Evaluation and Treatment of Sexual Dysfunction

Introduction

Sexual dysfunction is a common finding in both men and women with chronic kidney disease. Common disturbances include erectile dysfunction in men, menstrual abnormalities in women, and decreased libido and fertility in both sexes. These abnormalities are primarily organic in nature and are related to uremia as well as the other comorbid conditions that frequently occur in the chronic kidney disease patient. Fatigue and psychosocial factors related to the presence of chronic disease are also contributory factors.

Sexual Dysfunction in Uremic Men

Erectile dysfunction is one of the most common manifestations of sexual dysfunction in men with chronic kidney disease. The prevalence of this disorder has been reported to be as high as 70%–80% and is similar between patients on hemodialysis and patients on peritoneal dialysis. In addition to abnormalities in blood flow and neural input to the penis, abnormalities in the pituitary-gonadal axis play a prominent role in the genesis of this disorder.

Chronic kidney disease is associated with impaired spermatogenesis and testicular damage, often leading to infertility. Semen analysis typically shows decreased volume of ejaculate, either low or complete azoospermia, and a low percentage of sperm motility. Histologic findings include damage to the seminiferous tubules and interstitial fibrosis, and calcifications in the epididymis and corpora cavernosa. The factors responsible for testicular damage in uremia are not well understood, but chronic exposure to phthalates in dialysis tubing may play a role.

The endocrine function of the testes is also abnormal in chronic kidney disease ( Table 56.1 ). Total and free testosterone levels are typically reduced, although the binding capacity and concentration of sex hormone-binding globulin are normal. Low testosterone levels lead to increased plasma concentration of the pituitary gonadotropin, luteinizing hormone (LH) since testosterone normally inhibits LH release through a negative feedback loop. Low serum testosterone levels are associated with increased mortality in dialysis patients. Follicle-stimulating hormone (FSH) secretion is also increased in men with chronic kidney disease, although to a more variable degree such that the LH/FSH ratio is typically increased. FSH release by the pituitary normally responds to feedback inhibition by a peptide product of the Sertoli cells called inhibin. The plasma FSH concentration tends to be highest in those uremic patients with the most severe damage to the seminiferous tubules and presumably the lowest levels of inhibin. Increased FSH levels may be a predictor of incomplete recovery of spermatogenic function following kidney transplantation. Elevated plasma prolactin levels are commonly found in dialyzed men primarily due to increased production and, to a lesser extent, reduced metabolic clearance. Both increased parathyroid hormone and zinc deficiency may play a role in the increased levels.

Gynecomastia occurs in approximately 30% of men on maintenance hemodialysis. This disorder most often develops during the initial months of dialysis and then tends to regress as dialysis continues. The pathogenesis of gynecomastia is unclear. Although elevated prolactin levels and an increased estrogen-to-androgen ratio seem attractive possibilities, most data fail to support a primary role for abnormal hormonal function. Alternatively, a mechanism similar to that responsible for gynecomastia following refeeding of malnourished patients may be involved.