| pubmed-article:16788210 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16788210 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:16788210 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:16788210 | lifeskim:mentions | umls-concept:C0022646 | lld:lifeskim |
| pubmed-article:16788210 | lifeskim:mentions | umls-concept:C0033687 | lld:lifeskim |
| pubmed-article:16788210 | lifeskim:mentions | umls-concept:C0025519 | lld:lifeskim |
| pubmed-article:16788210 | lifeskim:mentions | umls-concept:C0052181 | lld:lifeskim |
| pubmed-article:16788210 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:16788210 | pubmed:dateCreated | 2006-8-22 | lld:pubmed |
| pubmed-article:16788210 | pubmed:abstractText | Increased plasma concentrations of apolipoprotein A-IV (apoA-IV) in chronic renal disease suggest a metabolic role of the kidney for this antiatherogenic protein. Therefore, we investigated patients with various forms of proteinuria and found increased serum concentrations of apoA-IV in 124 nephrotic patients compared with 274 controls (mean 21.9 +/- 9.6 vs. 14.4 +/- 4.0 mg/dl; P < 0.001). Decreasing creatinine clearance showed a strong association with increasing apoA-IV levels. However, serum albumin levels significantly modulated apoA-IV levels in patients with low creatinine clearance, resulting in lower levels of apoA-IV in patients with low compared with high albumin levels (21.4 +/- 8.6 vs. 29.2 +/- 8.4 mg/dl; P = 0.0007). Furthermore, we investigated urinary apoA-IV levels in an additional 66 patients with a wide variety of proteinuria and 30 controls. Especially patients with a tubular type of proteinuria had significantly higher amounts of apoA-IV in urine than those with a pure glomerular type of proteinuria and controls (median 45, 14, and 0.6 ng/mg creatinine, respectively). We confirmed these results in affected members of a family with Dent's disease, who are characterized by an inherited protein reabsorption defect of the proximal tubular system. In summary, our data demonstrate that the increase of apoA-IV caused by renal impairment is significantly modulated by low levels of serum albumin as a measure for the severity of the nephrotic syndrome. From this investigation of apoA-IV in urine as well as earlier immunohistochemical studies, we conclude that apoA-IV is filtered through the normal glomerulus and is subsequently reabsorbed mainly by proximal tubular cells. | lld:pubmed |
| pubmed-article:16788210 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16788210 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16788210 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16788210 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16788210 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16788210 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16788210 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16788210 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16788210 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:16788210 | pubmed:issn | 0022-2275 | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:KronenbergFlo... | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:KönigPaulP | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:LhottaKarlK | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:NeyerUlrichU | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:von... | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:DieplingerHan... | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:LingenhelArno... | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:SchoberMariaM | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:KronenbergMar... | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:RantnerBarbar... | lld:pubmed |
| pubmed-article:16788210 | pubmed:author | pubmed-author:HeidIris MIM | lld:pubmed |
| pubmed-article:16788210 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16788210 | pubmed:volume | 47 | lld:pubmed |
| pubmed-article:16788210 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16788210 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16788210 | pubmed:pagination | 2071-9 | lld:pubmed |
| pubmed-article:16788210 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:meshHeading | pubmed-meshheading:16788210... | lld:pubmed |
| pubmed-article:16788210 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16788210 | pubmed:articleTitle | Role of the kidney in the metabolism of apolipoprotein A-IV: influence of the type of proteinuria. | lld:pubmed |
| pubmed-article:16788210 | pubmed:affiliation | Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Innsbruck, Austria. | lld:pubmed |
| pubmed-article:16788210 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16788210 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:16788210 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:337 | entrezgene:pubmed | pubmed-article:16788210 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:16788210 | lld:entrezgene |
| lhgdn:association:35136 | lhgdn:found_in | pubmed-article:16788210 | lld:lhgdn |
