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Is Magnetic Resonance Imaging Detection of Kidney Iron Deposition Increased in
Haptoglobin 2-2 Genotype Carriers with Type 1 Diabetes?
Authors Costacou T, Orchard TJ, Moon CH, Bae KT, Fried L, Evans RW
Submitted By Tina Costacou on 2/19/2018
Status Published
Journal Antioxidants & redox signaling
Year 2018
Date Published 2/1/2018
Volume : Pages Not Specified : Not Specified
PubMed Reference
Abstract Haptoglobin's (Hp) main role is to bind free hemoglobin (Hb), reducing its
oxidative potential. The Hp-Hb complex formed is cleared from the circulation by
macrophage receptor CD163. In diabetes, impaired Hp 2-2-Hb CD163 clearance and
abnormal glomerular permeability allow the large Hp 2-2-Hb complex to cross the
barrier, where its redox active iron leads to cellular toxicity. Although Hp 2-2
predicts renal function decline, whether renal iron deposition differs by Hp is
unknown. We used renal quantitative T2* magnetic resonance imaging to estimate
iron level in the cortex and medullar of type 1 diabetes (T1D) adults [15 Hp 1-1
and 15 Hp 2-2 carriers of similar age (53 years), duration (45 years), and
gender]. Total kidney iron level was estimated as the sum of the cortex and
medullar iron. Albuminuria was defined as urinary albumin to creatinine ratio
>30?mg/g in two of three samples. Total kidney iron did not differ by gender or
Hp but was higher in those with albuminuria (p?=?0.05), an association confined
to Hp 2-2 carriers (p?=?0.04 vs. p?=?0.51 in Hp 1-1). These data lead to the
hypothesis that kidney iron deposition is increased among Hp 2-2 carriers with
albuminuria in T1D. Antioxid. Redox Signal. 00, 000-000.

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