South African Equine Veterinary Association Congress 2015 Protea Hotel Stellenbosch
Renal failure in horses: what can we do?
Schott HC*
Professor, Equine Internal Medicine
Department of Large Animal Clinical Sciences
D-202 Veterinary Medical Center
Michigan State University, East Lansing, MI 48824-1314
(517)-353-9710 [email protected]
Acute renal failure (ARF) remains a relatively uncommon problem in horses. Nevertheless, it is a
serious disorder that if not properly recognized and managed often has a poor outcome. ARF
usually develops as a complication of another disease process that causes hypovolemia and
decreased renal perfusion (colic, colitis, haemorrhage, or exhaustive exercise). Recently, there
have also been reports of ARF developing with leptospirosis in equids. Treatment with
nephrotoxic medications including aminoglycoside antibiotics, oxytetracycline (when
administered for correction of flexural deformities in neonatal foals), and nonsteroidal antiinflammatory drugs (NSAIDs) as well as exposure to endogenous pigments (myoglobin or
haemoglobin), vitamin D or vitamin K3, heavy metals (mercury, cadmium, zinc, arsenic and lead),
or acorns can also cause ARF. Due to widespread use of gentamicin and nonsteroidal antiinflammatory drugs (NSAIDs) in equine practice, potential nephrotoxicity with these medications
will be discussed in further detail below.
Clinical signs in horses with ARF commonly reflect the primary disease process: colic, diarrhoea,
or restricted gait and pigmenturia due to rhabdomyolysis. Subtle clinical signs that should prompt
investigation of possible secondary ARF include more severe lethargy or inappetance than are
typically manifested with the primary disease, especially in patients with nonoliguric ARF.
Persistent anuria or oliguria followed by development of oedema in the face of supportive fluid
therapy, along w ith weight gain due to fluid retention, are more obvious clinical signs of ARF.
Occasionally, horses with severe ARF may develop marked conjuctival oedema and they may
also be ataxic or manifest neurological signs similar to hepatoencepalopathy. Diarrhoea and
laminitis may develop in more serious cases.
When these clinical signs are observed, serum biochemical analysis is indicated to assess for
azotaemia. Azotaemia can be prerenal in origin, consequent to decreases in renal blood flow
(RBF) and glomerular filtration rate (GFR), or can be due to primary (intrinsic) ARF or
obstructive disease or disruption of the urinary tract (postrenal failure). The term "prerenal
failure" has been used to describe reversible increases in BUN and Cr associated with renal
hypoperfusion. Serum electrolyte concentrations are generally within reference ranges and urine
specific gravity is classically increased with prerenal failure. Although use of this term is firmly
entrenched in both the human and veterinary medical literature, its use likely contributes to a lack
of recognition of subclinical renal damage that accompanies a number of medical and surgical
conditions. This can be attributed to a large renal functional reserve capacity. In many patients
with reversible azotaemia, changes in glomerular and tubular function and integrity can be
demonstrated by proteinuria and cast formation, impaired concentrating ability (urine specific
gravity of 1.015-1.030 in a markedly dehydrated patient), and an increase in urine sodium
concentration (>20 mmol/L). Despite the reversible nature of these functional alterations, a degree
of nephron loss may occur with prerenal failure. To increase awareness of subclinical renal
damage in patients with decreased RBF and GFR, the term acute kidney injury (AKI) has been
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