Aluminium accumulation in chronic renal failure affects erythropoiesis

Summary: Aluminium (Al) toxicity has been associated with anaemia in exposed patients with chronic renal failure (CRF). the present study was undertaken to determine whether the ingestion of Al citrate was able to affect erythropoiesis in rats with normal or impaired renal function. the renal insufficiency was induced by surgical procedures and control rats were sham operated. Twenty‐four rats were allocated to four groups of six rats each: (A) Sham; (B) Sham+Al; (C) CRF; and (D) CRF+Al. the groups B and D received daily doses of Al citrate (0.5 μmol/g bodyweight) and the groups A and C, deionized water, via the intragastric route. At the end of the experimental period (15 weeks) cultures of late erythroid progenitor cells (CFU‐E) stimulated with erythropoietin were performed and haematological parameters determined. the liver, kidney, brain, bone and serum Al amounts were quantified. the results are expressed as median and interquartile range. the CFU‐E growth was found inhibited in B and D groups (A: 100; B: 74/54‐83; C: 86/54‐98; D: 46/39‐53 %). the haematocrit values were significantly diminished in rats with renal insufficiency when compared to controls (A: 42/40‐43; B: 45/42‐46; C: 37/32‐40 and D: 37/24‐39 %). Serum Al accumulation was observed in B and D groups receiving Al (A: 8/5‐12; B: 36/36‐44; C: 5/5‐6; D: 45/26‐132 μg Al/l). No differences among groups were found in the liver and kidney Al contents, but uraemic state favoured Al accumulation in brain (A: 6/5.0‐9.0; B: 4/3.8‐4.3; C: 2/1.0‐3.0; D: 15/12.0‐21.0 μg Al/g tissue) and bone (A: 29/27‐31; B: 30/29‐39; C: 42/33‐48; D: 68/56‐79 μg Al/g tissue). We suggest that the heavy accumulation of Al in the bone compartment may result in a protracted endogenous exposure of bone marrow cells, affecting the erythropoiesis in vivo.