Men with chronic renal failure have consistent reduction in circulating testosterone, accompanied by moderate elevations in luteinizing hormone (LH), follicle-stimulating hormone (FSH), and inhibin-a (1,12). The pathophysiological interpretation of these changes is complex. Prima facie elevated blood gonadotropin and inhibin concentrations, together with moderate reduction in sperm and testosterone production, are indicative of primary (testicular) hypogonadism. Nevertheless, the modest elevations in peptide hormones, despite markedly impaired peptide clearance, together with direct evidence of hypothalamic dysregulation of pulsatile LH and FSH secretion (13), suggest important defects in hypothalamic-pituitary regulation of gonadotropin secretion as well. This functional state of partial gonadotropin deficiency has interesting but largely unexplored therapeutic implications for adjuvant hormonal treatment. The hormonal changes of renal failure become evident with even moderate reduction in renal function (once serum creatinine is consistently elevated), and the effects progressively worsen as renal function deteriorates. The hormonal changes of uremia are minimally affected, or not improved, by dialysis, with the best results from intensive hemodialy-sis. Transplantation leading to restoration of normal renal function can reverse most hormonal changes of chronic renal failure, although some changes resulting from prolonged dialysis may be irreversible (14). The effects of immunosuppressive medication on human reproductive function are not well understood, because data are restricted to a few observational studies. Long-term surveillance suggests only minimal effects of conventional immunosuppressive regimens (azathioprine, prednisone, and cyclosporin) on male reproductive function (1,14,15), but further studies to clarify the effect of immunosuppressive agents on male reproductive function would be desirable.
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