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• W2092086586 abstract "Dear Sir,Markedly elevated Lp(a) concentrations have consistently been reported in patients with renal diseases and specifically in proteinuric patients and in patients receiving hemodialysis or chronic ambulatory peritoneal dialysis [1, 2, 3, 4]. Even though predialysis patients exhibit high serum Lp(a) levels [5, 6], there are sparse data with regard to serum Lp(a) concentrations in patients with mild/moderate renal failure [7, 8].Lipid parameters including Lp(a) were measured in the serum of 106 patients with mild/moderate renal failure (creatinine clearance 10–60 ml/min) of various causes. Patients with proteinuria (>0.5 g/24 h), severe secondary hyperparathyroidism (PTH levels >250 pg/ml), diabetes mellitus, endocrine or liver disease, malignancy, as well as patients treated with drugs that influence lipoprotein metabolism (lipid lowering agents, steroids, cyclosporin, and β-blockers) were excluded. One hundred and two healthy individuals matched for age and sex with the patients were used as controls. The serum lipid profile of both patients and controls is shown in table 1. Compared to the controls, patients with moderate renal failure exhibited increased serum concentration of triglycerides and decreased serum HDL cholesterol and ApoA1 levels. Serum Lp(a) concentration was also significantly increased in patients compared to controls. Additionally, the percentage of patients with increased (>30 mg/dl) serum Lp(a) levels was significantly higher in uremic patients compared to the control population (35 vs. 11.8%, p < 0.01). Serum Lp(a) levels were correlated with total cholesterol (r = 0.29, p < 0.02), LDL cholesterol (r = 0.35, p < 0.005) and ApoB (r = 0.32, p < 0.01) levels. On the other hand, no correlation was found between serum Lp(a) concentration and creatinine, albumin, PTH, as well as creatinine clearance, though there was a trend towards an inverse correlation between Lp(a) concentration and creatinine clearance (r = –0.24, p = 0.08).Our study showed that patients with mild-to-moderate renal failure devoid of factors that influence lipoprotein metabolism, such as hypoalbuminemia, glucose intolerance, and severe hyperparathyroidism exhibit increased serum Lp(a) concentration, along with the other more common lipid abnormalities observed in these patients. These results, as well as those previously found [7, 8], suggest that uremia per se could have influenced Lp(a) metabolism. It has been suggested that the kidney may play a direct role in the catabolism of Lp(a), and therefore the underlying renal failure, even though of modest degree, might result in elevated serum Lp(a) levels [1]. Alternatively, or synergically, the kidney may have an indirect influence on Lp(a) metabolism through either the secretion of a factor that regulates Lp(a) synthesis [9] or the presence of uremic toxins that can influence the regulatory mechanisms of Lp(a) synthesis in the liver and/or of the catabolic pathways [1].It should be mentioned that the weak positive correlation between total and LDL cholesterol as well as ApoB and Lp(a) is likely to reflect the possible, even though disputable, role of the LDL receptor in the Lp(a) catabolism." @default.
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• W2092086586 date "1998-01-01" @default.
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• W2092086586 title "Serum Lp(a) Levels in Patients with Moderate Renal Failure" @default.
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• W2092086586 doi "https://doi.org/10.1159/000045073" @default.
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