The Oxygen Affinity of Haemoglobin in Chronic Renal Failure

Mitchell, T. R.; Pegrum, G. D.

doi:10.1111/j.1365-2141.1971.tb02707.x

Cited by 48 publications

(18 citation statements)

References 18 publications

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“…In addition to damage of the EP-producing site, another mechanism which contributes to the development of anemia in uremic patients is increase in red cell inorganic phosphates, and 2,3-DPG [104,117]. This, in turn, causes the hemoglobin's affinity for oxygen to decrease, and thereby results in a more favorable oxygen delivery to the tissues.…”

Section: Clinical Manifestations O F Abnormalities In Erythropoietin mentioning

confidence: 99%

Erythropoietm and the Kidney

Fried¹

1975

Nephron

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Erythropoietin is a polypeptide hormone, which is produced in response to a deficit in the delivery of oxygen to the tissues relative to their oxygen needs; although other feedback mechanisms also modulate its production. The kidneys play a major role in the elaboration of this hormone. However, the precise action of the kidney is not yet known. Diseases of the kidneys cause profound alteration in the normal regulation of erythropoiesis. Some of these are reviewed here.

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Section: Clinical Manifestations O F Abnormalities In Erythropoietin mentioning

confidence: 99%

Erythropoietm and the Kidney

Fried¹

1975

Nephron

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“…In chronic anemia, oxygen extraction from hemoglobin can be facilitated by increases in the concentration of 2,3-DPG in red blood cells. Although difficult to estimate, the overall effect of this shift in the oxygen-binding curve does probably not compensate for more than 0.5 g/dl reduction in hemoglobin concentration [8]. Moreover, its effect is limited when baseline oxygen extraction is already high, as in the heart.…”

Section: Physiological Backgroundmentioning

confidence: 99%

Target Hemoglobin in Patients with Renal Failure

Eckardt¹

2001

Nephron

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15 years after recombinant erythropoietin (EPO) has become available for the treatment of renal anemia, the target hemoglobin concentration to be achieved is still controversial. A positive impact of partial correction of renal anemia on quality of life has been conclusively demonstrated. Several more recent studies indicate that further improvement of well-being can be achieved with normalization of hemoglobin levels. In addition, there is increasing evidence that anemia is associated with the progression of left-ventricular hypertrophy and mortality. These findings imply that correction of renal anemia has the potential to improve patient prognosis. However, in patients with advanced cardiac disease, the US normal hematocrit failed to demonstrate a prognostic benefit and instead suggested that the attempt to normalize hemoglobin may be harmful. Nevertheless, in patients with less advanced cardiac disease complete correction of renal anemia may prevent progressive ventricular dilatation. The impact of early anemia correction is currently tested in several trials in predialysis patients. Irrespective of the uncertainities about the upper target range, current US and European guidelines have defined a hemoglobin concentration of 11 g/dl as the lower target range on the basis of both symptomatic and prognostic considerations. In the majority of patients these minimum requirements are not yet achieved. Less then 10% of patients receive EPO prior to the onset of dialysis, the mean hemoglobin level at the start of dialysis is not higher than 9 g/dl and a significant proportion of patients permanently remain below 11 g/dl.

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“…The effect of increasing pH on blood oxygen tension is described by the equation Alog Pa02 = BA pH (Bohr effect), where B = -0.48 at oxygen saturations of 0-95% and B = -0.34 at oxygen saturations of 99% [25], The Bohr effect has its major role in the dissociation of oxy gen from blood at the tissue level where pH and PO2 may be quite low [26]. However, the association of oxygen with deoxygenated hemoglobin is very rapid and satura tion occurs in less than 1 ms [27], It is unlikely that the increase in association constant produced by an increase in pH has any effect on pulmonary end capillary POj when the transit time for pulmonary capillary blood approximates 750 ms [28], Blurnberg and Keller [29] measured in vitro and calcu lated in vivo shifts in oxygen tension at 50% hemoglobin saturation (P5o) during acetate dialysis and noted an insignificant increase in vitro and a significant decrease in vivo of 1.06 mm Hg.…”

Section: Effects O F Acid-base Changesmentioning

confidence: 99%

Determinants of Oxygenation during Hemodialysis and Related Procedures

Sherlock¹,

Ledwith²,

Letteri³

1984

Am J Nephrol

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A decrease in arterial oxygen tension during hemodialysis has been attributed to a number of factors. In order to more completely define these factors, we studied respiratory gas exchange, arterial blood gases and pH, and dialyzer flux of CO₂ during pure ultrafiltration, three types of acetate dialysis, and sorbent regenerated bicarbonate dialysis in which the dialysate concentration of bicarbonate varies. Changes due to position and extracorporeal circulation of a 300-ml volume of blood (sham dialysis) were studied for any effect contributing to the hypoxemia noted with circulation through the membrane and variation in dialysate. Alveolar oxygen tension (PAO₂) is calculated by the equation PAO₂ = PIO₂-PaCO₂ (FIO₂ + ^1-FIO2/_RE). RE is the ratio of CO₂ excretion by the lung (VCO₂) to oxygen consumption (VO₂). RE equals RQ (metabolic quotient) when no extrapulmonary CO₂ losses occur. Normals in a lounge chair had no change in RE and PACO₂. RE decreased to 0.75 during sham dialysis and PAO₂ decreased. During pure ultrafiltration RE decreased due to a decrease in VO₂ and VCO₂ with proportionately greater decrease in VCO₂. PAO₂ decreased accordingly. Acetate dialysis produced an increase in oxygen consumption without a proportional increase in CO₂ excretion and both RQ and RE decreased. When PAO₂ decreased during any of these procedures, arterial oxygen tension (PaO₂) decreased without a change in A-aO₂ gradient. No changes in PaCO₂ were noted. RQ did not change during bicarbonate dialysis. At high bicarbonate dialysate concentrations, however, PaCO₂ increased and PAO₂ decreased. The major reason for hypoxemia during acetate dialysis is a decrease in alveolar oxygen tension due to changes in metabolism and a decrease in pulmonary CO₂ excretion when CO₂ is lost from the dialyzer. The increasing pH may contribute to the metabolic change during acetate dialysis and the hypoventilation during bicarbonate dialysis. There is little evidence to support an effect of pulmonary capillary obstruction or changes in oxyhemoglobin association on the decrease in arterial oxygen tension observed.

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The Oxygen Affinity of Haemoglobin in Chronic Renal Failure

Cited by 48 publications

References 18 publications

Erythropoietm and the Kidney

Erythropoietm and the Kidney

Target Hemoglobin in Patients with Renal Failure

Determinants of Oxygenation during Hemodialysis and Related Procedures

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