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 acidbase 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.