Disturbance of secretion of erythropoetin at a chronic renal failure
All patients with a chronic renal failure in a varying degree have anemia. Weight of anemia approximately corresponds to degree of a renal failure though there are also exceptions. For example, at a polycystosis of kidneys expressiveness of anemia is less, and at a gemolitiko-uraemic syndrome and mikroangiopatichesky hemolitic anemia it is more, than it would be possible to expect, proceeding from weight of a renal failure.
Anemia, apparently, is caused by a number of factors, it is characterized by decrease in time of life of erythrocytes which extent, most likely, corresponds to expressiveness of uraemia, disturbance of an erythrogenesis and hemodilution. At increase in blood of content of urea in erythrocytes there are metabolic changes which have reversible character.
Reaction of marrow corresponds to expressiveness of anemia that is in turn caused, apparently, by inadequately low level of erythropoetin in which products kidneys play an important role. At the same time it is difficult to be sure of reliability of data on the low level of erythropoetin as sensitivity of modern methods of its definition in plasma is unsatisfactory. Besides, it is shown that at a chronic renal failure in erythrocytes contents 2,3-FDG increases and size intracellular rn increases. These changes reduce affinity of erythrocytes to oxygen and increase taking of the last fabrics thanks to what the need for bigger secretion of erythropoetin decreases. It is shown that uraemic serum is capable to reduce iron absorption by in vitro erythrocytes.
The effect of hemodilution is always variable, but is undoubted that at some patients because of existence of hemodilution anemia seems to heavier, than it is actually. At other patients with an accessory factor blood loss which most often happens in a digestive tract owing to erosive or a canker of a mucous membrane of a stomach is. Blood loss can result also from disturbance of coagulability of blood.
Anemia is normotsitarny and normokhromny, but erythrocytes in the form of a grinding stone occasionally meet. Their emergence is caused by changes of lipids of a cellular membrane. From other pathological forms find poikilocytes, triangular and shlemovidny cells. At gastrointestinal, bleedings hypochromia erythrocytes can appear. The morphology of leukocytes and thrombocytes is not changed, and the number of reticulocytes is very variable and can be reduced, normal or raised. Mikroangiopatichesky hemolitic anemia can meet, but its discussion is beyond the present chapter, and this disease will not be considered further. Changes of marrow are rather small. The expected strengthening of erythropoietic activity is absent, and at some patients the erythrogenesis is even lowered.
The basis of therapy is made by treatment of a chronic renal failure. There is no specific treatment, except for long administration of erythropoetin, but this drug is among extremely scarce. It is proved that other drugs, including androgenic steroids and cobalt, are inefficient. Hemotransfusion usually is not required, but it anyway has to be the iron, minimum because of danger of suppression of erythropoietic activity of marrow of the patient and an overload of an organism. Serumal hepatitis belongs to other risk factors connected with hemotransfusion.