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Article ; Online: Effect of Deferoxamine on Post-Transfusion Iron, Inflammation, and In Vitro Microbial Growth in a Canine Hemorrhagic Shock Model: A Randomized Controlled Blinded Pilot Study.

Claus, Melissa A / Smart, Lisa / Raisis, Anthea L / Sharp, Claire R / Abraham, Sam / Gummer, Joel P A / Mead, Martin K / Bradley, Damian L / Van Swelm, Rachel / Wiegerinck, Erwin T G / Litton, Edward

Veterinary sciences

2023 Volume 10, Issue 2

Abstract: Red blood cell (RBC) transfusion is associated with recipient inflammation and infection, which may be triggered by excessive circulating iron. Iron chelation following transfusion may reduce these risks. The aim of this study was to evaluate the effect ... ...

Abstract	Red blood cell (RBC) transfusion is associated with recipient inflammation and infection, which may be triggered by excessive circulating iron. Iron chelation following transfusion may reduce these risks. The aim of this study was to evaluate the effect of deferoxamine on circulating iron and inflammation biomarkers over time and in vitro growth of
Language	English
Publishing date	2023-02-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2768971-2
ISSN	2306-7381 ; 2306-7381
ISSN (online)	2306-7381
ISSN	2306-7381
DOI	10.3390/vetsci10020121
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Article ; Online: The multifaceted role of iron in renal health and disease.

van Swelm, Rachel P L / Wetzels, Jack F M / Swinkels, Dorine W

Nature reviews. Nephrology

2019 Volume 16, Issue 2, Page(s) 77–98

Abstract: Iron is an essential element that is indispensable for life. The delicate physiological body iron balance is maintained by both systemic and cellular regulatory mechanisms. The iron-regulatory hormone hepcidin assures maintenance of adequate systemic ... ...

Abstract	Iron is an essential element that is indispensable for life. The delicate physiological body iron balance is maintained by both systemic and cellular regulatory mechanisms. The iron-regulatory hormone hepcidin assures maintenance of adequate systemic iron levels and is regulated by circulating and stored iron levels, inflammation and erythropoiesis. The kidney has an important role in preventing iron loss from the body by means of reabsorption. Cellular iron levels are dependent on iron import, storage, utilization and export, which are mainly regulated by the iron response element-iron regulatory protein (IRE-IRP) system. In the kidney, iron transport mechanisms independent of the IRE-IRP system have been identified, suggesting additional mechanisms for iron handling in this organ. Yet, knowledge gaps on renal iron handling remain in terms of redundancy in transport mechanisms, the roles of the different tubular segments and related regulatory processes. Disturbances in cellular and systemic iron balance are recognized as causes and consequences of kidney injury. Consequently, iron metabolism has become a focus for novel therapeutic interventions for acute kidney injury and chronic kidney disease, which has fuelled interest in the molecular mechanisms of renal iron handling and renal injury, as well as the complex dynamics between systemic and local cellular iron regulation.
MeSH term(s)	Acute Kidney Injury/metabolism ; Erythropoiesis ; Erythropoietin/metabolism ; Homeostasis ; Humans ; Inflammation/metabolism ; Iron/metabolism ; Iron-Regulatory Proteins/metabolism ; Kidney/metabolism ; Kidney Tubules, Distal/metabolism ; Kidney Tubules, Proximal/metabolism ; Mitochondria/metabolism ; Nephrons/metabolism ; Oxidative Stress ; Renal Insufficiency, Chronic/metabolism
Chemical Substances	Iron-Regulatory Proteins ; Erythropoietin (11096-26-7) ; Iron (E1UOL152H7)
Language	English
Publishing date	2019-09-25
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-019-0197-5
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Article ; Online: Role of hepcidin in oxidative stress and cell death of cultured mouse renal collecting duct cells: protection against iron and sensitization to cadmium.

Probst, Stephanie / Fels, Johannes / Scharner, Bettina / Wolff, Natascha A / Roussa, Eleni / van Swelm, Rachel P L / Lee, Wing-Kee / Thévenod, Frank

Archives of toxicology

2021 Volume 95, Issue 8, Page(s) 2719–2735

Abstract: The liver hormone hepcidin regulates systemic iron homeostasis. Hepcidin is also expressed by the kidney, but exclusively in distal nephron segments. Several studies suggest hepcidin protects against kidney damage involving ... ...

Abstract	The liver hormone hepcidin regulates systemic iron homeostasis. Hepcidin is also expressed by the kidney, but exclusively in distal nephron segments. Several studies suggest hepcidin protects against kidney damage involving Fe
MeSH term(s)	Animals ; Apoptosis/drug effects ; Binding Sites ; Binding, Competitive ; Cadmium/administration & dosage ; Cadmium/toxicity ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Deferoxamine/pharmacology ; Female ; Gene Silencing ; Hepcidins/genetics ; Iron/administration & dosage ; Iron/toxicity ; Kidney Tubules, Collecting/cytology ; Kidney Tubules, Collecting/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism
Chemical Substances	Hamp protein, mouse ; Hepcidins ; Reactive Oxygen Species ; Cadmium (00BH33GNGH) ; Iron (E1UOL152H7) ; Deferoxamine (J06Y7MXW4D)
Language	English
Publishing date	2021-06-28
Publishing country	Germany
Document type	Journal Article
ZDB-ID	124992-7
ISSN	1432-0738 ; 0340-5761
ISSN (online)	1432-0738
ISSN	0340-5761
DOI	10.1007/s00204-021-03106-z
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Article ; Online: Investigating the Molecular Mechanisms of Renal Hepcidin Induction and Protection upon Hemoglobin-Induced Acute Kidney Injury.

Diepeveen, Laura E / Stegemann, Gaby / Wiegerinck, Erwin T / Roelofs, Rian / Naber, Myrthe / Lóreal, Olivier / Smeets, Bart / Thévenod, Frank / Swinkels, Dorine W / van Swelm, Rachel P L

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: Hemolysis is known to cause acute kidney injury (AKI). The iron regulatory hormone hepcidin, produced by renal distal tubules, is suggested to exert a renoprotective role during this pathology. We aimed to elucidate the molecular mechanisms of renal ... ...

Abstract	Hemolysis is known to cause acute kidney injury (AKI). The iron regulatory hormone hepcidin, produced by renal distal tubules, is suggested to exert a renoprotective role during this pathology. We aimed to elucidate the molecular mechanisms of renal hepcidin synthesis and its protection against hemoglobin-induced AKI. In contrast to known hepatic hepcidin induction, incubation of mouse cortical collecting duct (mCCD
MeSH term(s)	Acute Kidney Injury/chemically induced ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/physiopathology ; Animals ; Hemin/metabolism ; Hemoglobins/metabolism ; Hemolysis/physiology ; Hepcidins/metabolism ; Hepcidins/physiology ; Iron/metabolism ; Kidney/metabolism ; Kidney/pathology ; Kidney Tubules, Distal/metabolism ; Mice ; Mice, Knockout ; Oxidative Stress
Chemical Substances	Hamp protein, mouse ; Hemoglobins ; Hepcidins ; Hemin (743LRP9S7N) ; Iron (E1UOL152H7)
Language	English
Publishing date	2022-01-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23031352
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Article ; Online: Kidney tubule iron loading in experimental focal segmental glomerulosclerosis.

van Swelm, Rachel P L / Beurskens, Sanne / Dijkman, Henry / Wiegerinck, Erwin T G / Roelofs, Rian / Thévenod, Frank / van der Vlag, Johan / Wetzels, Jack F M / Swinkels, Dorine W / Smeets, Bart

Scientific reports

2022 Volume 12, Issue 1, Page(s) 1199

Abstract: ... in significant albuminuria at all time points (p < 0.01). Kidney iron loading, predominantly in distal tubules ... 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 ...

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.
MeSH term(s)	Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Animals ; Captopril/therapeutic use ; Deferoxamine/therapeutic use ; Disease Models, Animal ; Female ; Glomerulosclerosis, Focal Segmental/diet therapy ; Glomerulosclerosis, Focal Segmental/drug therapy ; Glomerulosclerosis, Focal Segmental/metabolism ; Iron/metabolism ; Kidney Tubules, Distal/metabolism ; Male ; Mice ; Receptors, Cell Surface/metabolism ; Siderophores/therapeutic use
Chemical Substances	24p3 receptor, mouse ; Angiotensin-Converting Enzyme Inhibitors ; Receptors, Cell Surface ; Siderophores ; Captopril (9G64RSX1XD) ; Iron (E1UOL152H7) ; Deferoxamine (J06Y7MXW4D)
Language	English
Publishing date	2022-01-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-05261-4
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Article ; Online: Endogenous hepcidin synthesis protects the distal nephron against hemin and hemoglobin mediated necroptosis.

van Swelm, Rachel P L / Vos, Madelon / Verhoeven, Frank / Thévenod, Frank / Swinkels, Dorine W

Cell death & disease

2018 Volume 9, Issue 5, Page(s) 550

Abstract: ... in Hb kidney injury was suggested by the induction of renal hepcidin synthesis (p < 0.001) in mice ...

Abstract	Hemoglobinuria is associated with kidney injury in various hemolytic pathologies. Currently, there is no treatment available and its pathophysiology is not completely understood. Here we studied the potential detrimental effects of hemoglobin (Hb) exposure to the distal nephron (DN). Involvement of the DN in Hb kidney injury was suggested by the induction of renal hepcidin synthesis (p < 0.001) in mice repeatedly injected with intravenous Hb. Moreover, the hepcidin induction was associated with a decline in urinary kidney injury markers 24p3/NGAL and KIM1, suggesting a role for hepcidin in protection against Hb kidney injury. We demonstrated that uptake of Hb in the mouse cortical collecting duct cells (mCCD
MeSH term(s)	Animals ; Hemin/metabolism ; Hemoglobins/metabolism ; Hemoglobinuria/metabolism ; Hemoglobinuria/pathology ; Hepcidins/biosynthesis ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; Kidney Tubules, Distal/metabolism ; Kidney Tubules, Distal/pathology ; Male ; Mice ; Necrosis
Chemical Substances	Hamp protein, mouse ; Hemoglobins ; Hepcidins ; Hemin (743LRP9S7N)
Language	English
Publishing date	2018-05-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-018-0568-z
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Article ; Online: Sustained Exposure to High Carbohydrate Availability Does Not Influence Iron-Regulatory Responses in Elite Endurance Athletes.

McKay, Alannah K A / Peeling, Peter / Pyne, David B / Tee, Nicolin / Welveart, Marijke / Heikura, Ida A / Sharma, Avish P / Whitfield, Jamie / Ross, Megan L / van Swelm, Rachel P L / Laarakkers, Coby M / Burke, Louise M

International journal of sport nutrition and exercise metabolism

2021 Volume 31, Issue 2, Page(s) 101–108

Abstract: ... 95% CI [1.8, 14.6]) between the dietary groups. Higher resting serum ferritin (p = .004) and hotter ... trial ambient temperatures (p = .014) were associated with greater hepcidin levels 3 hr postexercise ...

Abstract	This study implemented a 2-week high carbohydrate (CHO) diet intended to maximize CHO oxidation rates and examined the iron-regulatory response to a 26-km race walking effort. Twenty international-level, male race walkers were assigned to either a novel high CHO diet (MAX = 10 g/kg body mass CHO daily) inclusive of gut-training strategies, or a moderate CHO control diet (CON = 6 g/kg body mass CHO daily) for a 2-week training period. The athletes completed a 26-km race walking test protocol before and after the dietary intervention. Venous blood samples were collected pre-, post-, and 3 hr postexercise and measured for serum ferritin, interleukin-6, and hepcidin-25 concentrations. Similar decreases in serum ferritin (17-23%) occurred postintervention in MAX and CON. At the baseline, CON had a greater postexercise increase in interleukin-6 levels after 26 km of walking (20.1-fold, 95% CI [9.2, 35.7]) compared with MAX (10.2-fold, 95% CI [3.7, 18.7]). A similar finding was evident for hepcidin levels 3 hr postexercise (CON = 10.8-fold, 95% CI [4.8, 21.2]; MAX = 8.8-fold, 95% CI [3.9, 16.4]). Postintervention, there were no substantial differences in the interleukin-6 response (CON = 13.6-fold, 95% CI [9.2, 20.5]; MAX = 11.2-fold, 95% CI [6.5, 21.3]) or hepcidin levels (CON = 7.1-fold, 95% CI [2.1, 15.4]; MAX = 6.3-fold, 95% CI [1.8, 14.6]) between the dietary groups. Higher resting serum ferritin (p = .004) and hotter trial ambient temperatures (p = .014) were associated with greater hepcidin levels 3 hr postexercise. Very high CHO diets employed by endurance athletes to increase CHO oxidation have little impact on iron regulation in elite athletes. It appears that variations in serum ferritin concentration and ambient temperature, rather than dietary CHO, are associated with increased hepcidin concentrations 3 hr postexercise.
MeSH term(s)	Adult ; Dietary Carbohydrates/administration & dosage ; Dietary Carbohydrates/metabolism ; Ferritins/blood ; Hepcidins/blood ; Humans ; Interleukin-6/blood ; Iron/blood ; Male ; Oxidation-Reduction ; Physical Conditioning, Human/physiology ; Physical Endurance/physiology ; Sports/physiology ; Temperature ; Walking/physiology
Chemical Substances	Dietary Carbohydrates ; Hepcidins ; IL6 protein, human ; Interleukin-6 ; hepcidin 25, human ; Ferritins (9007-73-2) ; Iron (E1UOL152H7)
Language	English
Publishing date	2021-12-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	1101115-4
ISSN	1543-2742 ; 1050-1606 ; 1526-484X
ISSN (online)	1543-2742
ISSN	1050-1606 ; 1526-484X
DOI	10.1123/ijsnem.2020-0224
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Article ; Online: Kidney tubule iron loading in experimental focal segmental glomerulosclerosis

Rachel P. L. van Swelm / Sanne Beurskens / Henry Dijkman / Erwin T. G. Wiegerinck / Rian Roelofs / Frank Thévenod / Johan van der Vlag / Jack F. M. Wetzels / Dorine W. Swinkels / Bart Smeets

Scientific Reports, Vol 12, Iss 1, Pp 1-

2022 Volume 12

Abstract: ... deferoxamine; DFO). MAb injection resulted in significant albuminuria at all time points (p < 0.01). Kidney ... 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 ...

Abstract	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.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Investigating the Molecular Mechanisms of Renal Hepcidin Induction and Protection upon Hemoglobin-Induced Acute Kidney Injury

Laura E. Diepeveen / Gaby Stegemann / Erwin T. Wiegerinck / Rian Roelofs / Myrthe Naber / Olivier Lóreal / Bart Smeets / Frank Thévenod / Dorine W. Swinkels / Rachel P. L. van Swelm

International Journal of Molecular Sciences, Vol 23, Iss 1352, p

2022 Volume 1352

Abstract: ... and hemin significantly induced hepcidin synthesis ( p < 0.05). Moreover, iron/heme-mediated hepcidin ... as indicated by increased nuclear Nrf2 translocation and induced expression of Nrf2 downstream targets GCLM ( p ... < 0.001), NQO1 ( p < 0.001), and TXNRD1 ( p < 0.005), which could be prevented by the known Nrf2 ...

Abstract	Hemolysis is known to cause acute kidney injury (AKI). The iron regulatory hormone hepcidin, produced by renal distal tubules, is suggested to exert a renoprotective role during this pathology. We aimed to elucidate the molecular mechanisms of renal hepcidin synthesis and its protection against hemoglobin-induced AKI. In contrast to known hepatic hepcidin induction, incubation of mouse cortical collecting duct (mCCD cl1 ) cells with IL-6 or LPS did not induce Hamp1 mRNA expression, whereas iron (FeS) and hemin significantly induced hepcidin synthesis ( p < 0.05). Moreover, iron/heme-mediated hepcidin induction in mCCD cl1 cells was caused by the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, as indicated by increased nuclear Nrf2 translocation and induced expression of Nrf2 downstream targets GCLM ( p < 0.001), NQO1 ( p < 0.001), and TXNRD1 ( p < 0.005), which could be prevented by the known Nrf2 inhibitor trigonelline. Newly created inducible kidney-specific hepcidin KO mice demonstrated a significant reduction in renal Hamp1 mRNA expression. Phenylhydrazine (PHZ)-induced hemolysis caused renal iron loading and oxidative stress in both wildtype (Wt) and KO mice. PHZ treatment in Wt induced inflammatory markers ( IL-6 , TNFα ) but not Hamp1 . However, since PHZ treatment also significantly reduced systemic hepcidin levels in both Wt and KO mice (both p < 0.001), a dissection between the roles of systemic and renal hepcidin could not be made. Combined, the results of our study indicate that there are kidney-specific mechanisms in hepcidin regulation, as indicated by the dominant role of iron and not inflammation as an inducer of renal hepcidin, but also emphasize the complex interplay of various iron regulatory mechanisms during AKI on a local and systemic level.
Keywords	kidney ; iron ; hepcidin ; acute kidney injury ; hemoglobin ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Serum hepcidin concentrations in relation to iron status in children with type 1 diabetes.

Vreugdenhil, Mirjam / Akkermans, Marjolijn D / van Swelm, Rachel P L / Laarakkers, Coby M / Houdijk, Euphemia C A M / Bakker, Boudewijn / Clement-de Boers, Agnes / van der Kaay, Daniëlle C M / de Vries, Martine C / Woltering, M Claire / Mul, Dick / van Goudoever, Johannes B / Brus, Frank

Pediatric hematology and oncology

2020 Volume 38, Issue 2, Page(s) 108–123

Abstract: Chronic low-grade inflammation in type 1 diabetes (T1D) might increase hepcidin synthesis, possibly resulting in functional iron deficiency (FID). We hypothesized that in T1D children with FID, hepcidin concentrations are increased compared to those with ...

Abstract	Chronic low-grade inflammation in type 1 diabetes (T1D) might increase hepcidin synthesis, possibly resulting in functional iron deficiency (FID). We hypothesized that in T1D children with FID, hepcidin concentrations are increased compared to those with normal iron status and those with absolute iron deficiency (AID). We evaluated hepcidin concentrations in T1D children in relation to iron status, and investigated whether hepcidin is useful in assessing FID. A cross-sectional study was conducted. FID was defined as elevated zinc protoporphyrin/heme ratio and/or red blood cell distribution width, and AID as low serum ferritin concentration. Post-hoc analyses with different definitions of FID were performed, using transferrin saturation and reticulocyte hemoglobin content. Serum hepcidin concentrations were measured using mass-spectrometry. The IRODIAB-study is registered at www.trialregister.nl (NTR4642). This study included 215 T1D children with a median age of 13.7 years (Q
MeSH term(s)	Adolescent ; Anemia, Iron-Deficiency/blood ; Anti-Infective Agents/blood ; Cross-Sectional Studies ; Diabetes Mellitus, Type 1/blood ; Female ; Hepcidins/blood ; Humans ; Iron/blood ; Male
Chemical Substances	Anti-Infective Agents ; Hepcidins ; Iron (E1UOL152H7)
Language	English
Publishing date	2020-10-07
Publishing country	England
Document type	Journal Article
ZDB-ID	632914-7
ISSN	1521-0669 ; 0888-0018
ISSN (online)	1521-0669
ISSN	0888-0018
DOI	10.1080/08880018.2020.1820650
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