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Review
. 2019 Nov 1;8(11):1828.
doi: 10.3390/jcm8111828.

New Biomarkers of Ferric Management in Multiple Myeloma and Kidney Disease-Associated Anemia

Małgorzata Banaszkiewicz  1 , Jolanta Małyszko  2 , David H Vesole  3 , Karolina Woziwodzka  4 , Artur Jurczyszyn  5 , Marcin Żórawski  6 , Marcin Krzanowski  7 , Jacek Małyszko  8 , Krzysztof Batko  9 , Marek Kuźniewski  10 , Katarzyna Krzanowska  11
Affiliations
Review

New Biomarkers of Ferric Management in Multiple Myeloma and Kidney Disease-Associated Anemia

Małgorzata Banaszkiewicz et al. J Clin Med. .

Abstract

Multiple myeloma (MM) is a malignancy of clonal plasma cells accounting for approximately 10% of haematological malignancies. MM mainly affects older patients, more often males and is more frequently seen in African Americans. The most frequent manifestations of MM are anaemia, osteolytic bone lesions, kidney failure and hypercalcemia. The anaemia develops secondary to suppression of erythropoiesis by cytokine networks, similarly to the mechanism of anaemia of chronic disease. The concomitant presence of kidney failure, especially chronic kidney disease (CKD) and MM per se, leading to anaemia of chronic disease (ACD) in combination, provoked us to pose the question about their reciprocal dependence and relationship with specific biomarkers; namely, soluble transferrin receptor (sTfR), growth differentiation factor 15 (GDF15), hepcidin 25 and zonulin. One or more of these are new biomarkers of ferric management may be utilized in the near future as prognostic predictors for patients with MM and kidney failure.

Keywords: anaemia; growth differentiation factor 15; hepcidin; kidney disease; mieloma multiple; soluble transferrin receptor; zonulin.

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Conflict of interest statement

The authors declare that there is no conflict of interest regarding the publication of this paper. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Overview of iron physiology. Non-haem iron (after reduction to Fe2+ by membrane-bound enzymes), originating from dietary intake (mostly Fe3+), enters the enterocyte of the proximal intestine via the divalent metal transporter (DMT1), and exits the cell on the basolateral side through ferroportin (FPN), which is potentiated by an oxidase, hephaestein. Depending on the state of iron need, iron can be released from the cell or sequestered in the form of ferritin (a measure of body iron stores). Iron is bound by transferrin in plasma, which enables transport and distribution to other body tissues (this also depends on the presence of transferrin receptors). Hepcidin, which is a peptide hormone produced by the liver, negatively regulates iron absorption and release from cells (e.g., macrophages) depending on iron need.
Figure 2
Figure 2
Diagnostic and clinical scheme of multiple myeloma anaemia.
See this image and copyright information in PMC

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