Altered ET-1 levels may be involved in the pathogenesis of rebound hypertension and hypotension during HD.

Background. Researches have recently reported that serum cystatin C is a more sensitive marker of changes in glomerular filtration rate (GFR) than serum creatinine. We conducted this study to evaluate the significance of serum cystatin C as a more sensitive marker of GFR for early detection of renal impairment in special groups of patients with type 2 diabetes mellitus (DM).Methods. The present study included 40 patients with type 2 DM divided into four equal groups based on their urinary albumin excretion and renal function: group 1 was normoalbuminuric, group 2 was microalbuminuric, group 3 was macroalbuminuric, and group 4 was macroalbuminuric with renal dysfunction. All patients underwent a thorough history, full clinical examination, fasting, and renal function tests. Post-prandial blood glucose levels, glycosylated hemoglobin A1c (HbA1c), proteins, albumin in 24 hr urine, and serum cystatin C were collected. Results. Serum cystatin C and creatinine were significantly higher in macrolbuminuric type 2 diabetic patients with renal dysfunction (group 4: 2.26 ± 1.28, 4.21 ± 2.38 mg/dl, respectively; p < 0.001) than macrolbuminuric type 2 diabetic patients with normal renal function (group 3: 1.04 ± 0.24, 0.96 ± 0.20 mg/dl, respectively), the microalbuminuric group (0.87 ± 0.28, 0.71 ± 0.12 mg/dl, respectively), as well as the normoalbuminuric group (0.55 ± 0.41, 0.60 ± 0.18 mg/dl, respectively). ROC plots demonstrated that area under the curve (AUC) of cystatin C (0.74) was greater than that for creatinine clearance (cr.cl) (0.67) and serum creatinine (s-cr) (0.74); therefore, the sensitivity and diagnostic accuracy of cystatin c was better than cr. cl., and both were better than s-cr. Serum cystatin C showed significant correlation in groups 2-4 with s-cr, cr.cl, and 24 hr urine albumin, but no correlation was found in group 1. Conclusion. Serum cystatin C is a reliable and easily performed marker for GFR to detect renal impairment in patients with type 2 DM.

Background: The expression of human leukocyte antigen (HLA)-G was studied in certain malignancies and its role in escaping from immunosurveillance in cancers was proposed since HLA-G is a non-conventional HLA class I molecule that protects the fetus from immunorecognition during pregnancy. Some particles involved in the regulation of an immune system might represent prognostic value for B-cell chronic lymphocytic leukemia (B-CLL). The identification of novel prognostic factors in B-CLL may help define patient subgroups that may benefit from early therapeutic intervention. Objective: To evaluate the prognostic significance of HLA-G expression in B-CLL patients and its relationship with other well-established prognostic markers. Methodology: Thirty B-CLL patients diagnosed by clinical, morphological and immunophenotyping criteria were studied for HLA-G expression by flow cytometry. The relationship between HLA-G expression and some known prognostic markers was evaluated. Results: HLA-G was expressed in 36.7% of CLL patients at diagnosis, with a mean expression level of 35.31 ± 12.35%. A significant association between HLA-G expression and common prognostic markers of progressive disease was detected. The group of patients with positive HLA-G expression showed significantly higher absolute lymphocyte counts and serum levels of LDH and β₂-microglobulin, lower platelet counts, positive CD38 expression and advanced stages of Binet clinical staging. Conclusion: The present study demonstrated that HLA-G expression correlates with prognostic markers of a poor B-CLL outcome, mainly Binet clinical staging and CD38 expression by B-CLL cells, which indicates that this parameter may play a role as an important prognosticator of disease progression and consequently targeted therapy in B-CLL.

Background: This study was carried out to assess the efficacy of intravenous administration of alfacalcidol once weekly versus thrice weekly in patients with poorly controlled secondary hyperparathyroidism. Methods: Thirty-six hemodialysis patients with intact parathyroid hormone (i-PTH) > 31.8 pmol/L were divided into two groups. Eighteen patients (Group 1) were given once weekly alfacalcidol for 6 months. The starting dose was 3 μg, which was increased or decreased by 1 μg per week. Eighteen patients (Group 2) were given thrice weekly alfacalcidol for 6 months. The starting dose was 1 μg, which was increased or decreased by 0.5 μg per dose. The dose was increased or decreased according to serum-corrected calcium (CCa), phosphorus (P), and i-PTH. Serum-CCa and P were measured weekly, whereas serum i-PTH and alkaline phosphatase were determined every month. Results: Intact-PTH reduced significantly (p < 0.001) from 86 ± 33.20 pmol/L to 31.04 ± 7.77 pmol/L and from 83.64 ± 32.12 pmol/L to 33.09 ± 11.37 pmol/L post-treatment in Groups 1 and 2, respectively. Fifty-six percent of the patients had i-PTH ≤ 31.8 pmol/L at the last observation. Serum alkaline phosphatase reduced significantly (p < 0.001) from 227.94 ± 129.86 IU/L to 163.17 ± 95.29 IU/L and from 285.39 ± 232.36 IU/L to 202.56 ± 165.84 IU/L post-treatment in Groups 1 and 2, respectively. There were no significant differences in serum levels of CCa, P, or their product. Conclusion: Intravenous alfacalcidol thrice or once weekly is safe and effectively reduced the levels of i-PTH in hemodialysis patients.

Background. Monocyte chemoattractant protein-1 (MCP-1) can directly elicit an inflammatory response by inducing cytokine and adhesion molecule expression in the kidney. We investigated the role of MCP-1 in the development of early nephropathy in patients with type-1 diabetes mellitus, in addition to the effect of high-dose vitamin E treatment (8 weeks) on early stages of diabetic nephropathy. Methods. This study was carried out on 30 type-1 diabetic patients subdivided into two equal groups according to their urinary albumin excretion, in addition to 10 healthy matched volunteers included as controls. MCP-1, glycated hemoglobin (HbA1c), and albuminuria-before and after vitamin E treatment-were measured in all studied groups. Results. Serum MCP-1 and HbA1c were significantly elevated in patients with microalbuminuria and poor glycemic control (941.67 ± 47.03 pg/mL; 16.95 ± 2.74%) compared to normoalbuminuric diabetic patients (622.73 ± 103.23 pg/mL; 7.23 ± 0.86%), and controls (366.60 ± 129.01; 3.35 ± 0.66) (P = .001), respectively. There was positive correlation between MCP-1 and HbA1c. Both MCP-1 and albuminuria decreased significantly after using high-dose vitamin E treatment, though there was no change in HbA1c in type-1 diabetic patients with early nephropathy. Conclusion. These observations suggest that MCP-1 may be involved in the pathogenesis of diabetic nephropathy. High-dose vitamin E may provide a novel form of therapy for the prevention of microvascular complications in type-1 diabetic patients.