Inflammation, high ferritin, and erythropoietin resistance in indigenous maintenance hemodialysis patients from the Top End of Northern Australia.
Use of erythropoiesis-stimulating agents (ESAs) has improved the management of anemia in patients on maintenance hemodialysis (MHD). Iron deficiency and inflammation cause ESAs resistance and are both common among indigenous people of Northern Australia. As part of quality assurance in our Renal Anaemia Management program, we observed that there was use of higher doses of ESAs and adjuvant iron therapy in our MHD patients. This study aimed to explore the relationship among iron studies, inflammation, ESA responsiveness, and ESAs and iron requirements in indigenous patients on MHD from the Top End of Northern Australia. We performed a retrospective cohort analysis of anemia management in a cohort of our patients on MHD. We extracted data for 178 indigenous and 19 non-indigenous patients from 1 March 2009 to 28 February 2010 from the Renal Anaemia Management database, which collects data prospectively in MHD patients. Ninety-nine percent of the whole sample had a ferritin level above the international guidelines threshold of >500 µg/L. Indigenous patients had higher ferritin (1534 ± 245.5 µg/L vs. 1013 ± 323.3 µg/L, P = 0.002). C-reactive protein (CRP) was high in 56.9% of the total cohort. One hundred percent of those with normal CRP had high ferritin (>500 µg/L). C-reactive protein was higher in indigenous than in non-indigenous patients. Erythropoiesis-stimulating agents hyporesponsiveness was higher in indigenous patients (P < 0.0001). There was no significant difference in ESAs hyporesponsiveness among different levels of CRP (P = 0.116), ferritin (P = 0.408), and transferrin saturation (P = 0.503). Indigenous patients required higher total iron dose (2820.30 [2000-4350] vs. 2336.12 [1912-2900], P = 0.02). There was no significant relationship between the high ferritin and CRP. In indigenous dialysis patients, iron therapy and ESAs use are higher. The high iron use is due to a lack of published evidence to guide the administration of iron in patients with high ferritin. The high ferritin and ESAs resistance could not be fully explained by inflammation and need further evaluation. Further studies are required to determine the safe use of iron and management of ESAs resistance in our hemodialysis population.
Department of Nephrology, Division of Medicine, Royal Darwin Hospital, Casuarina, Northern Territory, Australia; Northern Territory Clinical School, Royal Darwin Hospital Campus, Flinders University, Tiwi, Northern Territory, Australia.
Sandawana William
SW
Majoni
Joy-Anne
JA
Ellis
Heather
H
Hall
Asanga
A
Abeyaratne
Paul D
PD
Lawton
D000740:Anemia / Q000188:drug therapy / Q000378:metabolism; D001315:Australia; D002097:C-Reactive Protein / Q000378:metabolism; D015331:Cohort Studies; D004351:Drug Resistance; D004921:Erythropoietin / Q000494:pharmacology; D005260:Female; D005293:Ferritins / Q000032:analysis / Q000097:blood*; D006397:Hematinics / Q000008:administration & dosage* / Q000494:pharmacology; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D007501:Iron / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000009:adverse effects / Q000379:methods*; D012189:Retrospective Studies
D006397:Hematinics; D004921:Erythropoietin; D002097:C-Reactive Protein; D005293:Ferritins; D007501:Iron
ESA resistance; Hemodialysis; erythropoiesis-stimulating agents; indigenous Australians; inflammation; iron therapy