2007 JASN IMPACT FACTOR 7.111	HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP
advanced	CURRENT ISSUE	ARCHIVES	JASN Express	ONLINE SUBMISSION

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by PRINSEN, B. H. C. M. T. Articles by RABELINK, T. J. Search for Related Content PubMed PubMed Citation Articles by PRINSEN, B. H. C. M. T. Articles by RABELINK, T. J.

Transferrin Synthesis Is Increased in Nephrotic Patients Insufficiently to Replace Urinary Losses

BERTHIL H. C. M. T. PRINSEN^*,,, MONIQUE G. M. DE SAIN-VAN DER VELDEN, GEORGE A. KAYSEN, HELMA W. H. C. STRAVER, HERMAN J. M. VAN RIJN, FRANS STELLAARD^||, RUUD BERGER and TON J. RABELINK^*

^* Department of Vascular Medicine and Metabolism, University Medical Center Utrecht, Utrecht, The Netherlands
Department of Clinical Chemistry, University Medical Center Utrecht, Utrecht, The Netherlands
Department of Metabolic Diseases, University Medical Center Utrecht, Utrecht, The Netherlands
Department of Medicine, Division of Nephrology, University of California-Davis, Davis, and Department of Veterans Affairs Northern California System of Clinics, Mather, California
^|| Department of Nutrition and Metabolism, University Hospital Groningen, Groningen, The Netherlands.

Correspondence to Dr. Monique G. M. de Sain-van der Velden, University Medical Center Utrecht, Department of Metabolic Diseases, H.P. KC-02.069.1, P.O. Box 85090, 3508 AB, Utrecht, The Netherlands. Phone: 31-30-2504294; Fax: 31-30-2504295; E-mail: M.G.deSain{at}lab.azu.nl

Abstract. The urinary loss of transferrin is sufficient to reduce plasma transferrin concentrations in the nephrotic syndrome. Hypotransferrinemia may lead to iron loss and microcytic anemia. The mechanism responsible for the hypotransferrinemia in the nephrotic syndrome is, however, unknown. In the present study, synthesis rate of transferrin was measured in vivo in nephrotic patients (n = 7) compared with control subjects (n = 6) using L-[1-¹³C]-valine. Plasma transferrin and iron concentration in the patients were significantly lower than in control subjects (transferrin, 1.39 ± 0.08 versus 2.57 ± 0.11 g/L, P < 0.0001; iron, 10.2 ± 0.8 versus 21.1 ± 4.5 µmol/L, P = 0.02). Furthermore, albuminuria correlated with transferrinuria (r² = 0.901, P = 0.001). The absolute synthesis rate of transferrin was increased in the patients (10.0 ± 1.1 versus 7.4 ± 0.7 mg/kg per d, P = 0.07), although this value failed to achieve significance. C-reactive protein, plasma iron, and proteinuria did not correlate with transferrin synthesis. In contrast, transferrin synthesis correlated with albumin synthesis (r² = 0.648, P = 0.03; n = 7). The present study indicates that increased transferrin synthesis occurs in nephrotic patients but is insufficient to compensate for urinary losses. Because, overall, no significant relationship was found between transferrin synthesis and either C-reactive protein or iron, it is unlikely that inflammation suppresses or that iron deficiency stimulates increased transferrin synthesis in these patients. The correlation between transferrin synthesis and albumin synthesis suggests that transferrin synthesis is a component of a general response in hepatic protein synthesis in the nephrotic syndrome. This suggests that a therapeutic approach to maximize plasma transferrin concentrations in nephrotic patients should be aimed primarily at reducing urinary protein excretion.

This article has been cited by other articles:

				M. S. Joy, M. La, and Bo Xiao Individualizing Therapy in Patients With Chronic Kidney Disease Journal of Pharmacy Practice, June 1, 2008; 21(3): 225 - 236. [Abstract] [PDF]

				A. J. W. Branten, D. W. Swinkels, I. S. Klasen, and J. F. M. Wetzels Serum ferritin levels are increased in patients with glomerular diseases and proteinuria Nephrol. Dial. Transplant., November 1, 2004; 19(11): 2754 - 2760. [Abstract] [Full Text] [PDF]

				P. H. Bisschop, M. G. M. de Sain-van der Velden, F. Stellaard, F. Kuipers, A. J. Meijer, H. P. Sauerwein, and J. A. Romijn Dietary Carbohydrate Deprivation Increases 24-Hour Nitrogen Excretion without Affecting Postabsorptive Hepatic or Whole Body Protein Metabolism in Healthy Men J. Clin. Endocrinol. Metab., August 1, 2003; 88(8): 3801 - 3805. [Abstract] [Full Text] [PDF]

				J. Yang, K. Mori, J. Y. Li, and J. Barasch Iron, lipocalin, and kidney epithelia Am J Physiol Renal Physiol, July 1, 2003; 285(1): F9 - F18. [Abstract] [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673