ArticleScientific reports2022
Kidney tubule iron loading in experimental focal segmental glomerulosclerosis.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Pilot pragmatic clinical trial of iron therapy in children with anemia of chronic kidney disease (FeTCh-CKD).Pediatric nephrology (Berlin, Germany) · 2026Trial
- IPNA Commentary on the KDIGO 2026 Clinical Practice Guideline for the Management of Anemia in CKD.Pediatric nephrology (Berlin, Germany) · 2026Article
- Impact of renal iron overload on sickle cell nephropathy in a humanized mouse model.American journal of physiology. Renal physiology · 2026Article
- Ferroptosis-related genes, a novel therapeutic target for focal segmental glomerulosclerosis.BMC nephrology · 2024Article
- Metalloporphyrins as Tools for Deciphering the Role of Heme Oxygenase in Renal Immune Injury.International journal of molecular sciences · 2023Review
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Kidney iron deposition may play a role in the progression of tubulointerstitial injury during chronic kidney disease. Here, we studied the molecular mechanisms of kidney iron loading in experimental focal segmental glomerulosclerosis (FSGS) and investigated the effect of iron-reducing interventions on disease progression. Thy-1.1 mice were injected with anti-Thy-1.1 monoclonal antibody (mAb) to induce proteinuria. Urine, blood and tissue were collected at day (D)1, D5, D8, D15 and D22 after mAb injection. Thy-1.1 mice were subjected to captopril (CA), iron-deficient (ID) diet or iron chelation (deferoxamine; DFO). MAb injection resulted in significant albuminuria at all time points (p < 0.01). Kidney iron loading, predominantly in distal tubules, increased in time, along with urinary kidney injury molecule-1 and 24p3 concentration, as well as kidney mRNA expression of Interleukin-6 (Il-6) and Heme oxygenase-1 (Ho-1). Treatment with CA, ID diet or DFO significantly reduced kidney iron deposition at D8 and D22 (p < 0.001) and fibrosis at D22 (p < 0.05), but not kidney Il-6. ID treatment increased kidney Ho-1 (p < 0.001). In conclusion, kidney iron accumulation coincides with progression of tubulointerstitial injury in this model of FSGS. Reduction of iron loading halts disease progression. However, targeted approaches to prevent excessive kidney iron loading are warranted to maintain the delicate systemic and cellular iron balance.
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Registered trials
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