Bile Acid-Induced Cholemic Nephropathy

Krones, Elisabeth; Wagner, Martin; Eller, Philipp; Rosenkranz, Alexander R.; Trauner, Michael; Fickert, Peter

doi:10.1159/000371689

Cited by 53 publications

(47 citation statements)

References 76 publications

(125 reference statements)

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“…Despite that creatinine increase cannot be unequivocally attributed to CIN because of possible concomitant factors for renal failure in patients with severe liver failure (e.g. hepato‐renal syndrome; jaundice‐related renal insufficiency), our data suggest that a particular caution should be paid to reduce ICM volume (for instance by using a 1:2 dilution with saline instead of the standard 1:1) in patients with acute‐on‐chronic liver failure.…”

Section: Discussionmentioning

confidence: 69%

Diagnostic hepatic haemodynamic techniques: safety and radiation exposure

Hari

Nair

Gottardi

et al. 2016

Liver International

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Section: Discussionmentioning

confidence: 69%

Diagnostic hepatic haemodynamic techniques: safety and radiation exposure

Hari

Nair

Gottardi

et al. 2016

Liver International

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“…[ 63 ] Bile acid cause oxidative damage to tubular cell membranes by stimulating the production of ROS from mitochondria. [ 64 ] Oxidative stress can promote the formation of vasoactive mediators. These mediators can affect renal function by causing renal vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Serum metabonomics analysis of quercetin against the toxicity induced by cadmium in rats

Jia

Guan

Zhang

et al. 2020

J Biochem & Molecular Tox

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This study aimed to investigate the protective effect of quercetin against the toxicity induced by chronic exposure to low levels of cadmium in rats by an ultra performance liquid chromatography mass spectrometer. Rats were randomly divided into six groups as follows: control group (C), low dose of quercetin group (Q1: 10 mg/kg·bw), high dose of quercetin group (Q2: 50 mg/kg·bw), cadmium chloride group (D), low dose of quercetin plus cadmium chloride group (DQ1), and high dose of quercetin plus cadmium chloride group (DQ2). Cadmium chloride (CdCl2) was administered to rats by drinking water ad libitum in a concentration of 40 mg/L. The final amount of CdCl2 ingested was estimated from the water consumption data to be 4.85, 4.91, and 4.89 mg/kg·bw/day, for D, DQ1, and DQ2 groups, respectively. After a 12‐week treatment, the serum samples of rats were collected for metabonomics analysis. Ten potential biomarkers were identified for which intensities were significantly increased or reduced as a result of the treatment. These metabolites included isorhamnetin 4′‐O‐glucuronide, 3‐indolepropionic acid, tetracosahexaenoic acid, lysophosphatidylcholine (LysoPC) (20:5), lysoPC (18:3), lysophosphatidylethanolamine (LysoPE) (20:5/0:0), bicyclo‐prostaglandin E2, sulpholithocholylglycine, lithocholyltaurine, and glycocholic acid. Results indicated that quercetin exerted a protective effect against cadmium‐induced toxicity by regulating lipid and amino acid metabolism, enhancing the antioxidant defense system and protecting liver and kidney function.

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“…Recently, BAs have been implicated in kidney injury due to longstanding jaundice. Cholemic nephropathy represents typical histopathological alterations including tubular epithelial cell injury and intratubular cast formation in patients with cholestasis [50, 51]. In addition, solubility of BAs is increased in acidic milieu such as metabolic acidosis, which may reflect another factor for urinary cast formation and interstitial tubular damage [52].…”

Section: Discussionmentioning

confidence: 99%

Circulating bile acids predict outcome in critically ill patients

Horvatits

Drolz

Rutter

et al. 2017

Ann. Intensive Care

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BackgroundJaundice and cholestatic hepatic dysfunction are frequent findings in critically ill patients associated with increased mortality. Cholestasis in critically ill patients is closely associated with stimulation of pro-inflammatory cytokines resulting in impaired bile secretion and subsequent accumulation of bile acids.Aim of this study was to evaluate the clinical role of circulating bile acids in critically ill patients.MethodsTotal and individual serum bile acids were assessed via high-performance liquid chromatography in 320 critically ill patients and 19 controls.ResultsTotal serum bile acids were threefold higher in septic than cardiogenic shock patients and sixfold higher than in post-surgical patients or controls (p < 0.001). Elevated bile acid levels correlated with severity of illness, renal dysfunction and inflammation (p < 0.05). Total bile acids predicted 28-day mortality independently of sex, age, serum bilirubin and severity of illness (HR 1.041, 95% CI 1.013–1.071, p < 0.005). Best prediction of mortality of total bile acids was seen in patients suffering from septic shock.ConclusionsIndividual and total BAs are elevated by various degrees in different shock conditions. BAs represent an early predictor of short-term survival in a mixed cohort of ICU patients and may serve as marker for early risk stratification in critically ill patients. Future studies should elucidate whether modulation of BA metabolism and signalling influences the clinical course and outcome in critically ill patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s13613-017-0272-7) contains supplementary material, which is available to authorized users.

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Bile Acid-Induced Cholemic Nephropathy

Cited by 53 publications

References 76 publications

Diagnostic hepatic haemodynamic techniques: safety and radiation exposure

Diagnostic hepatic haemodynamic techniques: safety and radiation exposure

Serum metabonomics analysis of quercetin against the toxicity induced by cadmium in rats

Circulating bile acids predict outcome in critically ill patients

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