ORIGINAL ARTICLE |
|
Year : 2015 | Volume
: 17
| Issue : 1 | Page : 149-153 |
|
Male patients with terminal renal failure exhibit low serum levels of antimüllerian hormone
Dag Eckersten1, Aleksander Giwercman2, Anders Christensson1
1 Department of Nephrology and Transplantation, Lund University, Skåne University Hospital, Malmö, Sweden 2 Reproductive Medicine Centre, Lund University, Skåne University Hospital, Malmö, Sweden
Correspondence Address:
Anders Christensson Department of Nephrology and Transplantation, Lund University, Skåne University Hospital, Malmö Sweden
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1008-682X.135124
|
|
Male reproductive function is impaired during end-stage renal disease (ESRD). Disturbance of the hypothalamic-pituitary-gonadal axis, and therefore the regulation of sex hormones, is one of the major causes. Our focus was to include antimüllerian hormone (AMH) and inhibin B concentrations. Twenty male patients on hemodialysis, median age 40 (26-48) years, were analyzed for follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, sex hormone-binding globulin (SHBG), testosterone, estradiol, AMH and inhibin B levels. We used 144 proven fertile men, median age 32 (19-44) years as a control group and analyzed differences using multiple linear regression. Males with ESRD demonstrated higher mean values for prolactin, 742 versus normal 210 mIE l−1 (95% confidence interval (CI): 60.3, 729), LH, 8.87 versus normal 4.5 IE l−1 (95% CI: 2.75, 6.14), and estradiol 89.7 versus normal 79.0 pmol l−1 (95% CI: −1.31, −0.15). Mean value for AMH was lower, 19.5 versus normal 47.3 pmol l−1 (95% CI: −37.6, −11.6). There were no differences found for FSH, SHBG, inhibin B and testosterone. The most important difference was found for AMH, a marker of Sertoli cell function in the testes, which decreased by close to 60% when compared with controls. Combined with an increase in LH, these findings may indicate a dysfunction of Sertoli cells and an effect on Leydig cells contributing to a potential mechanism of reproductive dysfunction in men with ESRD. |
|
|
|
[FULL TEXT] [PDF]* |
|
 |
|