Background: Statins can cause tubular proteinuria by inhibiting tubular reabsorption of urinary proteins. To distinguish between microalbuminuria originating from glomerular leakage of albumin and tubular microalbuminuria due to statin therapy, the alpha(1)-microglobulin/albumin ratio is evaluated in patients taking statins and compared to untreated patients.Methods: Ten apparently healthy subjects were given 40 mg of simvastatin and tested for urinary alpha(1)-microglobulin, albumin, creatinine and cystatin C, up to 24 h after administration. Additionally, urine samples of 76 statin-treated and 456 untreated patients presenting with micro-albuminuria (albuminuria range between 20 and 200 mg/L) were tested for alpha(1)-microglobulin and albumin. alpha(1)-Microglobulin/albumin ratios were compared. Total cholesterol was measured in 50 patients on statin therapy.Results: In the 10 apparently healthy subjects, a significant temporary increase of alpha(1)-microglobulin, albumin and alpha(1)-microglobulin/albumin ratio was observed after statin intake. In the group of 532 patients showing microalbuminuria, those treated with statins showed a significantly higher mean urinary alpha(1)-microglobulin/albumin ratio then untreated patients. Urinary albumin concentrations were significantly higher in patients taking simvastatin than in patients on rosuvastatin treatment and they were also higher in patients on statin therapy with a total serum cholesterol concentration below 3.88 mmol/L than in patients with a total serum cholesterol concentration above 5.17 mmol/L.Conclusions : Tubular proteinuria, caused by the use of statins, can be distinguished from glomerular proteinuria by a higher urinary alpha(1)-microglobulin/albumin ratio.

CONTEXT:Lipotoxicity is a risk factor for developing obesity-related metabolic complications, including non-alcoholic fatty liver disease, type 2 diabetes (DM2), cardiovascular disease and stroke. Yet, the mechanisms underlying the development of lipotoxicity itself remain poorly understood. Here, we investigated whether glucose intolerance aggravates lipotoxicity by evaluating the association between triglyceride (TG) concentrations and glucose tolerance status in a cross-sectional study on obese Caucasian women at risk for DM2.METHODS:913 obese females unknown to have diabetes were recruited (mean age: 41.2 ± SD 12.3; median BMI: 36.2, IQR 32.9-40.2). Visceral (VAT) and subcutaneous abdominal adipose tissue volumes were quantified with computed tomography. Glucose, insulin, and triglyceride concentrations were determined in fasting state and following a 75 gram oral glucose tolerance test.RESULTS:Based on fasting and 2 h post-load glucose levels, 27% of the women had impaired glucose tolerance (IGT), and 8% had newly diagnosed DM2. Fasting TG concentrations were similar between the IGT- and DM2-groups, and increased as compared to women with normal glucose tolerance (NGT). Even when adjusting for age, hip circumference and VAT, fasting TG concentrations remained elevated as compared to NGT. Mixed modelling analysis of post-load responses showed that TG concentrations declined more slowly in the DM2-group as compared to IGT and NGT. However, when adjusting for VAT the difference in decline between the glucose tolerance groups disappeared.CONCLUSIONS:Glucose intolerance associates with elevated fasting TG concentrations in obese Caucasian women. We propose that glucose intolerance and increased VAT reduce lipid disposal mechanisms and may accelerate lipotoxicity.

Background: Multiple human and animal studies have reviewed the (non-)actin scavenger functions of vitamin D binding protein (DBP). Recently, we demonstrated the partially lipid bound character of DBP. The purpose of the present study was to explore the link between actin, lipids and DBP in a cohort of patients undergoing cardiac surgery.Methods: The interplay between DBP, actin and lipids was investigated in a cohort study of 35 Caucasian patients who underwent cardiac surgery. Total and actin-free DBP concentrations were assessed by immunonephelometry and ELISA. Total cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, creatine kinase (-MB) and C-reactive protein (CRP) were measured using routine methods. Low-density lipoprotein cholesterol was calculated according to the Friedewald formula. The DBP phenotypes and the macromolecular bound DBP fractions were determined by polyacrylamide gel electrophoresis (PAGE) and confirmed by Western blotting.Results: Using PAGE and Western blotting with an antihuman DBP polyclonal antibody, the actin-bound DBP complex was identified in serum. Following cardiac surgery, total serum DBP concentrations were characterized by a two phased course. This was paralleled by a similar pattern in serum total cholesterol, HDL-cholesterol and triglyceride concentrations. Good correlation was found between total and actin free serum DBP concentrations (r=0.69, p<0.0001). The serum actin free DBP/total DBP ratio remained stable throughout the study period. Although no significant correlation between cumulative CK-MB enzyme release and delta serum total DBP concentration was observed (p=NS), the latter value correlated significantly with delta serum triglyceride concentrations (r=0.37, p<0.05).Conclusions: The lipid bound character is an underestimated property of DBP in the extracellular actin-scavenger system. Clin Chem Lab Med 2010;48:1345-50.

Cardiac autoimmunity has been widely studied over the last years. A lot of cardiac antigens have been identified. Laboratory tests for detection of antibodies against the heart are very helpful in diagnosing and monitoring cardiac autoimmune diseases, but the prevalence of anti-heart antibodies varies a lot between the tests. The aim of this paper is to review the number of laboratory assays used today and to determine the most suitable test for detection of cardiac autoantibodies in human serum.

Background: Vitamin D binding protein (DBP) is a multifunctional transport protein with a decreased serum concentration in cystic fibrosis (CF). The present study investigates the importance of DBP and its role as an alternative nutritional marker in CF.Methods: DBP phenotypes of 116 CF patients were determined electrophoretically. Serum DBP was measured by immunonephelometry. Parathormone was assessed by an immunoradiometric assay. Serum 25OH vitamin D-3, 1,25(OH)(2) vitamin D-3 and leptin concentrations were determined by a radioirnmunoassay. Serum a-tocopherol was measured by HPLC. Routine chemistry parameters were assessed using commercial methods. The Prognostic Inflammatory and Nutritional Index was calculated.Results: Decreased serum DBP concentrations were observed in the CF group. Total cholesterol, low-density lipoprotein (LDL)-cholesterol, triglyceride concentration, a-tocopherol and a low nutritional status correlated positively with DBP. Lipoprotein precipitation demonstrated a partial presence of DBP in very-low-density lipoprotein and LDL. Furthermore, DBP was positively correlated with serum leptin concentration.Conclusions: The present study demonstrates a positive correlation between DBP and serum lipids. Serum DBP concentration can be considered as a nutritional marker (especially for lipids).

OBJECTIVE:Vitamin D binding protein (DBP) is a polymorphic serum protein with a predominant role in a spectrum of biological activities. Chronic renal failure is characterized by deficient vitamin D metabolism. The present study investigates the impact of DBP polymorphism on the need for vitamin D in hemodialysis patients.DESIGN:This was a retrospective study.SETTING:This study included hemodialysis patients from the Renal Unit of Ghent University Hospital (Ghent, Belgium) and the Algemeen Stedelijk Ziekenhuis Geraardsbergen Hospital (Geraardsbergen, Belgium).METHODS:One hundred and ninety-one hemodialysis patients and 211 healthy subjects were recruited from the hemodialysis database. The DBP phenotypes were determined by polyacrylamide gel electrophoresis. Serum DBP, parathyroid hormone, 25-hydroxyvitamin D(3), 1,25-dihydroxyvitamin D(3), calcium, albumin, and phosphate were measured. Information regarding the intake of vitamin D analogues was collected.RESULTS:The phenotypic distributions of DBP were in agreement with Hardy-Weinberg equilibrium. Comparing allele frequencies of the two groups, there was an increased proportion of the DBP 2 allele in hemodialysis patients (P < .05). The median serum DBP concentration was lowest in the DBP 2-2 group. The need for oral vitamin D differed significantly (P < .01) between DBP phenotypes, and was greatest in DBP 2-2.CONCLUSIONS:The present study demonstrates an altered DBP allele frequency in hemodialysis patients, compared with the general population. More importantly, vitamin D intake differs depending on the DBP polymorphism, and is greatest for end-stage renal disease patients with a DBP 2-2 phenotype. Therefore, vitamin D treatment deserves more careful monitoring among DBP 2-2 patients with end-stage renal disease.

Journal of Pediatric Gastroenterology and NutritionVolume 42, Issue 5 p. E89-E90-E89-E90 Notices: 39th Annual Meeting of the European Society for Pediatric Gastroenterology, Hepatology and Nutrition Dresden, Germany, June 7-10, 2006: Abstracts: PN2-03 VITAMIN D SERUM LEVELS (VDSL) IN CYSTIC FIBROSIS (CF) RESULT FROM SUN NOT FROM ORAL SUPPLEMENTS ER Robberecht, ER Robberecht Cystic Fibrosis Center, Dept. Pediatrics, Ghent, BelgiumSearch for more papers by this authorSV Vandewalle, SV Vandewalle Cystic Fibrosis Center, Dept. Pediatrics, Ghent, BelgiumSearch for more papers by this authorCW Wehlou, CW Wehlou Cystic Fibrosis Center, Dept. Pediatrics, Ghent, BelgiumSearch for more papers by this author ER Robberecht, ER Robberecht Cystic Fibrosis Center, Dept. Pediatrics, Ghent, BelgiumSearch for more papers by this authorSV Vandewalle, SV Vandewalle Cystic Fibrosis Center, Dept. Pediatrics, Ghent, BelgiumSearch for more papers by this authorCW Wehlou, CW Wehlou Cystic Fibrosis Center, Dept. Pediatrics, Ghent, BelgiumSearch for more papers by this author First published: 01 May 2006 https://doi.org/10.1002/j.1536-4801.2006.tb01959.xRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Volume42, Issue5May 2006Pages E89-E90-E89-E90 RelatedInformation