Abstract
Fabry disease (FD) is an X-linked lysosomal storage disease caused by a deficiency in the enzyme, α-galactosidase A. FD has neurologic, cardiovascular, and kidney manifestations. Kidney dysfunction contributes significantly to mortality in people with FD. Analysis of the Fabry Registry showed that 57% of people with FD who died from cardiovascular causes had previously received kidney replacement therapy (KRT).1 Recombinant α-galactosidase A can be used to replace endogenous α-galactosidase A and has been available since 2001.
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