Early diagnosis of anemia associated with chronic kidney disease (CKD) and implementation of appropriate treatment changes patients’ lives in the short and long term. It not only improves their physical performance, cognitive abilities and sexual performance, but also reduces the risk of cardiovascular disease and delays the progression of CKD.
A common problem
Weakness, lack of energy while performing daily activities, headaches and dizziness, decreased concentration and attention – symptoms rightly associated with anemia are not alien to nephrological patients. Renal anemia is one of the important clinical syndromes during the development of chronic kidney disease (CKD). It is estimated that every fifth patient suffers from it, while in end-stage renal failure the percentage of patients with anemia increases to 50%. It is estimated that in Poland it is about 650 thousand. sick people, but most of them don’t even know it. Slowly and insidiously developing anemia, unfortunately, we accept it and go to the doctor when it is already very advanced. [1]
The primary and primary cause of renal anemia is deficiency of erythropoietin (EPO), a hormone that plays a key role in stimulating the bone marrow to produce red blood cells (erythrocytes). The very process of erythrocyte multiplication and differentiation from stem cells in the bone marrow of the flat bones and the epiphyses of long bones is called erythropoiesis.
In addition to insufficient EPO secretion, the main cause of anemia in CKD is iron deficiency, caused by reduced dietary iron intake, impaired absorption, blood loss through the gastrointestinal tract, and hormonal factors such as increased levels of hepcidin (a protein hormone whose task is to regulate iron levels in the blood). ) produced in the liver.
Malnutrition, vitamin B12 and folic acid deficiency, chronic inflammation and the use of angiotensin converting enzyme (ACE) inhibitors can also lead to the development of anemia in the course of CKD. [2]
Previous studies have shown that nephrogenic anemia is associated with high morbidity and mortality. Not only does it reduce the quality of life of CKD patients, negatively affecting all spheres of life: private, professional and sexual, but it also leads to many complications, including damage to the cardiovascular system. Hence, it is so important to recognize the causes of renal anemia early and implement appropriate treatment.
Reasonably and with sensitivity
Effective treatment of anemia in CKD became possible already in the 80s, with the introduction of the first form of recombinant erythropoietin into clinical practice, followed by erythropoiesis stimulating factors (ESAs – erythropoiesis-stimulating agents) with prolonged operation. The use of ESAs and the correction of anemia are associated with an improvement in the quality of life of patients, a slowing down of the progression of kidney damage and a reduction in cardiovascular mortality.
Currently, according to global and European recommendations, the treatment of renal anemia involves the administration of ESAs, supplementation with iron preparations and, in special clinical situations, blood transfusions. Importantly, the initiation of ESAs therapy should be preceded by a thorough diagnosis of the causes of anemia.
Considering that iron deficiency leads to an unsatisfactory response, and sometimes even a lack of response to treatment with standard doses of ESAs preparations, the state of iron metabolism should be assessed and corrected for any deficiency by oral or intravenous route before starting therapy. In the case of oral administration of iron, it is necessary to take into account the possibility of side effects from the gastrointestinal tract, as well as a decrease in the availability of iron in the case of simultaneous use of H2 receptor antagonists, proton pump inhibitors or calcium compounds. Hence, the intravenous route is preferred, and among the intravenous iron preparations, iron sucrose and iron gluconate are considered the safest. [3]
After iron deficiency has been corrected (ferritin levels> 100 ng / dl and transferrin saturation> 20%), it is time to properly treat anemia with ESAs. In patients with CKD during the period not requiring renal replacement therapy, both short-acting (alpha and beta) and long-acting erythropoietins (darbepoetin alfa and methoxypolyethylene glycol-epoetin beta) can be used. For all preparations, the subcutaneous route of drug administration is preferred. For practical reasons, the most widely used ESAs are nowadays.
The initial dose of ESAs should be determined individually, depending on the hemoglobin (Hb) concentration in the blood, the patient’s weight and the clinical situation. In turn, its further adjustment is made on the basis of the current Hb concentration in the blood, as well as the rate of increase in Hb concentration during the administration of ESAs. The current dose of ESAs as well as the clinical condition of the patient should be taken into account.
According to current guidelines, it is recommended not to exceed Hb values> 13,0 g / dl during treatment, and blood counts should be assessed at least monthly.
Although the widespread treatment with ESAs is undoubtedly a great breakthrough, it should be used wisely and sensitively. Before initiating therapy, it is advisable to weigh the potential benefits of reducing the number of blood transfusions and the clinical signs of anemia with the risk of complications from such therapy. Recognized risk factors for excessively rapid increases in blood Hb levels or elevations above 12,0 g / dl include: hypertension, stroke, thrombotic complications, including arteriovenous fistula thrombosis in chronic dialysis patients. ESAs should be used with particular caution in cardiovascular risk groups, especially in diabetic patients, but also in cancer patients (active or with a history of). [1]