Anemia in Hemodialysis Patients

Higgins, Michael R.; Grace, Michael; Ulan, Raymond A.; Silverberg, Donald S.; Bettcher, K. B.; Dossetor, John B.

doi:10.1001/archinte.1977.03630140028009

Cited by 19 publications

(6 citation statements)

References 18 publications

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“…Thus, during the hemodial ysis procedure, endogenous P, , increased by a total of about 20% and RBC survival de- A number of studies have demonstrated diminished RBC survival in patients with chronic renal failure [ 10-131. In the early days of dialysis, many reports documented relatively massive RBC destruction during hemodialysis due to exposure to excessively warm [18] or hypotonic [ 191 dialysate, or to excessive concentrations of nitrate [20], chloramine [21], or copper [22]. Formalin sensitivity [23] and obstruction of the extracorporeal circuit [24] also were reported to cause hemolysis during hemodialysis.…”

Section: Discussionmentioning

confidence: 99%

Use of alveolar carbon monoxide measurements to assess red blood cell survival in hemodialysis patients

1994

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We recently described a simple technique for measuring RBC survival based on measurements of the concentration of carbon monoxide (CO) in alveolar air, corrected for environmental CO using a device that equilibrates with atmospheric CO at the same rate as does the patient. The purpose of the present report is to demonstrate the clinical utility of this method via measurements of RBC turnover in hemodialysis patients. Prior to dialysis, the mean RBC survival of 9 chronic dialysis patients was 70 +/- 9 days, about 50% shorter than that of 32 healthy subjects. During the dialysis, the endogenous PCO increased by 14% (P < 0.05) while subjects not undergoing dialysis had a 6% fall in endogenous PCO over this same time period. Thus, this technique demonstrated that the hemodialysis procedure resulted in about a 20% increase in RBC destruction. This increased RBC destruction has not been detectable with previous methodologies (including conventional measurements of CO production) due to the insensitivity and lack of reproducibility of conventional techniques. We conclude that the simple, non-invasive measurement of endogenous PCO provides the most accurate available means of assessing the influence of a variety of acute manipulations on RBC survival.

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Section: Discussionmentioning

confidence: 99%

Use of alveolar carbon monoxide measurements to assess red blood cell survival in hemodialysis patients

1994

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“…Proinflammatory cytokines, elevated during critical illness, may also exacerbate intestinal or other bleeding disorders through vasodilation and increased permeability of the intestinal wall. 18 Coagulopathy, a commonly encountered problem in the ICU, may exacerbate the blood loss and make control of bleeding even more challenging.…”

Section: Active Bleedingmentioning

confidence: 99%

“…Available data indicate that there is an inverse correlation between red blood cell survival and serum blood urea nitrogen concentration. [18][19][20][21] In uremic patients, the normal response to hypoxemia is partially blunted. With initiation of dialysis, these patients usually show improvement in anemia symptoms and decreased transfusion requirements.…”

Section: Renal Failurementioning

confidence: 99%

“…Several studies have reported that the levels of these cytokines are elevated during critical illness, with the subsequent inhibition of the gene that encodes erythropoietin, suppression of erythropoietin production, and blunting of the erythropoietic response. 3,18,[25][26][27][28] Cytokines also appear to stimulate iron-binding proteins that sequester iron and also exert direct toxic effects on erythropoietin-producing cells. 29,30 Deficient erythropoiesis, as seen in inflammatory disease states, in which cytokines and other inflammatory mediators are elevated may explain why critically ill patients develop anemia despite the absence of active bleeding.…”

Section: Inflammationmentioning

confidence: 99%

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Anemia of Critical Illness

Asare

2008

Pharmacotherapy

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Anemia of critical illness, a commonly encountered clinical situation, is hematologically similar to that of chronic anemia, except that the onset is generally sudden. The etiology is usually multifactorial, occurring as a consequence of direct inhibitory effects of inflammatory cytokines, erythropoietin deficiency, blunted erythropoietic response, blood loss, nutritional deficiencies, and renal insufficiency. Although anemia is not well tolerated by critically ill patients, aggressive treatment of anemia can be just as detrimental as no treatment. Different types of anemia may coexist in a patient in the intensive care unit, making diagnosis and differentiation among these anemias complex, therefore requiring good diagnostic skills. Although several therapeutic options are available to treat anemia, critically ill patients often receive a transfusion, and yet, most recent studies indicate that blood transfusions in critically ill patients are associated with worse outcomes, including higher morbidity and mortality. These studies have generated interest in the administration of exogenous erythropoietin and iron therapy. Unfortunately, the accurate determination of iron status can be a rather difficult task, an undertaking that is made even more difficult by the presence of comorbid conditions that can affect the commonly used parameters for guiding iron therapy. The use of erythropoiesis-stimulating agents is rapidly gaining acceptance, although they also present potential problems of their own.

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“…Before the advent of rhEPO, severe anemia was a common complication in uremic individuals (45), resulting in disabling fatigue, diminished quality of life, and the need for frequent blood transfusions, which are potentially hazardous. In 1977, EPO was first purified by Miyake and colleagues (86).…”

mentioning

confidence: 99%

Renal anemia: from incurable to curable

Sato

Yanagita

2013

American Journal of Physiology-Renal Physiology

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Renal anemia has been recognized as a characteristic complication of chronic kidney disease. Although many factors are involved in renal anemia, the predominant cause of renal anemia is a relative deficiency in erythropoietin (EPO) production. To date, exogenous recombinant human (rh)EPO has been widely used as a powerful drug for the treatment of patients with renal anemia. Despite its clinical effectiveness, a potential risk for increased mortality has been suggested in patients who receive rhEPO, in addition to the economic burden of rhEPO administration. The induction of endogenous EPO is another therapeutic approach that might have advantages over rhEPO administration. However, the physiological and pathophysiological regulation of EPO are not fully understood, and this lack of understanding has hindered the development of an endogenous EPO inducer. In this review, we will discuss the current treatment for renal anemia and its drawbacks, provide an overview of EPO regulation in healthy and diseased conditions, and propose future directions for therapeutic trials that more directly target the underlying pathophysiology of renal anemia.

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Anemia in Hemodialysis Patients

Cited by 19 publications

References 18 publications

Use of alveolar carbon monoxide measurements to assess red blood cell survival in hemodialysis patients

Use of alveolar carbon monoxide measurements to assess red blood cell survival in hemodialysis patients

Anemia of Critical Illness

Renal anemia: from incurable to curable

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