Bone deposition after 1 year of treatment with LC is low (highest concentration: 5.5 microg/g). There is a slow release of lanthanum from its bone deposits 2 years after the discontinuation of the treatment and no association with aluminium-like bone toxicity.

No abstract

Patients with AIC and AMC are frequently found in the HD population. Screening for arterial calcifications in chronic kidney disease patients is suggested even in the early pre-dialysis period. The highest proportion of patients within the guidelines proposed range for bone and mineral metabolism markers was observed in the NC group. A longer period of data analysis is required in order to evaluate the possible role of some traditional and HD-specific risk factors for the development of arterial calcifications. The achievement of the K/DOQI guidelines is an important issue in the prevention of those conditions.

Our study showed that ER above 12 months before HD initiation and L-start of dialysis was associated with a reduced mortality risk in HD patients.

Acquired renal cystic disease (ARCD) is a well documented complication of end-stage renal disease, and it has been related to the duration of dialysis therapy. The association of this condition with renal cell adenoma or carcinoma has already been established. There have also been studies on the concentration of some tumor markers in hemodialysis (HD) patients, clinically free from neoplastic disease, where it was concluded that some tumor markers could be elevated, despite the absence of malignant disease, suggesting their altered metabolism i.e. clearance by the hemodialysis membrane. We compared the pre-dialysis serum concentration of several tumor markers in three groups of chronic HD patients, all of whom had been on maintenance HD treatment for more than 5 years. Group 1 consisted of 16 patients without ARCD with a mean HD treatment duration of 97.06 +/- 28.25 months. Group 2 consisted of 32 patients with a mean HD treatment of 105.62 +/- 24.4 months, who had ARCD with less than 10 renal cysts detected by ultrasonography. Group 3 consisted of 14 patients with a mean HD duration of 109.92 +/- 37.72 months, with ARCD and more than 10 renal cysts. Concentration of the following tumor markers was determined by EIA or ELISA methods: carcinoembryonic antigen (CEA), mucin-like carcinoma-associated antigen (MCA), neuron-specific enolase (NSE), carbohydrate antigen 19-9 (CA 19-9), prostatic specific antigen (PSA), carbohydrate antigen 125 (CA 125), alpha fetoprotein (AFP), cytokeratin 19-fragments 21-1 (CYFRA 21-1). The concentration of all the tumor markers was comparable in all three patient groups, with no statistically significant difference between groups. The mean concentrations of MCA, PSA, CA 125 and AFP were within the normal range. CEA and CYFRA 21-1 had mean values in the upper limit of their normal values, while NSE and CA 19-9 were increased by more than twofold in all three patient groups. We concluded that (i) tumor markers should be used with caution when diagnosing neoplastic diseases in chronic HD patients, because of their altered metabolism, and (ii) that in the follow up of ARCD with possible neoplastic alteration, imaging techniques remain dominant diagnostic tools.