title: Cholesterol synthesis, cholesterol absorption, and mortality in hemodialysis patients.
abstract: OBJECTIVE
  Recent clinical trials on cholesterol-lowering in patients with CKD yielded conflicting results, which might have resulted from different treatment strategies. Serum cholesterol levels are determined by endogenous synthesis and intestinal absorption, which are differentially influenced by various classes of cholesterol-lowering agents. Assessing markers of cholesterol metabolism has thus been proposed for guidance of lipid-lowering therapy. This study analyzed surrogate markers of cholesterol absorption and synthesis in hemodialysis (HD) patients.
  
  
  METHODS
  In 113 HD patients, lathosterol was measured as a marker of cholesterol synthesis and cholestanol was measured as a marker of cholesterol absorption via gas chromatography. Controls were 229 healthy persons. Overall survival in HD patients was recorded over 3.4-year follow-up.
  
  
  RESULTS
  Compared with controls, HD patients had lower lathosterol and higher cholestanol levels (P<0.001 for both). During follow-up, 58 patients died; higher cholestanol (indicating higher cholesterol absorption) predicted poor outcome among HD patients in multivariate Cox regression analysis after adjustment for potential confounders (hazard ratio for cholestanol above median, 2.24 [95% confidence interval (CI), 1.29-3.89]; P=0.004), whereas lower lathosterol (indicating lower cholesterol synthesis) did not (hazard ratio for lathosterol below median, 1.43 [95% CI, 0.81-2.50]; P=0.22).
  
  
  CONCLUSIONS
  This analysis of markers of cholesterol metabolism characterizes HD patients as cholesterol absorbers. In longitudinal analysis, higher levels of cholestanol were associated with all-cause mortality.
authors.affiliation: Department of Internal Medicine IV, Nephrology and Hypertension, Saarland University Medical Center, Homburg, Germany.
authors.forename: Kyrill S
authors.initials: KS
authors.lastname: Rogacev
authors.forename: Tobias
authors.initials: T
authors.lastname: Pinsdorf
authors.forename: Oliver
authors.initials: O
authors.lastname: Weingärtner
authors.forename: Markus K
authors.initials: MK
authors.lastname: Gerhart
authors.forename: Elena
authors.initials: E
authors.lastname: Welzel
authors.forename: Kai
authors.initials: K
authors.lastname: van Bentum
authors.forename: Julius
authors.initials: J
authors.lastname: Popp
authors.forename: Andreas
authors.initials: A
authors.lastname: Menzner
authors.forename: Danilo
authors.initials: D
authors.lastname: Fliser
authors.forename: Dieter
authors.initials: D
authors.lastname: Lütjohann
authors.forename: Gunnar H
authors.initials: GH
authors.lastname: Heine
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D004083:Cholestanol / Q000097:blood; D002784:Cholesterol / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D002849:Chromatography, Gas; D002908:Chronic Disease; D005260:Female; D005500:Follow-Up Studies; D005858:Germany; D006801:Humans; D007408:Intestinal Absorption; D053208:Kaplan-Meier Estimate; D007674:Kidney Diseases / Q000378:metabolism / Q000401:mortality / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016016:Proportional Hazards Models; D006435:Renal Dialysis / Q000009:adverse effects / Q000401:mortality*; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; C001521:lathosterol; D004083:Cholestanol; D002784:Cholesterol