Intra- and extracellular magnesium levels and atheromatosis in haemodialysis patients.

Traditional risk factors do not adequately explain the high prevalence of cardiovascular disease in patients with chronic renal insufficiency. Currently, there is a lot of evidence that hypomagnesaemia may play a significant role in the pathogenesis of cardiovascular diseases in general population. The aim of this study was to test the hypothesis that magnesium status in haemodialysis patients is related to the degree of atheromatosis of carotid arteries, as assessed by B-mode ultrasound. Intima-media thickness of both common carotids was assessed by B-mode ultrasound in 93 stable chronic haemodialysis patients and in 182 age- and sex-matched healthy controls. Intracellular magnesium as well as serum magnesium levels were obtained in the haemodialysis patients. Intracellular magnesium was estimated by determination of this ion in isolated peripheral lymphocytes. Haemodialysis patients had also a significantly higher mean common carotid intima-media thickness than controls (0.87+/-0.16 vs 0.76+/-0.13 mm, p < 0.001). Multivariate analysis revealed that in haemodialysis patients both serum magnesium and intracellular magnesium were negatively associated with common carotid intima-media thickness (p = 0.001 and p = 0.003 respectively). Significant associations between the age of the haemodialysis patients, the existence of diabetes mellitus as well as the serum calcium x serum phosphate product with common carotid intima-media thickness of haemodialysis patients were also observed. A strong negative association of both extracellular and intracellular magnesium with common carotid intima-media thickness exists in haemodialysis patients. The above finding suggests that magnesium may play an important protective role in the development and/or acceleration of arterial atherosclerosis in patients with chronic renal insufficiency.

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.