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Ovarian Function in Chronic Renal Failure: Evidence Suggesting Hypothalamic Anovulation

VICTORIA S. LIM, M.D.; CARLOS HENRIQUEZ, M.D.; GRANT SIEVERTSEN, M.D.; and LAWRENCE A. FROHMAN, M.D.
[+] Article and Author Information

Grant Support: By U. S. Public Health Service grants HD-10918 and AM 18722 and by the Michael Reese Medical Research Institute.

▸Requests for reprints should be addressed to Victoria S. Lim, M.D.; Renal Division, Michael Reese Hospital, 2900 S. Ellis; Chicago, IL 60616.


Chicago, Illinois


© 1980 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1980;93(1_Part_1):21-27. doi:10.7326/0003-4819-93-1-21
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The pathogenesis of ovarian dysfunction in uremia was evaluated in 24 patients by measurements of plasma levels of follicle-stimulating hormone (FSH), luteinizing hormone, prolactin, estradiol, and progesterone basally and after clomiphene, ethinyl estradiol, and bromocriptine. In the 17 premenopausal women, levels of plasma estradiol, progesterone, and FSH were comparable to those found in normal women during the follicular phase of the ovarian cycle; plasma luteinizing hormone was slightly elevated. In most patients, there was an absence of cyclicity. After clomiphene, plasma levels of luteinizing hormone, FSH, and estradiol rose; after ethinyl estradiol, plasma luteinizing hormone levels failed to increase. In seven postmenopausal patients, plasma estradiol was undetectable and gonadotropin levels were markedly elevated. Although plasma prolactin was generally elevated, suppression of prolactin with bromocriptine resulted in resumption of ovulation in only one patient; the other 2 remained amenorrheic. In uremic women, the continued secretion of estrogen, the rise of plasma levels of luteinizing hormone, FSH, and estradiol after clomiphene, and the elevated gonadotropin levels during menopause suggest that the negative estradiol feedback, the tonic gonadotropin secretion, and the pituitary ovarian axis were normal. The positive estradiol feedback associated with cyclic release of luteinizing hormone, however, was impaired as indicated by the prevalence of acyclicity and the failure of luteinizing hormone levels, to rise after ethinyl estradiol.

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