Ambühl Patrice M
Department of Nephrology, University Hospital, Zurich, Switzerland.
Curr Opin Nephrol Hypertens. 2007 Jul;16(4):379-87. doi: 10.1097/MNH.0b013e3281bd8860.
The occurrence and pathogenesis of metabolic acidosis after renal transplantation is reviewed. Posttransplant acidosis is shown to be a key mechanism for major metabolic complications in mineral and muscle metabolism, and for anemia, discussed in the context of both acidosis and renal transplantation.
Continuous improvement in kidney transplant survival has shifted attention to long-term outcomes, specifically to disorders linked to cardiovascular disease, physical capacity and quality of life. Metabolic acidosis is gaining growing acceptance as a clinical entity and has occasionally come into focus in the context of renal transplantation. The possible link to metabolic disturbances resulting in impairment of musculoskeletal disorders and physical limitations, however, has not been considered specifically.
Available evidence suggests a high prevalence of (compensated) metabolic acidosis after renal transplantation, presenting as low serum bicarbonate and impaired renal acid excretion. This condition is associated with relevant disorders in mineral metabolism and muscle function. Current knowledge about the effects of acidosis on renal electrolyte handling, mineral metabolism and protein synthesis suggests that acid/base derangements contribute to the muscle and bone pathology, as well as anemia, encountered after kidney transplantation. Consequently, posttransplant acidosis may be a relevant factor in the causal pathway of impaired physical capacity observed in this patient group.
