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Nocturnal hypoxemia secondary to sleep apnea has long been implicated as a cardiovascular risk factor in renal failure, but to date there is no study that links nocturnal hypoxemia to cardiovascular outcomes in end-stage renal disease. Fifty uremic patients on regular dialysis treatment without
Using a dialysis electrode, previous studies showed a clear biphasic release of glutamate during anoxia and ischemia. In this study, we examined two hypotheses: (1) glutamate is of vesicular origin and its release is thus Ca2+- and ATP-dependent in the first phase, while in the second phase
We report the beneficial effect of control of anemia on hyperinsulinemia and hypoxemia in a hemodialysis patient with corrected transposition of the great arteries. The patient's hemoglobin (Hb) level of 10.3 g/dl on admission represents good control for hemodialysis (HD) patients, but it was too
The background of this study is the occurrence during acetate hemodialysis (HDA) of arterial hypoxemia associated with well described vasodilatator hemodynamic changes. Our aim was to evaluate the relationship between these 2 phenomena. Eleven patients (7 males, 4 females, mean age 54 years) were
Decrease in arterial oxygen tension has been reported during hemodialysis.(1-3) The etiology of the hypoxemia has not been clearly demonstrated. Intravascular leukostasis,(1) pulmonary arterial microembolization,(3) and loss of CO(2) through the dialyzer are some of the explanations given for this
Five mechanically ventilated patients were studied during hemodialysis. The aim was to determine if hypoxemia would develop, and to identify the causes. Respiratory variables (dynamic compliance, peak airway pressure, CO2production); oxygen uptake, and transport variables (alveolar and arterial PO2,
Arterial hypoxemia occurs frequently during hemodialysis. Proposed mechanisms for this phenomenon have included hypoventilation and embolism of granulocyte aggregates. We studied 18 patients with endstage renal failure who required chronic hemodialysis, and measured arterial blood gases, pulmonary
In a study of 72 patients treated with acetate and bicarbonate dialysis, the Authors verified if hypoxic hypoxia caused by dialysis depends on a deficit in oxygen content with an inherent risk of tissue hypoxia. PO2uv (uncompensated venous oxygen partial pressure) and CQ (cardiac compensation
Arterial oxygen partial pressure decreases during hemodialysis if acetate as buffer is used or if certain types of bioincompatible dialyzer membranes are used. Several hypotheses considering the main cause of this hypoxemia have been proposed. To gain more insight into the mechanisms leading to this
Dialysis-associated hypoxemia is frequently of clinically significant magnitude and is incompletely understood. In order to investigate the hypoxemia directly we labelled a patient's white blood cells with 111Indium-oxine prior to hemodialysis with acetate or bicarbonate baths. Both dialysate
To investigate whether hypoxia extends into the post-hemodialysis period, nine clinically stable-end stage renal disease patients were dialyzed against bicarbonate and one against an acetate batch, all with bioincompatible dialyzers. None had clinical evidence of cardiopulmonary overload on the day
In order to examine the effect of different dialysates on hemodialysis-induced hypoxemia, 6 stable patients with chronic pulmonary disease (CPD) were compared with 8 control subjects using, alternately, acetate and bicarbonate in the dialysate. These patients were also studied during acetate
We studied the role of blood-dialyzer-membrane interactions in hemodialysis-induced hypoxemia by measuring PaO2 and white blood cell counts during isolated ultrafiltration (UF). These values were compared to those obtained from the same patients during subsequent hemodialysis (HD; utilizing the same
Hypoxemia during hemodialysis may result from several differing processes. We initially studied patients undergoing standard acetate hemodialysis. At 15 minutes of dialysis, leukopenia (primarily neutropenia), a decline of platelet count, and hypoxemia occurred, but without a significant change in
Hypoxemia during hemodialysis has variously been attributed to worsening ventilation-perfusion (VA/Q) relationships, alveolar hypoventilation combined with a reduced respiratory quotient, increased right-to-left shunting, and diffusion impairment. It is difficult to separate out these various