PON1 and uremia: Interestingly, toxins such as the reactive aldehyde acrolein are elevated in uremia, removed via hemodialysis, and demonstrate dose‐ and time‐dependent PON inactivation that is attenuated with N‐acetylcysteine.33 Similar to hemodialysis, renal transplantation also appears to normalize PON activity in ESRD.27 Interestingly, changes in PON‐1 activity within the chronic renal failure population do not appear to be linked to genetic polymorphisms,34–35 whereas genetic polymorphisms are linked to systemic PON activity measures in subjects with normal renal function.20,36–37