moderate positive correlation between SA and serum creatinine (103.8 ± 50.6 vs 89.9 ± 20.9; r = 0.48; p = 0.029), and between SL and serum creatinine (61.2 ± 40.1 vs 89.9 ± 20.9; r = 0.47; p = 0.034) in group I. Mean SA values were significantly higher in group I in comparison with group II: 103.8 ± 50.6 vs 64.1 ± 31.5 U/L; p = 0.005, and mean SL values were significantly higher in group I in comparison with group II: 61.2 ± 40.1 vs 31.8 ± 17.7 U/L; p = 0.002. Conclusion: Our results indicate that elevated serum levels of pancreatic enzymes in ESRD patients on maintenance HD is slight but frequently occurs. There is a general agreement that reduced glomerular filtration rate would be the cause. The occurrence of hypothetical concomitant pancreatic damage has been suggested and the complex hemodynamic, biochemical, and physiological alterations in uremia were speculated to cause an excessive release of pancreatic enzymes.


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