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Originally published In Press as doi:10.1194/jlr.M600178-JLR200 on June 20, 2006

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Journal of Lipid Research, Vol. 47, 2071-2079, September 2006
Copyright © 2006 by American Society for Biochemistry and Molecular Biology

Patient-Oriented Research

Role of the kidney in the metabolism of apolipoprotein A-IV: influence of the type of proteinuria

Arno Lingenhel*, Karl Lhotta{dagger}, Ulrich Neyer§, Iris M. Heid**,{dagger}{dagger}, Barbara Rantner*, Martina F. Kronenberg*, Paul König{dagger}, Arnold von Eckardstein§§, Maria Schober***, Hans Dieplinger* and Florian Kronenberg1,*

* Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Innsbruck, Austria
{dagger} Department of Clinical Nephrology, Innsbruck Medical University, Innsbruck, Austria
§ Department of Nephrology and Dialysis, Academic Teaching Hospital, Feldkirch, Austria
** Institute of Epidemiology, GSF-National Research Center for Environment and Health, Neuherberg, Germany
{dagger}{dagger} Institute of Biostatistics and Epidemiology, Ludwig-Maximilians-Universität München, Munich, Germany
§§ Institute of Clinical Chemistry, University and University Hospital of Zürich, Zürich, Switzerland
*** Central Laboratory of University Clinics, Innsbruck Medical University, Innsbruck, Austria

Published, JLR Papers in Press, June 20, 2006.

1 To whom correspondence should be addressed. e-mail: florian.kronenberg{at}i-med.ac.at


ABSTRACT

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.

Supplementary key words nephrotic syndrome • tubular proteinuria • atherosclerosis • Dent's disease


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B. C.H. Kwan, F. Kronenberg, S. Beddhu, and A. K. Cheung
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