Low serum testosterone, arterial stiffness and mortality in male haemodialysis patients.

BACKGROUND: In the general population, accumulating data support a link between low testosterone levels and mortality by all causes, but especially by cardiovascular disease (CVD). Also, accelerated arterial stiffness has been recognized as an important cardiovascular risk factor. Here, we explored the association between testosterone levels and risk of death in male haemodialysis (HD) patients, whose arterial system is characterized by generalized stiffening. METHODS: In this three-centre prospective observational study, 111 male HD patients after completion of baseline assessment, including measurement of male sex hormones and pulse wave velocity (PWV), were followed up for CVD and all-cause mortality. RESULTS: Of the 111 patients studied, 54 were found with and 57 without testosterone deficiency, defined as testosterone levels <8 nmol/L. During a median follow-up period of 37 months, 49 deaths occurred, 28 (57%) of which were caused by CVD. Testosterone deficiency patients had increased CVD and all-cause mortality {crude hazard ratio: 3.14 [95% confidence interval (CI), 1.21-8.16] and 3.09 (95% CI, 1.53-6.25), respectively}, even after adjustment for age, body mass index, serum albumin and C-reactive protein, prevalent CVD and HD vintage. The association of testosterone with CVD mortality, but not with all-cause mortality, was lost after adjusting for PWV, an index of arterial stiffness. Testosterone levels were inversely related to PWV (r = -0.441; P < 0.001). CONCLUSION: We showed that testosterone deficiency in male HD patients is associated with increased CVD and all-cause mortality and that increased arterial stiffness may be a possible mechanism explaining this association.

Magnesium carbonate for phosphate control in patients on hemodialysis. A randomized controlled trial.

BACKGROUND: Magnesium salts bind dietary phosphorus, but their use in renal patients is limited due to their potential for causing side effects. The aim of this study was to evaluate the efficacy and safety of magnesium carbonate (MgCO(3)) as a phosphate-binder in hemodialysis patients. METHODS: Forty-six stable hemodialysis patients were randomly allocated to receive either MgCO(3) (n=25) or calcium carbonate (CaCO(3)), (n=21) for 6 months. The concentration of Mg in the dialysate bath was 0.30 mmol/l in the MgCO(3) group and 0.48 mmol/l in the CaCO(3) group. RESULTS: Only two of 25 patients (8%) discontinued ingestion of MgCO(3) due to complications: one (4%) because of persistent diarrhea, and the other (4%) because of recurrent hypermagnesemia. In the MgCO(3) and CaCO(3) groups, respectively, time-averaged (months 1-6) serum concentrations were: phosphate (P), 5.47 vs. 5.29 mg/dl, P=ns; Ca, 9.13 vs. 9.60 mg/dl, P<0.001; Ca x P product, 50.35 vs. 50.70 (mg/dl)(2), P=ns; Mg, 2.57 vs. 2.41 mg/dl, P=ns; intact parathyroid hormone (iPTH), 285 vs. 235 pg/ml, P<0.01. At month 6, iPTH levels did not differ between groups: 251 vs. 212 pg/ml, P=ns. At month 6 the percentages of patients with serum levels of phosphate, Ca x P product and iPTH that fell within the Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines were similar in both groups, whereas more patients in the MgCO(3) group (17/23; 73.91%) than in the CaCO(3) group (5/20, 25%) had serum Ca levels that fell within these guidelines, with the difference being significant at P<0.01. CONCLUSION: Our study shows that MgCO(3) administered for a period of 6 months is an effective and inexpensive agent to control serum phosphate levels in hemodialysis patients. The administration of MgCO(3) in combination with a low dialysate Mg concentration avoids the risk of severe hypermagnesemia.

Prostate-specific antigen in hemodialysis patients and the influence of dialysis in its levels.

The determination of prostate-specific antigen (PSA) is a useful tool in the diagnosis and follow-up of prostate cancer in males, but its diagnostic validity is uncertain in hemodialysis patients. We prospectively evaluated PSA in male hemodialysis patients as well as the influence of a single dialytic session on its levels. We measured pre- and postdialysis total PSA (tPSA) in 63 hemodialysis patients (mean age 68.44 +/- 11.16 years, range 33-86 years) who had received dialysis with low flux membranes as well as in 729 normal subjects (mean age 63.22 +/- 16.85 years, range 28-92 years). We also measured pre- and postdialysis hematocrit (Hct) in patients in order to estimate the degree of hemoconcentration after the dialysis session. If any of the examined patients or subjects had abnormal tPSA levels then free PSA (fPSA) and the f/tPSA ratio were additionally measured. Patients had lower levels of tPSA compared with those of the subjects (2.41 +/- 4.06 vs. 3.76 +/- 7.16 ng/ml, p < 0.05) while both of the two groups had near equal prevalence of individuals with abnormal values of tPSA or f/tPSA ratio (patients 12.69 and 7.93%, subjects 11.01 and 7.11%, respectively; nonsignificant. Dialysis resulted in a 9.48% increase in mean tPSA levels (2.41 +/- 4.06 vs. 2.69 +/- 4.06 ng/ml, nonsignificant) and in a 10.09% increase in mean Hct; the correlation between these increases was significant (r = 0.79, p < 0.001). In conclusion, our male hemodialysis patients had lower PSA levels compared with the general population, while both groups of individuals had a similar prevalence of abnormal values of tPSA and f/tPSA ratio. Dialysis with low flux membranes does not eliminate PSA and its postdialysis increase is due to hemoconcentration.