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Hypoproliferative anemias: causes, symptoms, diagnosis, treatment
Last reviewed: 05.07.2025
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Hypoproliferative anemias are the result of erythropoietin (EPO) deficiency or decreased response to it; they are usually normochromic and normocytic. Kidney disease, metabolic disease, and endocrine disease are the most common causes of this type of anemia. Treatment is aimed at correcting the underlying disease and sometimes using erythropoietin.
Hypoproliferation is the most common mechanism of anemia in renal disease, hypometabolic states or endocrine failure (e.g., hypothyroidism, hypopituitarism), and hypoproteinemia. The mechanism of anemia is due to either inadequate efficiency or inadequate production of erythropoietin. In hypometabolic states, there is also an inadequate bone marrow response to erythropoietin.
Anemia in kidney disease
Insufficient production of erythropoietin by the kidneys and the severity of anemia correlate with the progression of renal dysfunction. Anemia occurs when creatinine clearance is less than 45 ml/min. Disorders of the glomerular apparatus (e.g., against the background of amyloidosis, diabetic nephropathy) usually manifest themselves with the most pronounced anemia for their degree of excretory insufficiency.
The term "anaemia due to kidney disease" reflects only that the cause of the anemia is a decrease in erythropoietin, but other mechanisms may increase its intensity. Moderate hemolysis may develop in uremia, the mechanism of which is not fully understood. Rarely, there is fragmentation of red blood cells (traumatic hemolytic anemia), which occurs when the renovascular endothelium is damaged (for example, in malignant hypertension, polyarthritis nodosa, or acute cortical necrosis). Traumatic hemolysis in children can be acute, often fatal, and is called hemolytic uremic syndrome.
The diagnosis is based on the presence of renal failure, normocytic anemia, reticulocytopenia in the peripheral blood, and insufficient erythroid hyperplasia for the given degree of anemia. Fragmentation of erythrocytes in a peripheral blood smear, especially when combined with thrombocytopenia, suggests the presence of traumatic hemolysis.
Therapy is aimed at improving renal function and increasing red blood cell production. As renal function normalizes, anemia gradually normalizes. In patients undergoing long-term dialysis, erythropoiesis may improve, but complete normalization is rarely achieved. The treatment of choice is erythropoietin at a dose of 50 to 100 U/kg intravenously or subcutaneously 3 times a week, along with iron. In almost all cases, the maximum increase in red blood cell levels is achieved by 8 to 12 weeks. Reduced doses of erythropoietin (approximately 1/2 of the initial dose) can then be administered 1 to 3 times a week. Transfusions are usually not necessary.
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Other hypoproliferative anemias
The clinical and laboratory features of other hypoproliferative normochromic, normocytic anemias are similar to those of renal disease. The mechanism of anemia in protein deficiency may be due to general hypometabolism, which may reduce the bone marrow response to erythropoietin. The role of protein in hematopoiesis is still unclear.