Serum erythropoietin and its relation with soluble transferrin receptor in patients with different types of anaemia in a locally defined reference population

Roque, Marta Elena; Sandoval, Marisa Julia; Aggio, Mario Carlos

doi:10.1046/j.1365-2257.2001.00413.x

Cited by 15 publications

(19 citation statements)

References 21 publications

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“…Several hypotheses could explain our findings. First, it is known that the kidney is closely associated with erythropoiesis since low levels of oxygen present in hemolytic anemia induce increases in HIF-1, which in turn plays an important role in the expansion of committed erythroid progenitors and in the terminal differentiation of erythroid cells (31). This could explain hematological restoration to hemolytic anemia (6,14).…”

Section: Discussionmentioning

confidence: 99%

Role of the kidney in iron homeostasis: renal expression of Prohepcidin, Ferroportin, and DMT1 in anemic mice

Veuthey

D'Anna²,

Roque³

2008

American Journal of Physiology-Renal Physiology

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It is known that renal tissue plays a role in normal iron homeostasis. The current study examines kidney function in iron metabolism under hemolytic anemia studying renal expression of Prohepcidin, Ferroportin (MTP1), and divalent metal transporter 1 (DMT1). The relationship between these proteins and iron pigments was also investigated. Immunohistochemical procedures to study renal expression of Prohepcidin, MTP1, and DMT1 were performed in healthy and anemic mice. Renal tissue iron was determined by Prussian blue iron staining. To assess anemia evolution and erythropoietic recovery, we used conventional tests. In healthy mice, Prohepcidin expression was marked in proximal tubules and inner medulla and absent in outer medulla. Cortical tissue of healthy mice also showed MTP1 immunostaining, mainly in the S2 segment of proximal tubules. Medullar tissue showed MTP1 expression in the inner zone. In addition, S2 segments showed intense DMT1 immunoreactivity with homogeneous DMT1 distribution throughout renal medulla. The main cortical findings in hemolytic anemia were in S2 segments of proximal tubules where we found that decreased Prohepcidin expression coincided with an increment in Ferroportin and DMT1 expression. This expression pattern was concomitant with increased iron in the same tubular zone. However, in medullar tissue both Prohepcidin and MTP1 decreased and DMT1 was detected mainly in larger diameter tubules. Our findings clearly demonstrate that in hemolytic anemia, renal Prohepcidin acts in coordination with renal Ferroportin and DMT1, indicating the key involvement of kidney in iron homeostasis when iron demand is high. Further research is required to learn more about these regulatory mechanisms.

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Section: Discussionmentioning

confidence: 99%

Role of the kidney in iron homeostasis: renal expression of Prohepcidin, Ferroportin, and DMT1 in anemic mice

Veuthey

D'Anna²,

Roque³

2008

American Journal of Physiology-Renal Physiology

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“…Although erythropoiesis is usually increased in patients with AIHA, natural ESAs might be diminished, at least in some patients. Until now, ESA concentrations have only been measured in a few patients with AIHA; thus no conclusions can be drawn from these results [16]. The notion that ESAs might be rather decreased in AIHA is supported by findings in ITP patients where TPO has been observed to be decreased rather than increased [17].…”

Section: Discussionmentioning

confidence: 70%

The Effect of Erythropoiesis-Stimulating Agents in Patients with Therapy-Refractory Autoimmune Hemolytic Anemia

Salama

Hartnack

Lindemann

et al. 2014

Transfus Med Hemother

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Background: Many patients with autoimmune hemolytic anemia (AIHA) do not respond to standard therapy and/or may develop severe complications which can be of fatal outcome. There is some evidence that erythropoiesis-stimulating agents (ESAs) may be helpful in the management of such patients. Methods: We describe the effect of ESAs in 12 new patients with therapy-refractory AIHA (7 of warm type and 5 of cold type) and review 5 previously reported cases. Serological testing was performed using standard methods. Results: All patients responded well to treatment with ESAs. At least 5 of the 17 patients demonstrated complete recovery, and none of the patients developed significant adverse reactions due to treatment with ESAs. Conclusion: The mechanism by which ESAs improves hemolysis in AIHA is not completely clear. In addition to increased production and prolonged RBC survival, it may inhibit eryptosis (programmed cell death). ESAs represent a new option in the treatment of decompensated and/or refractory AIHA of warm and cold type. However, more information is required to assess which patients can be treated with ESAs.

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“…EPO is made predominantly in the kidney, and during anemia, caused by either reduced iron intake or by blood loss, the healthy kidney can increase EPO production by at least tenfold [3][4][5]. EPO production is impaired in renal disease, which contributes to the anemia of kidney failure.…”

Section: Interaction Among Components Of the Iron Cycle To Maintain Nmentioning

confidence: 99%

“…The oxygen content of the renal blood supply declines during anemia, and the normal kidney responds by increased EPO output, which may increase in the bloodstream from 15 to 35 mU/ ml after a single blood donation [19] and 150-200 mU/ml during severe iron-deficiency anemia [3][4][5].…”

Section: Classical Anemia: Insufficent Dietary Iron Intakementioning

confidence: 99%

Iron and anemia in human biology: a review of mechanisms

2008

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The biology of iron in relation to anemia is best understood by a review of the iron cycle, since the majority of iron for erythropoiesis is provided by iron recovered from senescent erythrocytes. In iron-deficiency anemia, storage iron declines until iron delivery to the bone marrow is insufficient for erythropoiesis. This can be monitored with clinical indicators, beginning with low plasma ferritin, followed by decreased plasma iron and transferrin saturation, and culminating in red blood cells with low-Hb content. When adequate dietary iron is provided, these markers show return to normal, indicating a response to the dietary supplement. Anemia of inflammation (also known as anemia of chronic disease, or ACD) follows a different course, because in this form of anemia storage iron is often abundant but not available for erythropoiesis. The diagnosis of ACD is more difficult than the diagnosis of iron-deficiency anemia, and often the first identified symptom is the failure to show a response to a dietary iron supplement. Confirmation of ACD is best obtained from elevated markers of inflammation. The treatment of ACD, which typically employs erythropoietin (EPO) supplements and intravenous iron (i.v.-iron), is empirical and often falls shorts of therapeutic goals. Dialysis patients show a complex pattern of anemia, which results from inadequate EPO production by the kidney, inflammation, changes in nutrition, and blood losses during treatment. EPO and i.v.-iron are the mainstays of treatment. Patients with heart failure can be anemic, with incidence as high as 50%. The causes are multifactorial; inflammation now appears to be the primary cause of this form of anemia, with contributions from increased plasma volume, effects of drug therapy, and other complications of heart disease. Discerning the mechanisms of anemia for the heart failure patient may aid rational therapy in each case.

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Serum erythropoietin and its relation with soluble transferrin receptor in patients with different types of anaemia in a locally defined reference population

Cited by 15 publications

References 21 publications

Role of the kidney in iron homeostasis: renal expression of Prohepcidin, Ferroportin, and DMT1 in anemic mice

Role of the kidney in iron homeostasis: renal expression of Prohepcidin, Ferroportin, and DMT1 in anemic mice

The Effect of Erythropoiesis-Stimulating Agents in Patients with Therapy-Refractory Autoimmune Hemolytic Anemia

Iron and anemia in human biology: a review of mechanisms

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