Ben,

I'd suggest to merely use the value that most determines
physiological consequence: ammonia.  Here are 2 relevant excerpts:

1.  For levels ...

"Ammonia levels above 200 micromol/l are usually caused by
inherited metabolic diseases and it is essential to make a diagnosis
for genetic counselling, even if the patients die. The aim of treatment
is to lower the ammonia concentrations as fast as possible. Sodium
benzoate, sodium phenylbutyrate and arginine can exploit alternative
pathways for the elimination of nitrogen but haemodialysis or
haemofiltration should be instituted if ammonia concentrations are
>500 micromol/l or if they do not fall promptly. Long-term management
involves drugs, dietary protein restriction and use of an emergency
regimen during illness. Severe hyperammonaemia is usually
associated with irreversible neurological damage, particularly if levels
have been above 800 micromol/l for >24 hours ..."

Leonard JV, Morris AA. Urea cycle disorders. Semin Neonatol. 2002
Feb;7(1):27-35.


2. And one for relevant interventions ...

"In a patient with a presumed inherited metabolic disorder, the aim of
therapy should be to normalize blood ammonia levels. Recent
experience has provided treatment guidelines that include minimizing
endogenous ammonia production and protein catabolism, restricting
nitrogen intake, administering substrates of the urea cycle,
administering compounds that facilitate the removal of ammonia
through alternative pathways, and, in severe cases, dialysis therapy."

Mathias RS, Kostiner D, Packman S. Hyperammonemia in urea cycle
disorders: role of the nephrologist. Am J Kidney Dis. 2001
May;37(5):1069-80.

Ed