While I also find that Rohde's explanation (which I read a long time ago)
of the interrelationship of all the above concepts is excellent, my
understanding of it is very different from yours.
It seems to me there is an obvious contradiction in your assertions that
ammonia is acidic and that at the same time "excreting ammonia lets the
body get rid of some excess acid", which is why Rohde calls protein a very
basic food. Indeed, if ammonia were acidic, excreting it would only add to
PRAL, rather than reducing it. I believe that Rohde implies that ammonia
(or, to be more precise, ammonium hydroxide NH4OH) is alkaline and thus
enables excretion of acids, e.g. ketones (since the NH4+ cation forms a
salt with the anion from the acid). If I am wrong, could you please provide
a reference about acidity of ammonia?
In accordance with that, I believe you are mistaken when you ascribe
toxicity of ammonia to its acidity: as far as I know ammonia toxicity (and
thus protein toxicity) has nothing to do with acid-base balance, but with
interruption of Krebs' cycle in the brain (energy deprivation of neurons)
and neurotransmitter imbalance. (See U.C. Davis lecture notes on metabolism
at http://www.zonehome.com/met/metprotnit.htm).
Your conclusions about harmfulness of gluconeogenesis and absoluteness of
protein ceiling are diametricaally opposite to what I see as the main ideas
of Rohde.
In my interpretation Rohde essentially says that acid-base balance is
irrelevant in the context of a low-carb high protein diet owing to
neutralization of excess acid in kidney by ammonia. Furthermore, it is my
understanding that this ammonia is generated in the first step of
gluconeogenesis in kidney (from glutamine), thus gluconeogenesis does
definitely not cause excess acidity. Rather, the gradual  translocation
(the so called acid-base metabolic switch) of
gluconeogenesis from liver (with alanine as substrate) to kidney seems to
occur in response to rise in blood acidity (e.g. ketosis or protein-induced
acidosis).
Thus, I would expect that a higher fat intake could raise the protein
ceiling since there would be less need for gluconeogenesis in liver due to
higher ketosis and resultant acid-base metabolic switch. (Incidentally, it
is not ammonia, as Richard Archer stated, but alanine, which is converted
into urea in liver  - ammonia normally does not appear in blood-stream or
liver due to its toxicity in brain; it is produced only in kidney where it
is immediately secreted.)

Regards

Darko