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Nov. 16, 2006 -- Kidney patients get high doses of an anemia drug have a higher risk of heart disease, stroke, and death, new clinical studies show.
The drug is epoetin alfa, a man-made form of a red-blood-cell-boosting protein normally made in the kidneys. The drug is sold by Amgen as Epogen and by Johnson & Johnson as Procrit. Amgen also makes a similar drug, darbepoetin alfa, sold as Aranesp. Another similar drug, epoetin beta, is sold in Europe as NeoRecormon by Roche.
Amgen, Johnson & Johnson, and Roche are WebMD sponsors.
People with chronic kidney diseasekidney disease often suffer anemia. Anemia has been linked to increased risk for heart disease complications and related death in people with chronic kidney disease.
Epoetin successfully treats anemia. High doses of the drug can raise red blood cell levels back to normal.
That was supposed to be a good thing. But two major clinical trials now show that it is not.
A 16-month, 1,432-patient clinical trial shows that kidney patients whose red blood cell count is normalized with epoetin alfa have a 34% higher risk of death, heart failureheart failure, heart attackheart attack, and stroke than patients who take lower doses of the drug.
And a three-year study of epoetin beta shows that when it is used to normalize red blood cell counts in kidney patients, it does not reduce their risk of heart disease or stroke compared with patients who take lower doses of the drug.
Both studies appear in the Nov. 16 issue of The New England Journal of Medicine.
It is not yet clear what the results mean. It could be that the real problem is whatever causes anemia in kidney patients -- not the anemia itself. Or it could be that correcting red blood cell levels comes at the cost of complications that counterbalance the benefit.
Either way, the trials seem likely to put an end to routine, high-dose epoetin treatment in kidney patients, note Giuseppe Remuzzi, MD, and Julie R. Ingelfinger, MD, in an editorial accompanying the studies.
"It seems wisest to refrain from complete correction of anemia in persons with chronic kidney disease," Remuzzi and Ingelfinger conclude.
SOURCES: Drueke, T.B. The New England Journal of Medicine, Nov. 16, 2006; vol 355: pp 2071-2084. Singh, A.K. The New England Journal of Medicine, Nov. 16, 2006; vol 355: pp 2085-2098. Remuzzi, G. and Ingelfinger, J.R. The New England Journal of Medicine, Nov. 16, 2006; vol 355: pp 2144-2146.