Regarding renal failure in ferrets:
 
I missed the initial posting, but a few comments on renal failure in
ferrets.
 
Renal failure is a common finding in older ferrets due to the kidneys
lack of significant regenerative capacity.  As all animals age, including
humans, as kindey tissue wears out, it is not replaced by more kidney
tissue, but by fibrous connective tissue, which doesn't do anything (just
takes up space, like a scar.) Over a lifetime, we continually lose renal
tissue, and our kindeys lose ability to perform necessary tasks, such as
to filter waste into the urine, and reclaim water as necessary to maintain
proper hydration.  As we get older, this is manifested by having to urinate
more frequently, etc.
 
Now, renal failure as a DISEASE is when the kidney loses its ability to
perform these functions earlier in life.  There are actually two types of
renal failure - acute and chronic (with chronic being the more common.)
Acute renal failure is that seen with drug intoxications, and some
hypotensive episodes.  Animals can recover from some types of acute renal
failure, with proper support.  In acute failure, you do not see the fibrous
connective tissue replacement - simply death of kidney tubule cells.  If
the animal has enough kidney left (usually 25%), there will be regeneration
of the cells and the animal will recover.  Acute renal failure is generally
a single, generalized insult over a short period of time, such as
administration of a drug (Gentamicin is a classic example in ferrets.)
The trick is support, but with acute renal failure, there is a chance of
recovery.
 
Chronic renal failure on the other hand, happens over a number of years,
and because renal tissue is replaced by scar tissue, there is no hope of
recovery.  We all lose reanl tissue by fair wear and tear, as do ferrets,
but usually the animals die of other causes before the critical 75% loss
is reached.  Ferrets that reach that point earlier in life will generally
die of renal failure.
 
How do you measure renal failure?  In general, by measuring certain blood
and urine parameters which only go awry once critical renal mass is lost.
After around 66% of the kidneys are lost, you lose the ability to
concentrate urine.  Measurements of the specific gravity of the kidneys
will be low and the animal's frequency of urination will increase.
However, very few of us watch closely enough to pick up the early signs.
AFter 75% of the kindey is lost, certain substances which are normally
excreted by functional kidneys tend to back up and are present in increased
levels in the blood - urea, creatinine, and phosphorus - which can be
picked up by routine blood tests.  As the level of blood urea nitrogen
(BUN) increases, the animal will start to feel ill and may go off food.
This is probably the first obvious sign of renal failure that is seen by
owners.  Severely increased BUN may result in an ammonia smell to the
breath and the presence of mouth ulcers (which are far more rare in ferrets
than in dogs or cats with renal failure.)
 
There really is no cure for chronic renal failure, as that tissue will
never be replaced, only palliative treatment designed to decrease levels
of toxic substances in the blood and thus clinical signs.  When the levels
are high, large amounts of intravenous or subcutaneous fluids will help to
flush out some of these substances and decrease the levels.  They will of
course, build up again over time, with animals with less functional renal
tissue having faster increases.
 
Common wisdom in veterinary medicine suggests that lower protein diets are
renal-sparing, and we generally reduce protein content markedly in the
diets of animals with renal failure.  As a precaution in cats and ferrets,
two species who suffer inordinately high rates of renal failure as a
species, it is probably a good idea to decrease feed protein at the times
when renal changes are first seen microscopically - about 3.5 years in
ferrets.  At or arond that age, I personally change my ferrets over to
adult cat maintenance feeds and Totally Ferret geriatric food.
 
Bruce Williams, DVM
[Posted in FML issue 3218]