First cause:Less hemopoietin.
1. EPO, secreted by kidneys and liver, is a kind of glycoprotein hormone stimulating differentiation and fission of precursors of red cells(PRC). Interstitial fibroblast of kidneys is the main secreting part. The decisive factor of renal fibrosis is the damage of renal intrinsic cells. Interstitial fibroblast transforms into myofibroblast, leading to glomerulosclerosis, tubulointerstitial fibrosis and sclerosis. Hereto, the producing channel of hemopoietin breaks down completely.
2. Toxin prevents bone marrow from producing blood.
In the end stage of renal fibrosis, amounts of toxin accumulated in blood restrain bone marrow producing blood, such as middle molecular substance—peptide, others like amine, phenol and so on.
3. Lack of ferride.
4. Lack of folic acid.
Second cause:Increasing damaged red blood cells causing renal anemia.
Blood plasma.
Polyamine in blood during end stage of renal fibrosis shortens life expectancy of red cells and make red cells antolysis.
Metabolic block and brittleness of red cells also reasons for antolysis.
The damaged renal cells make red cells bear mechanical damage.
Third cause:Increasing lose of red cells.
Due to the damaged filtrating function of kidneys, reabsorption function of kidney tubules breaks down and that makes part of red cells lose in urine. In addition to the lose of left red cells during hemadialysis. These factors aggravate renal anemia.
Forth cause:Hyperthyroidism.
parathyroid hormone has the functions of antagonism against EPO, restraining the formation of red cells.Meanwhile, it can increase brittleness of red cells and can shorten life expectancy. In addition that parathyroid hormone can induce marrow fibrosis and makes marrow reduce. Therefore, parathyroid hormone is closely relevant with renal anemia.
