When hgb, hct and iron sat are running low, but ferritin is over 800, should iron be held while giving the appropriate dose of epo?
Another question I have is, in some home programs epo is given once a week in a larger dose instead of spread out over 3 txs a week as is done in-center. Is the effectiveness and safety still the same?
I would say that you should ask the doctor what could be causing the increase in ferritin when the other labs are low. First, here’s information on ferritin from MedlinePlus:
Here’s a response to a similar question that I found on the National Anemia Action Council website along with 19 other questions for medical professionals:
Q3. How do you approach high ferritin, low iron saturation anemia (eg, as seen in renal failure and certain chronic diseases)?
A3. By NAAC Hematologist John W. Adamson, MD. Posted 8/22/03.
The issue here is whether or not the patient is iron deficient with an inflammatory process that raises the ferritin level and invalidates that measurement as a reflection of iron stores. The easiest way to address this is by giving iron and looking for an erythropoietic response (increase in hemoglobin or hematocrit) over time. In the old days, a bone marrow aspirate might have been done to look for stainable iron stores.
We have asked why ferritin remains elevated, but have gotten a could be this or that type answer. A nurse once said it is due to an iron load given in the past.
Is Adamson, MD saying here that an inflammatory process could cause a ferritin result to be inaccurate, so by giving some iron and seeing the hgb and hct increase, it would show that iron is necessary despite what the ferritin is?
That’s the way I read it. However, one thing I heard years ago was that high ferritin could make someone at risk of infection. So I’d ask the doctor about the association between ferritin and infection/inflammation and how to tell if the patient has an underlying and undiagnosed inflammation.
Also, here’s a study that discusses patients with low responsiveness to EPO and high ferritin levels and how vitamin C supplementation helped. You might want to discuss this with the nephrologist and see if he/she thinks vitamin C might help.
Am J Kidney Dis. 2006 Apr;47(4):644-54.
Effect of intravenous ascorbic acid in hemodialysis patients with EPO-hyporesponsive anemia and hyperferritinemia.
Attallah N, Osman-Malik Y, Frinak S, Besarab A.
Division of Nephrology and Hypertension, Henry Ford Hospital, Detroit, MI 48202, USA. email@example.com
BACKGROUND: Although erythropoietin (EPO)-hyporesponsive anemia in hemodialysis patients most commonly results from iron deficiency, the contributory role of chronic inflammation and oxidative stress in its pathogenesis is poorly understood. We conducted an open-label prospective study to assess the effect of vitamin C, an antioxidant, on EPO-hyporesponsive anemia in hemodialysis patients with unexplained hyperferritinemia. METHODS: Forty-six of 262 patients in an inner-city hemodialysis center met the inclusion criteria (administration of intravenous iron and EPO for > or = 6 months at a dose > or = 450 U/kg/wk, average 3-month hemoglobin [Hb] level < or = 11.0 g/dL [<or> or = 500 ng/mL (microg/L), and transferrin saturation [TSAT] < or = 50%). Patients were excluded if they had a clear explanation for the EPO hyporesponsiveness. Four patients refused to participate. The remaining patients were randomly assigned; 20 patients to receive standard care and 300 mg of intravenous vitamin C with each dialysis session (group 1) and 22 patients to receive standard care only (group 2). Study duration was 6 months. During the study, 1 patient from group 1 was removed (upper gastrointestinal bleeding) from final analysis. Monthly assessment included Hb level, mean corpuscular volume, iron level, iron-binding capacity, ferritin level, TSAT, and Hb content in reticulocytes. In addition, biointact parathyroid hormone, aluminum, C-reactive protein (CRP), and liver enzymes were measured every 3 months. RESULTS: Age, sex, race, and time on dialysis therapy were similar in both groups. At 6 months, Hb levels significantly increased from 9.3 to 10.5 g/dL (93.0 to 105.0 g/L) in group 1, but not group 2 (9.3 to 9.6 g/dL [93.0 to 96.0 g/L]; P = 0.0001). Similarly, TSAT increased from 28.9% to 37.3% in group 1, but not group 2 (28.7% to 29.3%; P = 0.0001). EPO dose (477 to 429 versus 474 to 447 U/kg/wk), iron-binding capacity (216 to 194 versus 218 to 257 microg/dL [38.7 to 34.7 versus 39 to 46 micromol/L]), and CRP level (2.8 to 0.9 versus 2.8 to 2.2 mg/dL) decreased significantly in group 1, but not in controls. Changes in Hb content in reticulocytes and ferritin level also were statistically significant in group 1. There was no change in biointact parathyroid hormone levels. Although serum iron levels and intravenous iron doses changed within each group, changes were equal between the 2 groups. CONCLUSION: In hemodialysis patients with refractory anemia and hyperferritinemia, vitamin C improved responsiveness to EPO, either by augmenting iron mobilization from its tissue stores or through antioxidant effects.
Iron management on dialysis patients is difficult that it fluctuates and cannot be kept at steady level, so iron given intervenously usually brings the levels up instantly, but also can cause an iron overload that liver carries an excess iron load. Other iron overload problems come from past blood transfusions…in that case, they’d administer such drug therapies such as Desferal to reduce the overload…, but I think patients who have an iron overload are not given any iron supplements at all. For me, this is something that has happened in the past… it took about 3 years for my iron overload to come down…