Page 959 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

934 CHAPTER 7

VetBooks.ir develop complications such us generalised oedema, chapter (p. 958) for detailed information regarding
aminoglycoside administration.
laminitis or encephalopathy or those that remain
oliguric despite fluid therapy have a poor progno-
Increases in urinary GGT may be present with
sis for recovery, and generally go into CKD. Horses early tubular necrosis; however, this is a non-specific
that have recovered from AKI are more prone to finding. Monitoring of urine for casts can be useful
develop renal failure in the future. The prognosis for although their presence is transient and urinalysis
post-renal failure depends on the ability to correct must be performed repeatedly throughout the day.
the underlying problem and whether intrinsic renal Monitoring of SG and blood urea and creatinine lev-
failure has developed. els can be performed, but no changes will be detected
until at least 70% of renal function has been lost.
SPECIFIC AETIOLOGIES ASSOCIATED Therefore, efforts are best addressed at preventing
WITH ACUTE KIDNEY INJURY aminoglycoside-associated renal failure.

Aminoglycoside toxicity Non-steroidal anti-inflammatory
Aminoglycoside toxicity is a common cause of intrin- drugs
sic AKI in horses. Neomycin is the most nephrotoxic NSAID use may lead to AKI, particularly if used
of the aminoglycosides and streptomycin the least. at excessive doses or in dehydrated or hypotensive
Gentamicin, kanamycin and amikacin are placed horses. The pathological lesion of medullary crest
between neomycin and streptomycin. Gentamicin is necrosis is caused by disruption of renal synthesis of
most commonly associated with renal failure because prostaglandins, which have an important function in
of its widespread use. regulating renal perfusion. Characteristic signs of
Aminoglycosides may accumulate within tubu- renal failure are displayed. Haematuria may also be
lar epithelial cells, disrupt phospholipid metabolism present.
and cause tubular necrosis. They also cause renal If NSAID-associated AKI is suspected, NSAID
vasoconstriction. Damage to the tubular epithelial administration should be ceased, if possible. If anal-
cells usually develops after 3–5 days of aminoglyco- gesia is required, alternative drugs, including alpha-2
side administration and most commonly occurs in agonists and/or opioids, given parenterally, trans-
dehydrated and/or hypotensive animals. Concurrent dermally or via the epidural route, should be consid-
treatment with NSAIDs, diuretics, cisplatin and/or ered. If NSAIDs must be used, the lowest possible
cephalosporins may aggravate the disease. Diagnosis doses should be administered, and normal hydra-
is based on a history of aminoglycoside adminis- tion and blood pressure must be maintained. Of the
tration, clinical signs and a laboratory diagnosis of NSAIDs commonly used in horses, phenylbutazone
intrinsic AKI as discussed above. is suggested to be the most nephrotoxic, followed by
Nephrotoxic drugs should be promptly discon- flunixin meglumine and ketoprofen. Treatment of
tinued in horses that show any sign of AKI. Horses NSAID-associated AKI is as described above.
with aminoglycoside-associated AKI are usually
polyuric. Progression to oliguric or anuric renal Pigment nephropathy
failure is rare and recovery occurs on discontinuing Haemoglobin and myoglobin are potentially neph-
the drug and provision of supportive care in most rotoxic. Horses with severe haemolysis or rhab-
cases. domyolysis are at risk of developing pigment
A variety of measures can be used in an attempt nephropathy, particularly if dehydrated or hypoten-
to prevent aminoglycoside-associated AKI. The sive. Nephropathy is thought to be associated with
most important is to ensure that patients are ade- direct tubular toxicity (heme-mediated proximal
quately hydrated and have no underlying renal dis- tubular cell toxicity), tubular obstruction (intratu-
ease. Monitoring of peak and trough drug levels is bular cast formation) and renal vasoconstriction.
very useful, where possible. The reader should refer Coagulopathies that may be associated with severe
to the renal pharmacology section at the end of this haemolysis also affect renal vasculature integrity.