title: Mechanism underlying an elevated serum bile acid level in chronic renal failure patients.
abstract: BACKGROUND
  Bile acids play an important role in the digestion of dietary lipids. Bile acid metabolism is regulated by the digestive system. The kidney is an important organ of the urinary system and is believed to play a minor role in bile acid excretion; however, many recent studies have reported an increased serum bile acid level and alterations in bile acid homeostasis in both clinical and animal model studies on chronic renal failure. The existing research findings on the mechanisms underlying this phenomenon were mostly derived from animal model studies, but clinical investigations have been limited.
  
  
  METHODS
  Kidney tissues and serum and urine samples from CRF patients and normal controls were studied.
  
  
  RESULTS
  We found increased serum bile acid levels and decreased urine bile acid output levels in chronic renal failure patients. Mesangial cell and endothelial cell proliferation, glomerular sclerosis, renal interstitial fibrosis, and intrarenal vascular sclerosis were observed based on hematoxylin-eosin and Masson trichrome staining pathology analysis. Scatter diagram and Pearson correlation analysis showed that in chronic renal failure patients, the estimated glomerular filtration rate and serum bile acid level were interrelated. Reverse transcription polymerase chain reaction and Western blotting results indicated that reabsorption and secretion of bile acid at the apical surface of the proximal renal tubular did not contribute to the elevated serum BA level.
  
  
  CONCLUSIONS
  The increase in plasma bile acid is due to decreased bile acid filtration through the kidneys in CRF patients.
authors.affiliation: Department of Minimally Invasive Urology Center, Provincial Hospital Affiliated to Shandong University, 9677 Jingshi Road, Jinan, Shandong, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Chu
authors.forename: Kangkang
authors.initials: K
authors.lastname: Zhang
authors.forename: Yingying
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xunbo
authors.initials: X
authors.lastname: Jin
authors.forename: Huaxin
authors.initials: H
authors.lastname: Jiang
mesh_terms: D000328:Adult; D001647:Bile Acids and Salts / Q000097:blood / Q000378:metabolism*; D049109:Cell Proliferation; D042783:Endothelial Cells / Q000502:physiology; D005260:Female; D005355:Fibrosis; D005919:Glomerular Filtration Rate; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007687:Kidney Tubules, Proximal / Q000378:metabolism; D008297:Male; D026901:Membrane Transport Proteins / Q000235:genetics; D050527:Mesangial Cells / Q000502:physiology; D008875:Middle Aged; D000089762:Multidrug Resistance-Associated Protein 2; D027425:ATP-Binding Cassette, Sub-Family C Proteins / Q000235:genetics; D029363:Organic Anion Transporters, Sodium-Dependent / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D012598:Sclerosis; D027981:Symporters / Q000235:genetics
chemical_list: D001647:Bile Acids and Salts; D026901:Membrane Transport Proteins; D000089762:Multidrug Resistance-Associated Protein 2; D027425:ATP-Binding Cassette, Sub-Family C Proteins; D029363:Organic Anion Transporters, Sodium-Dependent; D012333:RNA, Messenger; D027981:Symporters; C476575:organic solute transporter alpha, human; C476577:SLC51B protein, human; C071908:sodium-bile acid cotransporter