Dyslipoproteinemia and oxidative modification of low-density lipoprotein (oxLDL) contribute to the development of oxidative stress and atherosclerosis in chronic kidney disease (CKD). On the contrary, high-density lipoprotein cholesterol (HDL-C), especially HDL3-C subtype, has protective effect against oxidative damage. There is limited evidence referring HDL-C subclass levels in patients on dialysis. This study was designed to compare lipid abnormalities and oxLDL levels in hemodialysis (HD) and peritoneal dialysis (PD) patients. Serum lipids, HDL subclasses, and oxLDL were measured in 55 patients with CKD-stage 5 (31 patients on HD and 24 patients on PD) and in 21 normal controls (NC). The results showed that in dialysis patients, triglycerides were higher than in controls (p < 0.0001) and HDL-C was significantly lower (p < 0.0001). The HDL2-C subclass concentration did not differ significantly between patients and controls, while HDL3-C was lower in patients (11 ± 0.5 mg/dL) than in NC (23 ± 1, p < 0.0001). oxLDL levels were markedly increased in patients (1.92 ± 0.29 mg/L) compared to NC (0.22 ± 0.05, p < 0.0001). Patients on PD had higher levels of cholesterol (p < 0.001) and apolipoprotein B (p < 0.05) than patients on HD. However, HDL-C, HDL-C subclasses, and oxLDL concentrations did not differ significantly between PD and HD patients. It is concluded that patients with CKD have a nearly 10-fold elevation of oxLDL compared with NC. Patients on PD have differences in the lipid profile compared with patients on HD; however, both modalities seem to possess similar potential to atherosclerosis development.

In the article ''Oxidative stress markers and C-reactive protein in end-stage renal failure patients on dialysis'' by Elisabeth C. Samouilidou, Eirini J. Grapsa, Ioannis Kakavas, Antonios Lagouranis and Basilis Agrogiannis, published in International Urology and Nephrology-issue 35(3), pages 393-397, Fig. 2 was incorrect. Please find the correct figure below.

Patients with chronic kidney disease (CKD) are at high risk of atherosclerotic events; dyslipoproteinemia and the decrease of the HDL-linked enzyme paraoxonase 1 (PON1), might have a major role. This study intends to compare the association between lipid profile and serum PON1 levels in renal failure (RF) and hemodialysis (HD) patients. Serum lipids, HDL-subclasses and PON1 concentration were evaluated in 90 patients with CKD, divided into groups: RF (n ¼ 46) and HD (n ¼ 44), and in 30 normal individuals (control group). The results showed that PON1 was significantly lower in HD patients than in RF and controls (p50.001). In RF patients under statin therapy, PON1 did not differ from that of patients without statins. In HD patients without statins, PON1 was considerably low, whereas in HD with statins (30.42 ± 12.62 mg/mL) was lower than RF with statins (49.31 ± 14.94, p50.001). PON1 concentration was significantly and positively associated with HDL-C, HDL3-C and Apo A1 in all groups. Additionally, in HD patients PON1 was negatively associated with LDL-C. Multiple regression analysis revealed that LDL-C and statin treatment were independently related to PON1 concentration in HD patients (b ¼ À0.331, p ¼ 0.026 and b ¼ 0.344, p ¼ 0.020, respectively). In RF patients, HDL3-C and Apo A1 are strong determinants of PON1 levels. It is concluded that different parameters of lipid profile seem to affect serum PON1 concentration of RF and HD patients and probably contribute to the delay of atherosclerosis.ARTICLE HISTORY

Dialysis is associated with an impairment of antioxidant defense and an overproduction of oxidative stress markers. This study focuses on the comparison of plasma total antioxidant capacity (TAC) and lipid peroxidation products in patients on hemodialysis (HD) before and after treatment and in peritoneal dialysis (PD) patients. Plasma TAC, malonaldehyde (MDA), and 4-hydroxyalkenal concentrations were measured in 31 HD patients, in 24 PD patients, and in 17 normal controls (NC). It was found that before HD, TAC and MDA levels were higher than those in the NC (p < 0.001). After HD, these levels decreased significantly but were higher than in NC and lower than in PD patients (p < 0.001). The levels of 4-hydroxyalkenals were elevated in patients as compared with NC, but did not differ between HD and PD patients. The MDA concentrations correlated positively with the TAC in the patients. It is concluded that the oxidative status of patients on HD is similar to that of patients on PD and that the susceptibility to oxidative stress is strongly related to the levels of MDA produced in plasma.

SUMMARYIn a prospective study of 152 HIV-1 patients (with and without progression to AIDS) we examined CD28 MoAb costimulation and CD3 MoAb response using whole blood culture at baseline and up to either the time of AIDS diagnosis or the end of the observation period. CD28 antigen expression on both CD4 1 and CD8 1 T lymphocytes was also studied in both groups of patients. In patients who progressed to AIDS, CD28 MoAb costimulation was found to be decreased. Univariate time-dependent analysis showed that decreases in (i) absolute numbers of either CD4 1 , CD4 1 CD28 1 , CD8 1 CD28 1 T cells, (ii) CD28 MoAb costimulation, and (iii) CD3 MoAb response, and an increase in CD8 1 CD28 2 %, are significant predictors for progression to AIDS. In addition, multivariate time-dependent analysis demonstrated that a decrease in CD28 MoAb costimulation (but not a decrease in CD3 MoAb response) was predictive for progression to AIDS, as were decreases in the percentage of CD4 1 T cells and the absolute number of CD4 1 CD28 1 T cells. Thus, CD28 MoAb costimulation can be considered a useful assay for monitoring HIV-1 infection. Furthermore, apart from the early increase in the percentage of CD8 1 CD28 2 T cells and an increase in the percentage of CD28 2 on CD8 1 T cells in both groups of patients at baseline compared with normal controls, a negative correlation was found to exist between the percentages of CD4 1 or CD4 1 CD28 1 T cells and the percentage of CD8 1 CD28 2 T cells; this suggests that these cells are probably mutually regulated.

Thyrotropin receptors are expressed in several extrathyroidal tissues including bone. We investigated whether the increase of thyroid-stimulating hormone (TSH) levels, under stable thyroid hormone levels, affects the bone markers. Thirty-two postmenopausal women, with papillary thyroid carcinoma, previously treated with near-total thyroidectomy and I131 remnant ablation underwent routine evaluation for residual disease by using injections of recombinant human TSH (rhTSH) without withdrawal from thyroxine therapy. Changes in TSH levels and various serum and urine markers of bone metabolism were followed before and 1, 2, 5, and 7 days after the rhTSH injections. A transient, significant decrease in serum calcium and urinary excretion of C- and N-terminal telopeptides of type I collagen was observed after the injections of rhTSH. Serum parathyroid hormone (PTH) started to rise along with TSH, but a significant increase of PTH was only reached on Day 5 when the TSH concentration had fallen more than 80% of the peak value. Bone alkaline phosphatase and osteocalcin did not show any significant change over time. There was no significant correlation between TSH concentration and the various parameters we measured. The study provides evidence that rhTSH produces a transient inhibition of bone resorption, as well as an attenuation of osteoblast response in spite of the PTH activation. Additional studies are needed to resolve the mechanisms by which TSH alters the response of the bone cells.

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Background:Dyslipoproteinemia and oxidative modification of LDL (oxLDL) are common symptoms in patients suffering from chronic renal failure on hemodialysis (HD), and contribute to the development of oxidative stress. High-density lipoprotein cholesterol (HDL-C) protects against atherosclerosis by inhibiting the oxidation of lipoproteins and by supporting reverse cholesterol transport. This study intends to examine the association of oxLDL with HDL2 and HDL3 subclasses of HDL-C in HD patients, in order to elucidate whether oxidative stress influences HDL-C composition. Methods: Thirty-four patients on HD and 21 age- and sex-matched controls were studied. HDL2 and HDL3-C subclasses were isolated from serum according to a single-step precipitation method following a homogenous HDL-C assay. oxLDL was measured by ELISA. Results: In HD patients, oxLDL concentration was higher compared to the controls (1.40 ± 0.47 vs. 0.21 ± 0.05 mg/l, p = 0.017) and was significantly associated to total cholesterol (r = 0.480, p = 0.044), LDL-C (r = 0.544, p = 0.019), HDL-C (r = –0.589, p = 0.027) and C-reactive protein (r = 0.578, p = 0.024). Comparing HDL-C subclasses, only HDL2-C was negatively correlated to oxLDL levels (r = –0.565, p = 0.035). Conclusions: In HD patients, high serum levels of oxLDL are associated with low HDL2-C subclass levels. This might suggest that oxidative stress affects the HDL subclass more related to the protecting activity of HDL-C, contributing to atherosclerosis development.