Adaptive Mechanisms of Renal Bile Acid Transporters in a Rat Model of Carbon Tetrachloride-Induced Liver Cirrhosis.
acute kidney injury
bile acids
choleric nephropathy
liver cirrhosis
organic transport proteins
rat model
serum inflammation biomarkers
urinary tubular injury biomarkers
Journal
Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588
Informations de publication
Date de publication:
27 Jan 2022
27 Jan 2022
Historique:
received:
21
12
2021
revised:
19
01
2022
accepted:
23
01
2022
entrez:
15
2
2022
pubmed:
16
2
2022
medline:
16
2
2022
Statut:
epublish
Résumé
Acute kidney injury (AKI) is common in advanced liver cirrhosis, a consequence of reduced kidney perfusion due to splanchnic arterial vasodilation and intrarenal vasoconstriction. It clinically manifests as hepatorenal syndrome type 1, type 2, or as acute tubular necrosis. Beyond hemodynamic factors, an additional mechanism may be hypothesized to explain the renal dysfunction during liver cirrhosis. Recent evidence suggest that such mechanisms may be closely related to obstructive jaundice. Given the not completely elucidated role of bile acids in kidney tissue damage, this study developed a rat model of AKI with liver cirrhosis induction by carbon tetrachloride (CCl No renal histopathological alterations were found at sacrifice. Comparing treated rats with controls, organic anion transporters were differentially expressed and localized. High serum bile acid values were detected in cirrhotic animals, while caspase-3 staining was negative in both groups. Increased levels of serum inflammatory and urinary tubular injury biomarkers were observed during cirrhosis progression, with a peak after 4 and 8 weeks of treatment. These findings suggest possible adaptive tubular mechanisms for bile acid transporters in response to cirrhosis-induced AKI.
Sections du résumé
BACKGROUND
BACKGROUND
Acute kidney injury (AKI) is common in advanced liver cirrhosis, a consequence of reduced kidney perfusion due to splanchnic arterial vasodilation and intrarenal vasoconstriction. It clinically manifests as hepatorenal syndrome type 1, type 2, or as acute tubular necrosis. Beyond hemodynamic factors, an additional mechanism may be hypothesized to explain the renal dysfunction during liver cirrhosis. Recent evidence suggest that such mechanisms may be closely related to obstructive jaundice.
METHODS
METHODS
Given the not completely elucidated role of bile acids in kidney tissue damage, this study developed a rat model of AKI with liver cirrhosis induction by carbon tetrachloride (CCl
RESULTS
RESULTS
No renal histopathological alterations were found at sacrifice. Comparing treated rats with controls, organic anion transporters were differentially expressed and localized. High serum bile acid values were detected in cirrhotic animals, while caspase-3 staining was negative in both groups. Increased levels of serum inflammatory and urinary tubular injury biomarkers were observed during cirrhosis progression, with a peak after 4 and 8 weeks of treatment.
CONCLUSIONS
CONCLUSIONS
These findings suggest possible adaptive tubular mechanisms for bile acid transporters in response to cirrhosis-induced AKI.
Identifiants
pubmed: 35160088
pii: jcm11030636
doi: 10.3390/jcm11030636
pmc: PMC8836491
pii:
doi:
Types de publication
Journal Article
Langues
eng
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