American Journal of Nephrology
Original Report: Laboratory Investigation
Reduced Serum Fetuin-A in Nephrotic Children: A Consequence of Proteinuria?Fischer D.-C.a, b · Schaible J.b · Wigger M.b · Staude H.b · Drueckler E.b · Kundt G.c · Haffner D.aaDepartment of Pediatric Kidney, Liver and Metabolic Diseases, Hannover Medical School, Hannover, and bDepartment of Pediatrics and cInstitute of Medical Informatics and Biometry, University of Rostock, Rostock, Germany
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Article / Publication Details
Received: May 27, 2011
Accepted: July 22, 2011
Published online: September 02, 2011
Issue release date: October 2011
Number of Print Pages: 8
Number of Figures: 5
Number of Tables: 3
ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)
For additional information: https://www.karger.com/AJN
Abstract
Background: The extracellular protein fetuin-A is a potent soluble inhibitor of calcification, and its deficiency has been associated with vascular calcification in dialysis patients. In proteinuric patients, significant urinary losses of fetuin-A may cause low serum fetuin-A levels. Methods: In a cross-sectional study, urinary/serum concentrations of fetuin-A were investigated in proteinuric children with glomerular diseases and preserved renal function (n = 58) in comparison to healthy controls (n = 246). Results: Mean fetuin-A serum concentrations were clearly reduced in children with nephrotic syndrome (0.25 ± 0.14 g/l, p < 0.001), slightly reduced in children with large proteinuria (0.39 ± 0.15 g/l, p < 0.05), and comparable to controls in those with mild proteinuria (0.45 ± 0.14 vs. 0.46 ± 0.12 g/l). Fetuin-A was positively correlated with serum protein (r = 0.58), albumin (r = 0.57), and calcium (r = 0.64), but negatively correlated with proteinuria (r = –0.41), albuminuria (r = –0.46), and urinary fetuin-A excretion (r = –0.48; each p < 0.001). The fractional excretion of fetuin-A was significantly associated with the degree of proteinuria and serum fetuin-A levels. However, the urinary loss of fetuin-A and albumin in nephrotic children differed by three orders of magnitude and the mean fractional excretion of fetuin-A was only 1/10 of that of albumin (0.016 ± 0.029 vs. 0.162 ± 0.403%; p < 0.001). Conclusions: Fetuin-A is clearly reduced in children with nephrotic syndrome and associated with the degree of hypoalbuminemia. This is due to urinary fetuin-A loss and/or reduced hepatic synthesis. Persistent fetuin-A deficiency may have an impact on cardiovascular morbidity in nephrotic children.
© 2011 S. Karger AG, Basel
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Article / Publication Details
Received: May 27, 2011
Accepted: July 22, 2011
Published online: September 02, 2011
Issue release date: October 2011
Number of Print Pages: 8
Number of Figures: 5
Number of Tables: 3
ISSN: 0250-8095 (Print)
eISSN: 1421-9670 (Online)
For additional information: https://www.karger.com/AJN
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