Fp206role of Iron and Renal Transferrin Expression on Contrast Induced Acute Kidney Injury

Sridharan, Badrinathan; Annamalai, Chandrashekar; Singhh, Shivendra Pratap; Ganesh, Rajesh Nachiappa; Viswanathhan, Pragasam

doi:10.1093/ndt/gfv172.34

Cited by 1 publication

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[25][26][27] Experimental studies have also reported pathological alterations in the expression of several iron-regulatory proteins together with the accumulation of iron in renal tissues obtained from CKD, acute kidney injury (AKI), and chronic iron overloading. [28][29][30][31][32] Nevertheless, little is currently known regarding the effects of acute iron toxicity on the expression of ironhomeostatic proteins in renal tissues. 12,27,33 This study, therefore, measured the effects of acute sublethal iron overloading on the expression of iron-regulatory proteins together with several markers of oxidative stress and ferroptosis in renal tissues, and the results were compared with those obtained from controls and following chronic iron overloading.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Acute and Chronic Iron Overloading Differentially Modulates the Expression of Cellular Iron-homeostatic Molecules in Normal Rat Kidney

Refaat

Abdelghany

BaSalamah

et al. 2018

J Histochem Cytochem.

View full text Add to dashboard Cite

Little is known about the renal responses to acute iron overloading. This study measured the renal tubular expression of transferrin receptor-1 (TfR1), cubilin/megalin receptors, hepcidin, ferroportin, and ferritin chains following subacute intoxication of 40 male Wistar rats with a single oral dose of ferrous iron (300 mg/kg). The animals were randomly subdivided into 4 equal subgroups at the time of necropsy (1, 2, 4, and 8 hr). The results were compared with the controls ( n=15) and with the chronic group ( n=15), which received iron for 4 weeks (75 mg/kg/day; 5 days/week). Although both toxicity models inhibited TfR1, they upregulated the cubilin/megalin receptors and hepcidin, and triggered iron deposition in tubular cells. The ferritin heavy-chain and ferroportin were downregulated in the 2-hr and 4-hr acute subgroups, whereas chronic toxicity promoted their expression, compared with controls. Moreover, the 4-hr and 8-hr subgroups had higher intracellular Fe and marked cell apoptosis compared with the chronic group. In conclusion, the kidney appears to sustain iron reabsorption in both intoxication models. However, the cellular iron storage and exporter proteins were differentially expressed in both models, and their inhibition post-acute toxicity might contribute toward the intracellular accumulation of Fe, oxidative stress, and ferroptosis.

show abstract

Section: Introductionmentioning

confidence: 99%

“…25–27 Experimental studies have also reported pathological alterations in the expression of several iron-regulatory proteins together with the accumulation of iron in renal tissues obtained from CKD, acute kidney injury (AKI), and chronic iron overloading. 28–32…”

Section: Introductionmentioning

confidence: 99%