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INTRODUCTION: Insulin resistance (IR) is a known complication of end-stage kidney disease (ESKD). It may be an important therapeutic target in stages of chronic kidney disease. AIM: The study was conducted to evaluate the effect of short-term treatment with recombinant human erythropoietin (rHuEpo) therapy on IR, serum leptin, and neuropeptide Y in ESKD patients on hemodialysis. MATERIALS AND METHODS: Thirty ESKD patients were enrolled in the study and were randomly assigned into two groups. Erythropoietin (rHuEpo) group consisted of 15 patients (7 females, 8 males, mean age 47.8 ± 9.3 years) treated with rHuEpo therapy after each session of dialysis. No-rHuEpo group consisted of 15 patients (7 females, 8 males, mean age 45.5 ± 8.6 years) not treated with rHuEpo. In addition to, control group consisted of 15 healthy controls (6 females, 9 males, mean age 48.8 ± 11 years). RESULTS: The mean fasting insulin (11 ± 4.2 mU/L) and homeostatic model assessment of IR (HOMA-IR) test (2.6 ± 1.1) were significantly higher in ESKD patients than control group (6.6 ± 1.4 mU/L and 1.5 ± 0.3, respectively). There were significant decreases in glycated hemoglobin (HbA1c) (5.6 ± 1%), fasting insulin level (9.3 ± 3.1 µU/mL), HOMA-IR (2.2 ± 0.7), and serum leptin levels (17.4 ± 8.7 ng/mL) also significant increase in neuropeptide Y levels (113 ± 9.9 pg/mL) after 3 months of rHuEpo therapy, in addition to further significantly decrease fasting insulin levels (7.1 ± 2.1 µU/mL) and HOMA-IR (1.7 ± 6) after 6 months in rHuEpo group. In contrast, there were significantly increases in HbA1c% (5.9 ± 0.5%) and leptin levels (42.3 ± 25.3 ng/mL) in No-rHuEpo group throughout the study. CONCLUSION: IR and hyperleptinemia are improved by recombinant human erythropoietin therapy.
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BACKGROUND: Uremia is a vasculopathic process, and both cardiac calcification and vascular calcification seen from the early stages of chronic kidney disease. Osteoprotegerin could play a crucial role in atherosclerotic plaque formation, maturation and calcification. The goal of this study was to determine the relationship of serum osteoprotegerin with vascular calcification in patients with end stage kidney disease who were maintained on regular hemodialysis. METHODS: Sixty clinically stable chronic renal failure patients undergoing regular hemodialysis were enrolled in this cross sectional study. Thirty patients (mean age 56.7 ± 10.5 years) with abdominal aortic calcification were selected by basal abdominal X-ray who underwent multi-slice computerized tomography scan to measure coronary artery calcification score; and thirty patients (mean age 56.5 ± 8.4 years) without abdominal aortic calcification. All patients were evaluated by serum calcium, phosphorus, albumin, lipid profile, intact parathyroid hormone (iPTH), serum creatinine, serum urea, serum uric acid, serum C-reactive protein, and hemoglobin. Serum osteoprotegerin samples were collected before dialysis and estimated by the ELISA kit. RESULTS: Serum osteoprotegerin level was significantly higher in patients with vascular calcification than in those without calcifications. Serum osteoprotegerin correlated positively with serum phosphorus, calcium phosphorus product, alkaline phosphatase, iPTH, C-reactive protein, serum uric acid, low-density lipoprotein (LDL) and left ventricular mass index (LVMI) (p < 0.005), and negatively with hemoglobin, ejection fraction (p < 0.005) and HDL (p < 0.05). CONCLUSIONS: These findings suggest that osteoprotegerin may be involved in the development of vascular calcification in hemodialysis patients.
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BACKGROUND: Leukocyte adhesion molecules are important for migration of the inflammatory cells into sites of inflammation. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are members of the immunoglobulin superfamily that are expressed in normal kidney. Their expression is up-regulated in the renal tissue of patients with lupus nephritis (LN). OBJECTIVES: We evaluated whether changes in urinary levels of ICAM-1 and VCAM-1 reflect renal tissue damage in LN. We related the levels of these molecules to other laboratory findings, especially complement C3/C4 levels. We also tested the hypothesis that changes in urinary levels of ICAM-1 and VCAM-1 reflect the severity of renal tissue damage in LN. PATIENTS AND METHODS: This study included 30 systemic lupus erythematosus (SLE) patients with LN (16 with mild histological changes, i.e., with World Health Organization (WHO) class I and II LN, and 14 with advanced histological changes, i.e., class III, IV, and V LN) and 20 with SLE without nephritis. In addition, 20 healthy individuals of comparable age were included as a control group. The levels of urinary ICAM-1 and VCAM-1 were measured by enzyme-linked immunosorbent assay (ELISA) and related to the clinical, laboratory [rheumatoid factor(RF), antinuclear antibodies (ANA), anti-double-stranded DNA (anti-dsDNA), complements C3 and C4] and histological findings. RESULTS: Levels of urinary ICAM-1 and VCAM-l in LN patients with advanced histological changes (renal damage) were statistically significantly higher than those in other groups (LN patients with mild histological changes or SLE patients without nephritis and control group; p < 0.01). In contrast, serum levels of C3 and C4 in LN patients with advanced histological changes were significantly lower than those in other groups (p < 0.01). There was a significant negative correlation between the levels of urinary adhesion molecules and serum complement levels (p < 0.01). CONCLUSIONS: The significantly high urinary levels of the adhesion molecules in the LN group with advanced histological changes may reflect their renal tissue expression and therefore the severity of the nephritis. Renal tissue damage in these cases may be the result of transmigration of activated inflammatory cells, inducing serious tissue damage. The hypocomplementemia combined with increased urinary levels of adhesion molecules seems to be a useful biomarker of disease severity in LN.