https://www.kidney-international.org/article/S0085-2538(15)32377-2/pdf

Leukopenia, hypoxia, and complement function with different hemodialysis membranes

Alterations in respiratory drive, mechanics, muscle function, and gas exchange are frequent if not invariable consequences of uremia. Pulmonary dysfunction may be the direct result of circulating uremic toxins or may result indirectly from volume overload, anemia, immune suppression, extraosseous calcification, malnutrition, electrolyte disorders, and/or acid-base imbalances. The pulmonary system is unique because it is affected by the disease and its treatment. Acetate hemodialysis reduces alveolar ventilation and PaO2 due to extrapulmonic CO2 unloading. Peritoneal dialysis increases alveolar ventilation and intraperitoneal pressure. The latter leads to an elevated and lengthened diaphragm, a reduced functional residual capacity, basilar atelectasis, possible hypoxemia, and altered respiratory muscle function. In patients on chronic peritoneal dialysis, adaptations may occur that limit the reductions in lung volumes, PaO2, and respiratory muscle strength that are often observed during acute peritoneal dialysis. This review details how uremia and dialysis interact to alter pulmonary function.

Effect of uremia and its treatment on pulmonary function.

Effect of uremia and its treatment on pulmonary function: Commentary

https://www.ajkd.org/article/S0272-6386(88)80133-1/pdf

Hypoxemia During Hemodialysis: A Critical Review of the Facts

https://www.ajkd.org/article/S0272-6386(82)80078-4/pdf

Del Monte Ml

Papers

Consumpton of CO2 in metabolism of acetate as an explanation for hypoventilation and hypoxemia during hemodialysis.