Pathophysiology of anemia in chronic kidney diseases: A review

Abstract

Backgroud. Anemia is one of the laboratory and clinical findings of chronic kidney diseases (CKD). The presence of anemia in patients with CKD has a wide range of clinically important consequences. Some of the symptoms that were previously attributed to reduced renal function are, in fact, a consequence of anemia. Anemia contributes to increased cardiac output, the development of left ventricular hypertrophy, angina, and congestive heart failure. According to current knowledge, anemia also contributes to the progression of CKD and is one of the factors that contribute to the high morbidity and mortality in patients with chronic renal failure and their reduced survival. Methods. MEDLINE search was performed to collect both original and review articles addressing anemia in CKD, pathophysiology of renal anemia, erythropoiesis, erythropoietin, iron metabolism, inflammation, malnutrition, drugs, renal replacement therapy and anemia management Conclusion. The present review summarized current knowledge in the field of the pathophysiology of renel anemia. Understanding the pathophysiology of anemia in CKD is crucial for the optimal treatment of anemia according to recent clinical practice guidelines and recommendation, and correct recognition of causes of resistence to treatment of erythropoietin stimulating agents (ESA).

Relation between anaemia and bone marrow features and serum erythropoietin in dogs with chronic kidney disease

“…Chronic anaemia, usually of the normocytic normochromic nonregenerative type, is a common and invariable complication of chronic kidney disease (CKD), resulting from decreased erythrocyte half-life, iron and folic acid deficiency, the action of uremic toxins and, especially, erythropoietin deficiency (Waki et al 2010, Macdougal 2011, Polzin 2011, Zadrazil & Horak 2014.…”

The Role of Hypercortisolemia in Ischemic Heart Disease Based on Comorbidity

“…2, у обстежених з ІХС та ане-мією легкого ступеня тяжкості у порівнянні із паці-єнтами контрольної групи спостерігалась активація периферійної ланки гіпоталамо-гіпофізарно-надниркової системи. Очевидно, анемія поглиблює гіпоксію, що має місце при ІХС внаслідок знижено-го серцевого викиду і недостатньої перфузії орга-нів і тканин [10], у результаті чого компенсаторно активується секреція кортизолу як основного адап-тогенного гормону в організмі людини. В подаль-шому із наростанням анемії спостерігається тенде-нція до виснаження глюкокортикоїдної функції кори надниркових залоз зі зниженням вмісту кортизолу в сироватці крові, яке, однак, не носить статистич-но вірогідний характер (р>0,05).…”

TLR4 and TLR9 Polymorphisms Effect on Inflammatory Response in End-Stage Renal Disease Patients

“…In the course of the inflammatory response, the absorption of iron as well as the mobilization of iron from the reticuloendothelial system, needed for erythroid cell proliferation and differentiation, is impaired, blunting, therefore, the response to rhEPO. An erythropoiesis-suppressing effect has been attributed to increased activity ofproinflammatory cytokines, and this relationship has been also proposed as a potential factor associated to rhEPO therapy resistance (2,3,5,6). Moreover, previous studies on ESRD patients showed evidence of a T-helper I polarized T-cell activation process, as well as neutrophil activation based on elastase plasma levels has also been associated with poor response to rhEPO (4).…”

“…Nevertheless, anemia is still highly prevalent among ESRD patients and 5-10% of patients developed resistance to rhEPO therapy (2,3). This may be explained by the inflammatory response, which alters the iron metabolism.…”

“…ESRD is strongly associated with a proinflammatory state and anemia, which are the most prevalent complications presented by these patients (2), although these two events may already exist in patients with CKD in pre-dialysis stages (3).…”