Contribution to the issue of hepatorenal damage and failure
Authors:
V. Teplan
Authors place of work:
Klinické a výzkumné centrum pro střevní záněty ISCARE I. V. F. a. s., Praha 1. LF UK, Praha Subkatedra nefrologie, Institut postgraduálního vzdělávání ve zdravotnictví, Praha Katedra interních oborů, LF OU, Ostrava
Published in the journal:
Gastroent Hepatol 2018; 72(3): 242-250
Category:
doi:
https://doi.org/10.14735/amgh2018242
Summary
Kidney and liver are the most metabolically active solid organs in the human body, helping to maintain a balanced protein, carbohydrate, lipid and energy metabolism and contributing to mineral and water stability and hormonal activities. They can be simultaneously damaged by diseases of different aetiology, most frequently of immunologic, hereditary, infectious origin, or related to pregnancy, circulation and use of medical drugs; or a serious damage of one organ can be followed by subsequent damage of the other one. Liver failure in cirrhosis leads to acute kidney injury of prerenal aetiology, i.e. to the development of the hepatorenal syndrome. Its prognosis depends on the degree of liver damage. In type I hepatorenal syndrome, there is a rapid progression and worse prognosis as compared to type II. The primary renal illness can be followed by secondary liver damage due to toxic effect on liver tissue by hepatic clearance of drugs, e. g. antibiotics. Evaluation scores (MELD, Child-Pugh or King‘s College) have been developed for the most seriously ill patients with liver failure and kidney failure, allowing to enrol patients on priority positions in the waiting lists for liver or combined liver and kidney transplantation.
Key words:
liver function – kidney function – hepatorenal syndrome – liver and kidney transplantation
The author declares he has no potential conflicts of interest concerning drugs, products, or services used in the study.
The Editorial Board declares that the manuscript met the ICMJE „uniform requirements“ for biomedical papers.
Submitted: 13. 5. 2018
Accepted: 1. 6. 2018
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