VIDEO: Managing anemia in patients with CKD

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Well, the first step is diagnosis. We have to be screening for anemia among our patients with chronic kidney disease. And I think that requires that we understand that this is a fairly prevalent complication of CKD even in earliest stages. It's estimated that patients with stages three or even two CKD have a about a 15 to 20% prevalence of anemia as defined by the World Health Organization. That would be a hemoglobin less than 12 in women and less than 13 in men. As you get to stage three CKD, it's up to 30 or 40%. And when you get to stage four CKD, it's up to 50%. And patients who are not on dialysis and stage five CKD, it's about 50%. And then when you get up to stage five CKD on dialysis, the instance of anemia is 90%.

So unless we're screening for what's essentially a very prevalent complication among our patients with chronic kidney disease, we're not going to make the diagnosis. We can't wait until the patients say "Oh my God, I'm so tired, I can't function. "You know, please help me," and then do a CBC. We have to understand that that's really way too late in the natural history of the anemia with progressive decreases in their hemoglobin over time, and it would be nice to be able to catch the anemia earlier so that we can work it up, figure out what's causing the anemia, and ultimately, to try to treat it effectively before it gets to the point where the patients are totally disabled, and have a significant decrease in their quality of life. So again, diagnosis is key. We’ve got to be screening our patients with CKD for anemia.

The second is evaluating it. Not everybody with CKD who has anemia is it due to erythropoietin deficiency causing decreased red cell production. It's estimated that 50% of patients who have anemia in the setting of CKD have iron deficiency. So we need to be working up the anemia if it's present by screening for iron deficiencies. It's not very difficult. It's an easy test to order, and it's a relatively easy test to interpret. The anemia guidelines from the National Kidney Foundation define iron deficiency in the setting of chronic kidney disease as a serum ferritin less than a hundred, or at transferrin saturation of less than 20%. Those are higher thresholds for the diagnosis than we see in the general population, and it reflects the fact that the inflammatory state of chronic kidney disease requires that patients have higher iron levels in order to avoid the impairment of iron transport to the marrow that occurs in in the setting of CKD. So again, unless you're familiar with these thresholds for the definition of iron deficiency, you're going to overlook the iron deficiency, and you're going to under treat it.

The third is the issue of whether or not oral iron supplements should either be tried, or should, how long should they be continued? Again, in the setting of inflammation, oral iron supplements are very poorly absorbed. There's a tendency by many practitioners to probably wait too long for patients to fail oral iron therapy before they decide to do something else, and there's also a very high resistance to the prescription of IV iron because of fears about allergic reactions, anaphylaxis, and things like that, which I think are wildly exaggerated. There were some older agents that were on the market that were associated with anaphylactic reactions that had black box warnings, but most of the more current IV iron agents are very, very safe if administered at the appropriate rate, and patients benefit from them much quicker and to a much greater degree than they do from oral iron agents.

Finally, you need to maybe screen for other things. Is the patient having other issues that may be contributing to the anemia? Are they having GI bleeding? Are they having, you know, malignancy? Are there other things that could be contributing to anemia that might require further evaluation? So once you've ruled out iron deficiency, which is the easiest thing to diagnose and treat, and you can't find any other cause, then the diagnosis of exclusion in patients with chronic kidney disease, and especially in patients with more advanced chronic kidney disease, is erythropoietin deficiency, both due to the decreased numbers of erythropoietin producing cells in the diseased kidney as well as what I mentioned before. The decreases in hypoxia inducible factor because of the perception by the kidney tissue that the oxygen tension is fine even though there's less oxygen delivery.

And then we have the issue of who should we be prescribing exogenous erythropoietin the therapy to among patients with chronic kidney disease? And you know, I must say that there's a lot of reluctance to use these agents as well. They have a black box warning. The FDA has come down pretty hard on them in terms of safety issues, and you're not generally encouraged to start ESA therapy until the hemoglobin is less than 10. Well, unfortunately, many patients are already symptomatic at a hemoglobin less than 10 when you consider that normal hemoglobin is greater than 12 in women and greater than 13 men. So it's unfortunate that we have to wait that long to use ESA therapy. ESA therapy in patients with chronic kidney disease can be cumbersome because it's injectable. The patient either has to learn how to self-inject at home or has to go to an infusion center to get the injections by a nurse. And many patients, again, especially if they're socioeconomically disadvantaged, may not be able to get the transportation to get these drugs, may not have enough money to pay the co-insurance on these drugs, or may not have adequate insurance at all to pay for these drugs, and therefore, many of these patients will develop more severe anemia, and that's obviously very frustrating for the clinician in terms of being able to offer the patient treatment that will improve their quality of life.