Abstract
Chronic kidney disease (CKD) is a global health problem characterized by progressive kidney failure due to uremic toxicity and the complications that arise from it. Anemia consecutive to CKD is one of its most common complications affecting nearly all patients with end-stage renal disease. Anemia is a potential cause of cardiovascular disease, faster deterioration of renal failure and mortality. Erythropoietin (produced by the kidney) and iron (provided from recycled senescent red cells) deficiencies are the main reasons that contribute to CKD-associated anemia. Indeed, accumulation of uremic toxins in blood impairs erythropoietin synthesis, compromising the growth and differentiation of red blood cells in the bone marrow, leading to a subsequent impairment of erythropoiesis. In this review, we mainly focus on the most representative uremic toxins and their effects on the molecular mechanisms underlying anemia of CKD that have been studied so far. Understanding molecular mechanisms leading to anemia due to uremic toxins could lead to the development of new treatments that will specifically target the pathophysiologic processes of anemia consecutive to CKD, such as the newly marketed erythropoiesis-stimulating agents.
Highlights
Chronic kidney disease (CKD) is a global public health problem characterized by a progressive loss of kidney function through the accumulation of uremic toxins leading to inflammation and endothelial dysfunction [1,2]
The European Uremic Toxin (EUTox) Work Group has compiled an authoritative list of 146 compounds as known uremic toxins and classified them into 3 groups based on their physicochemical characteristics such as the molecular weight, protein-binding capacity and removal pattern by dialysis [3,4,5,6,7]
With the exception of genetic polycystic disease; cases of enlarged kidneys in diabetic and amyloid nephropathies with deposits of amorphous specific material have a reduction of EPO-producing cells), together with a lowered set point for EPO production in case of hemorrhage. This decrease in EPO production is associated with true iron deficiency related to blood loss due to uremic enteropathy and hemodialysis treatment aggravated by iron-restricted anemia
Summary
Chronic kidney disease (CKD) is a global public health problem characterized by a progressive loss of kidney function through the accumulation of uremic toxins leading to inflammation and endothelial dysfunction [1,2]. EPO deficiency and iron deficiency are the main reasons contributing to anemia, a well-known consequence of CKD In this disease, the best available indicator of kidney function is the glomerular filtration rate (GFR), which estimates the total amount of blood filtered by the kidney that passes. Some of the risk factors that lead to common complications for CKD below 15% of its normal capacity. Some of the risk factors that lead to common complications for are shown in Figure [14,15,16]. Is the the complications could could be the be consequence of a strategy treatment of a risk It is theItcase of case of the development of hyperkalemia that is common in patients with heart anddisease.
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