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.

In order to define the type of renal disease, renal biopsy was performed in 1304 patients, aged 14-72 years. Their biopsies were processed for light and immunofluorescence microscopy, and electron microscopy in some cases. The diagnosis of primary glomerular disease was confirmed in 716 patients with the following incidence: minimal change nephrotic syndrome in 52 (7.2%), focal segmental glomerulosclerosis in 72 (9.9%), membranous nephropathy in 97 (13.5%), IgA nephropathy in 85 (11.8%), diffuse mesangial glomerulonephritis (GN) without IgA in 32 (4.4%), focal mesangial GN in 97 (13.5%), membranoproliferative GN in 59 (8.4%), acute GN in 88 (12.3%), crescentic GN in 53 (7.4%) and sclerosing GN in 46 patients (6.4%).

No abstract

Mycophenolate mofetil (MMF) is an immunosuppressive drug successfully used for the prevention of acute and chronic rejection of renal allografts, as well as in the therapy of glomerular disorders. We treated three groups of patients with lupus nephritis: the first group of patients had a high histologic activity index (AI), 13.4 +/- 2.34; the second group of patients had a high histologic chronicity index (CI), 6.0 +/- 0.7; and the third group consisted of only two patients, one with low AI (3.5) and another with low CI (1.5). The patients were treated for 2 years. MMF was initiated at a dose of 2 g/daily for the first 6 months and the dose was decreased to 1.5 g/daily for the further 18 months. Steroids, 0.4 mg/kg/day, were the concomitant therapy for the first 6 months, with slow tapering for the further 18 months. Patients with high AI presented significant decrease of serum creatinine after 2 years, 286 +/- 112.95 to 131.2 +/- 44.65 micromol/L. Two of the patients, with acute oligoanuria, were withdrawn from dialysis treatment. Significant improvement was also noted, 6.97 +/- 1.81 to 0.9 +/- 0.31 g/day. Patients with high CI had nonsignificant decrease of serum creatinine, 178.5 +/- 47.73 to 129.25 +/- 22.88 micromol/L, and significant improvement of proteinuria, 4.63 +/- 1.57 to 1.14 +/- 0.39 g/day. The patient with low AI showed recovery of renal function (serum creatinine from 196 to 72 micromol/L) and alleviation of proteinuria, 7.93 to 3.4 g/day. The patient with low CI did not respond to the therapy and renal function slowly worsened. MMF has emerged as a promising therapeutic approach for both the induction and maintenance phase in patients with lupus nephritis.

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.