Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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Chapter | 28 Avian Clinical Biochemistry
be elevated when renal function is below 30% of its original
capacity. For elevated UA and UR during starvation and
endurance flight see Sections III.B and III.C.
B . Articular and Visceral Gout
Hyperuricemia can result in precipitation of monosodium
urate monohydrate (MSUM) crystals in joints (articular
gout) and on visceral surfaces (visceral gout). The exact
mechanism of deposition or the predilection for certain
sites is unknown, although lower temperatures at predilection
sites have been suggested. Gout should not be
regarded as a disease but as a clinical sign of any severe
renal function disorder.
When birds are provided with dietary protein in excess of
their requirements, the surplus protein is catabolized and the
N released converted to UA. The total amount of UA formed
may surpass the clearing capacity of this substance from the
body and hyperuricemia, and articular gout may result. The
use of high-protein poultry pellets as the bulk food in psittacines
may result in an increased incidence of gout.
There is no consensus on the different etiologies of
articular and visceral gout in birds. The following hypothesis,
however, seems to explain all known facts about avian
gout. A plasma UA concentration that is slightly above the
solubility of MSUM will lead to UA precipitates in the body.
Predilection sites are those areas where the solubility of
MSUM is lower than in other areas. The joints and synovial
sheaths may be predilection sites because of a comparatively
low temperature. Articular gout is a sign of chronic moderate
hyperuricemia. MSUM deposits grow with time with chronic
hyperuricemia and form the typical tophi of articular gout.
If urates precipitate in the tubules or collecting ducts of the
kidney or the ureters (e.g., severe dehydration of long duration,
vitamin A deficiency), this will lead to an acute obstructive
uropathy (postrenal obstruction). Anuria or gross oliguria
and tubular secretion of UA are severely compromised. This
leads to a rapid and severe increase in plasma UA with precipitation
of urate crystals on many visceral surfaces and those
predilection sites for articular gout. This condition of visceral
gout will rapidly lead to death of the affected animal. This
hypothesis is based on the fact that no inflammation or tophi
are seen in typical predilection sites for articular gout, because
the condition has a rapidly fatal course. There is no time for an
inflammatory reaction or tophi to develop. In this situation, the
kidney tubules, collecting ducts, and ureters may contain UA
deposits. An alternative situation could occur in acute tubular
failure. In this condition, visceral gout could develop without
UA deposits in the tubules, collecting ducts, and ureters.
C . Acute versus Chronic Renal Failure
Renal function disorders may result from any progressive
destructive condition affecting both kidneys (chronic renal
failure), or from conditions wherein the function of the kidneys
is rapidly and severely, but often reversibly, compromised
(acute renal failure). In the latter condition, oliguria is
usual, whereas in the former situation, polyuria is normally
observed. It is important to differentiate between reversible
conditions (e.g., prerenal renal failure caused by dehydration
or shock of any cause, urolithiasis [postrenal renal failure]
and acute nephritis) and chronic irreversible renal failure.
Appropriate and timely treatment of acute renal failure can
often prevent further damage and in some cases result in
improved function. Extrarenal factors such as infection, gastrointestinal
hemorrhage, and hypovolemia can disturb an otherwise
stable, well-compensated asymptomatic chronic renal
patient and precipitate a desperately dangerous condition.
D . Prerenal Azotemia
Prerenal azotemia can be defined as the clinical condition
associated with reduced renal arterial tension leading to oliguria
and retention of nitrogenous waste products in the
blood. It is often seen during shock or severe dehydration.
No increased plasma UA concentrations were observed in
4-day dehydrated racing pigeons, whereas plasma UR concentration
had a significant 6.5- to 15.3-fold increase. Plasma
UR appeared to be the single most useful variable for early
detection of prerenal causes of renal failure ( Lumeij, 1987c ).
This is because UR is excreted by glomerular filtration,
whereas tubular reabsorption is dependent on urine flow,
which in turn depends on the state of hydration. During
hydration, almost all of the filtered UR is excreted and during
dehydration nearly all of the filtered UR is reabsorbed.
The active tubular secretion of UA, on the other hand, is not
dependent on arterial pressure, because the tubules of the
reptilian type nephrons are supplied by venous blood through
the renal portal system. The tubular reabsorption of UR in
conditions of renal failure accompanied by a low urine flow
(e.g., dehydration) in combination with a nearly unchanged
tubular secretion of UA causes a disproportionate increase in
plasma UR concentration, resulting in an elevated UR/uric
acid ratio. Although potentially useful for judging the hydration
status of a bird, UR is normally present in low concentration
in avian plasma and has traditionally been considered
an inappropriate variable to evaluate renal function in birds.
When the dehydration becomes more severe, this may
eventually lead to hyperuricemia. This might be caused by
reduced tubular blood supply which leads to reduced uric
acid secretion. Urates may also precipitate in the tubules
when there is active tubular secretion of UA in the absence
of urine flow. The latter condition looks much like acute
uric acid nephropathy in humans ( Watts, 1978 ).
E . Urea versus BUN
There is a great deal of confusion with respect to the conversion
of urea (CH 4 N 2 O) to blood UR nitrogen or “ BUN. ” Apart