Ovarian Function in Chronic Renal Failure: Evidence Suggesting Hypothalamic Anovulation

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Abstract
The pathogenesis of ovarian dysfunction in uremia was evaluated in 24 patients by measurements of plasma levels of follicle-stimulating hormone (FSH), luteinizing hormone [LH], prolactin, estradiol and progesterone basally and after clomiphene, ethynyl 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 LH was slightly elevated. In most patients, there was an absence of cyclicity. After clomiphene, plasma levels of LH, FSH and estradiol rose; after ethynyl estradiol, plasma LH levels failed to increase. In 7 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 1 patient; the other 2 remained amenorrheic. In uremic women, the continued secretion of estrogens, the rise of plasma levels of luteinzing 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 LH was impaired as indicated by the prevalence of acyclicity and the failure of LH levels to rise after ethynyl estradiol.