title: Endogenous testosterone, endothelial dysfunction, and cardiovascular events in men with nondialysis chronic kidney disease.
abstract: OBJECTIVE
  Deterioration of kidney function impairs testosterone production, with hypogonadism being common in men with chronic kidney disease (CKD). In nonrenal populations, testosterone is suggested to participate in the atherosclerotic process. In male dialysis patients, we showed that low testosterone increases the risk of mortality. We here studied plausible links among testosterone levels, vascular derangements, and cardiovascular events in nondialysis CKD men.
  
  
  METHODS
  This was a cross-sectional analysis in which flow-mediated dilation (FMD) was assessed in 239 CKD male patients (stages 1 to 5; mean age 52 ± 12 years), together with routine measurements, serum total and free testosterone, and follow-up for cardiovascular outcomes.
  
  
  RESULTS
  Total and free testosterone levels decreased in parallel with the reduction of kidney function. Multiple regression analyses showed that total and free testosterone significantly and independently contributed to explain the variance of FMD. After a median follow-up of 31 months (range 8 to 35 months), 22 fatal and 50 nonfatal cardiovascular events occurred. In Cox analysis, the risk of cardiovascular events was reduced by 22% for each nanomole-per-liter increment of total testosterone. This reduced risk persisted after adjustment for age, renal function, diabetes mellitus, previous cardiovascular history, C-reactive protein, albumin, and FMD. The same was true for free testosterone concentrations.
  
  
  CONCLUSIONS
  The reduction in endogenous testosterone levels observed with progressive CKD was inversely associated with endothelial dysfunction and exacerbated the risk of future cardiovascular events in nondialysis male CKD patients.
authors.affiliation: Department Nephrology, School of Medicine, Ankara, Turkey. Juan.jesus.carrero@ki.se
authors.forename: Mahmut Ilker
authors.initials: MI
authors.lastname: Yilmaz
authors.forename: Alper
authors.initials: A
authors.lastname: Sonmez
authors.forename: Abdul Rashid
authors.initials: AR
authors.lastname: Qureshi
authors.forename: Mutlu
authors.initials: M
authors.lastname: Saglam
authors.forename: Peter
authors.initials: P
authors.lastname: Stenvinkel
authors.forename: Halil
authors.initials: H
authors.lastname: Yaman
authors.forename: Tayfun
authors.initials: T
authors.lastname: Eyileten
authors.forename: Kayser
authors.initials: K
authors.lastname: Caglar
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Oguz
authors.forename: Abdullah
authors.initials: A
authors.lastname: Taslipinar
authors.forename: Abdulgaffar
authors.initials: A
authors.lastname: Vural
authors.forename: Mahmut
authors.initials: M
authors.lastname: Gok
authors.forename: Hilmi Umut
authors.initials: HU
authors.lastname: Unal
authors.forename: Mujdat
authors.initials: M
authors.lastname: Yenicesu
authors.forename: Juan Jesús
authors.initials: JJ
authors.lastname: Carrero
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology / Q000401:mortality / Q000503:physiopathology; D016009:Chi-Square Distribution; D002908:Chronic Disease; D003430:Cross-Sectional Studies; D015536:Down-Regulation; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D007006:Hypogonadism / Q000097:blood / Q000150:complications* / Q000401:mortality; D007674:Kidney Diseases / Q000097:blood / Q000150:complications* / Q000401:mortality / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D016016:Proportional Hazards Models; D012044:Regression Analysis; D018570:Risk Assessment; D012307:Risk Factors; D013739:Testosterone / Q000097:blood*; D013997:Time Factors; D014421:Turkey; D014463:Ultrasonography; D014664:Vasodilation
chemical_list: D015415:Biomarkers; D013739:Testosterone