IRON DEFICIENCY IS A COMMON CAUSE OF ANEMIA IN CHRONIC KIDNEY
DISEASE AND CAN OFTEN BE CORRECTED WITH INTRAVENOUS IRON
L Gotloib, D Silverberg, R Fudin, and A Shostak
J Nephrol, March 1, 2006; 19(2): 161-7.
BACKGROUND: There is some epidemiological and clinical
evidence that the anemia seen in chronic kidney disease (CKD) in patients not on
dialysis could be due to a significant extent to iron deficiency, and that
adequate iron replacement could cause a marked improvement in the anemia even
without the use of erythropoietin (EPO). The purpose of this work was to study
the effects of intravenous (i.v.) iron administration (ferric gluconate -
Ferrlecit) on hemoglobin (Hb) of patients with CKD.
METHODS: Forty-seven consecutive patients with CKD with Hb
<12 g/dL in whom no underlying cause for the anemia could be found underwent
sternal bone marrow biopsy and had their red cell and blood iron parameters
measured. They then received 250 mg of ferric gluconate (Ferrlecit)
intravenously twice monthly for 3 months, and had their blood parameters
measured 1 month later. No patient received erythropoietin (EPO).
RESULTS: Forty-six patients had no evidence of any iron
deposits in the bone marrow - consistent with the presence of severe iron
deficiency. The mean serum ferritin and %transferrin saturation prior to
treatment were 235.9 +/- 54.3 ug/L and 13.5 +/- 4.1%, respectively, and both
increased significantly with the iron treatment. Mean Hb increased from 10.16
+/- 1.32 to 11.96 +/- 1.52 g/dL, an increase of 1.80 +/- 1.72 g/dL (p<0.01).
Twenty-six patients (55.3%) reached the target Hb of 12 g/dL. Ten patients
(21.3%) had an increase of 0.1-0.9 g/dL, nine patients (19.1%) had an increase
of 1-1.9 g/dL and 23 patients (48.9%) had an increase of >or= 2 g/dL.
CONCLUSIONS: Iron deficiency is frequently seen in anemic
CKD patients not on dialysis and its correction with i.v. iron will often cause
a marked increase in the Hb level, and the achievement of the target Hb of 12
g/dL even without EPO.
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