IMPOTENCE: II
Authors: Charney David L. , Walton Daniel F. , Cheung Alfred K. 
Published: October 2007

In January of 1992, a 61‐year‐old white male chronic hemodialysis patient complained of impotence. He described a decrease in the rigidity and the length of time he could maintain an erection, as well as a decrease in the frequency of erections. He had been on maintenance hemodialysis since April, 1989 when he presented with end‐stage renal disease (ESRD) of unknown etiology. He had a remote history of renal calculi and pyelonephritis. Prior to starting dialysis, he had been treated for hypertension with clonidine and later enalapril. His noninsulin‐dependent diabetes mellitus was diet controlled for four years prior to his being seen at this institution. He had smoked less than five pack years in the remote past.

Since starting dialysis he had required no medication for diabetes or hypertension. Subcutaneously administered erythropoietin was used to maintain his hematocrit at 33%‐35%. Other routine medications included vitamins and phosphate binders. He occasionally used ibuprofen for capsulitis of the right shoulder, concurrently with ranitidine for ulcer prophylaxis. He declined renal transplantation. His only problem on dialysis had been interdialytic weight gains of 3–6 kg. Benign gynecomastia noted after the initiation of dialysis therapy resolved spontaneously, prior to the development of impotence. His dialysis dosage was considered reasonable, with multiple evaluations yielding an average delivered Kt/V of 1.4.

Psychological evaluation found him to be well adjusted to dialysis and to have a stable family life. He had no prior history of sexual problems and the onset of his problem was described as gradual. His sexual dysfunction began more than two years after starting dialysis and affected erectile function rather than libido.

Physical examination revealed a robust appearing, normotensive 61‐year‐old man weighing 102 kg, with a height of 1.8 meters. Cardiopulmonary examination was within normal limits. Abdominal examination was free of bruits and hepatosplenomegaly. Pulses were full and equal in the extremities. Rectal examination was unremarkable, with a normal prostate and rectal sphincter tone. Testes were normal in size and free of masses. Phallus was normal in appearance and no plaques of Peyronie's disease were detected. Gait was normal and there was no evidence of peripheral neuropathy.

After discussion of the various treatment options, empiric therapy was started at the patient's request with testosterone enanthate 200 mg IM every two weeks. Although the patient reported a slight improvement shortly after the dose was given and requested a dosage increase, the overall response to six months of therapy was unsatisfactory. An endocrinologic evaluation was performed to determine the adequacy of the prescribed dose. This revealed a testosterone level of 351 ng/dl (normal 300–890 ng/dl). Follicle‐stimulating hormone (FSH) and luteinizing hormone (LH) levels were both found to be appropriately suppressed at <0.3 mIU/ml (normal LH 0.9–10.6 mIU/ml and FSH 2.4–19.9 mIU/ ml). A serum prolactin level drawn simultaneously was mildly elevated at 22.9 ng/ml (normal 0.1–18.1 ng/ml). Thyroid function tests were normal. Intact parathyroid hormone levels during this time period ranged from 13–66 pcg/ml (normal 10–75 pcg/ml) and aluminum levels were 10 μg/ml (normal 1–39 μg/ml). No increase in dose of testosterone was given. Of note is that elevations of serum triglycerides occurring during the testosterone therapy required the addition of gemfibrozil for treatment.

Urologic consultation was obtained and the patient initially considered the purchase of a vacuum‐constrictor device. However, this proved to be too costly and he therefore agreed to learn to perform self‐injection of intracavernosal papaverine, and to be tapered off testosterone injections.