UCL Discovery
UCL home » Library Services » Electronic resources » UCL Discovery

Iron handling by the human kidney: glomerular filtration and tubular reabsorption both contribute to urinary iron excretion

van Raaij, SEG; Rennings, AJ; Biemond, BJ; Schols, SEM; Wiegerinck, ETG; Roelofs, HMJ; Hoorn, EJ; ... van Swelm, RPL; + view all (2019) Iron handling by the human kidney: glomerular filtration and tubular reabsorption both contribute to urinary iron excretion. American Journal of Physiology - Renal Physiology , 316 (3) F606-F614. 10.1152/ajprenal.00425.2018. Green open access

[thumbnail of Walsh Manuscript iron in urine study Sanne 180730.pdf]
Preview
Text
Walsh Manuscript iron in urine study Sanne 180730.pdf - Accepted Version

Download (604kB) | Preview

Abstract

In physiological conditions, circulating iron can be filtered by the glomerulus and is almost completely reabsorbed by the tubular epithelium to prevent urinary iron wasting. Increased urinary iron concentrations have been associated with renal injury. However, it is not clear whether increased urinary iron concentrations in patients are the result of increased glomerular iron filtration and/or insufficient tubular iron reabsorption and if these processes contribute to renal injury. We measured plasma and urine iron parameters and urinary tubular injury markers in healthy human subjects (n = 20), patients with systemic iron overload (n = 20), and patients with renal tubular dysfunction (n = 18). Urinary iron excretion parameters were increased in both patients with systemic iron overload and tubular dysfunction, whereas plasma iron parameters were only increased in patients with systemic iron overload. In patients with systemic iron overload, increased urinary iron levels were associated with elevated circulating iron, as indicated by transferrin saturation (TSAT), and increased body iron, as suggested by plasma ferritin concentrations. In patients with tubular dysfunction, enhanced urinary iron and transferrin excretion were associated with distal tubular injury as indicated by increased urinary glutathione S-transferase pi 1-1 (GSTP1-1) excretion. In systemic iron overload, elevated urinary iron and transferrin levels were associated with increased injury to proximal tubules, indicated by increased urinary kidney injury marker 1 (KIM-1) excretion. Our explorative study demonstrates that both glomerular filtration of elevated plasma iron levels and insufficient tubular iron reabsorption could increase urinary iron excretion and cause renal injury.

Type: Article
Title: Iron handling by the human kidney: glomerular filtration and tubular reabsorption both contribute to urinary iron excretion
Open access status: An open access version is available from UCL Discovery
DOI: 10.1152/ajprenal.00425.2018
Publisher version: https://doi.org/10.1152/ajprenal.00425.2018
Language: English
Additional information: This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions.
Keywords: Science & Technology, Life Sciences & Biomedicine, Physiology, Urology & Nephrology, filtration, injury, iron, reabsorption, urine, TRANSFERRIN-BOUND IRON, LABILE PLASMA IRON, THALASSEMIC PATIENTS, NEPHROTIC SYNDROME, BETA-THALASSEMIA, SERUM FERRITIN, BODY IRON, HEPCIDIN, INJURY, HEMOGLOBIN
UCL classification: UCL
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Div of Medicine
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Div of Medicine > Renal Medicine
URI: https://discovery.ucl.ac.uk/id/eprint/10077372
Downloads since deposit
42Downloads
Download activity - last month
Download activity - last 12 months
Downloads by country - last 12 months

Archive Staff Only

View Item View Item