Page 960 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Urinary system 935

VetBooks.ir essential, as is aggressive fluid therapy. Treatment oxytetracycline, NSAIDs, endogenous pigments
Identification and control of the inciting cause are
(myoglobin or haemoglobin), heavy metals, vitamin
of pigment nephropathy is as described for AKI.
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stitial nephritis, renal microvascular thrombosis,
Sodium bicarbonate is indicated also when myoglob- D or K and plant toxins. Glomerulonephritis, inter-
ulinuria is associated with the AKI, as alkalisation of renal amyloidosis, renal pelvic calculi and renal neo-
the urine increases urinary myoglobin solubility and plasia may lead to CKD.
reduces intrinsic damage to the kidney. CKD develops when tubular and glomerular dam-
age exceeds renal reserve capacity. As renal function
Miscellaneous drug and decreases, surviving nephrons undergo functional
other toxicities changes that permit the horse to regulate water and
Horses may encounter a variety of nephrotox- solute homeostasis. However, if disease progresses,
ins, including cisplatin, proton pump inhibitors this compensatory mechanism may be overwhelmed.
(omeprazole), vitamin K , vitamin D, tetracycline,
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polymixin B, amphotericin B and heavy metals. Clinical presentation
Additionally, ingestion of acorns, ochratoxins and Anorexia and weight loss are the most common
cantharidin may induce renal failure. Cestrum diur- presenting complaints (Fig. 7.16). Poor athletic
num (flowering jasmine) contains vitamin D metabo- performance may also be detected early in the dis-
lites, which may cause severe renal disease in horses ease. With progression of uraemia, depression and
through their ability to disrupt calcium metabolism. lethargy develop. Rough hair coat, ventral oedema
Treatment involves removal of the initiating factor and PU/PD are commonly associated with CKD,
and should follow general principles for the treat- although PU/PD may not be identified in horses that
ment of AKI. If nephrotoxins have recently been are kept on pasture with free access to water. Urea
ingested, the stomach should be lavaged and charcoal may be converted to ammonia on mucosal surfaces
administered orally (1–3 g/kg via nasogastric tube). of the GI tract, resulting in ulceration. Uraemic hal-
Treatment with laxatives is also warranted after itosis and excessive dental tartar formation may be
charcoal treatment (MgSO at 0.5–1 g/kg mixed in present (Fig. 7.17). Encephalopathy is a possible but
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water via a nasogastric tube; Na SO at 1 g/kg mixed uncommon sequela of uraemia.
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in water via a nasogastric tube). MgSO and Na SO
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2
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can cause an electrolyte imbalance. Differential diagnosis
Differential diagnoses include pleuropneumonia,
CHRONIC KIDNEY DISEASE peritonitis, malabsorbtion/maldigestion syndrome,
Definition/overview
CKD results from irreversible loss of functional 7.16
nephrons. Serious clinical signs only occur when the
number of functioning nephrons decreases below
20–30%. All causes of AKI can lead to CKD and in
addition, several other metabolic, immunological,
infectious, obstructive and congenital disorders can
cause CKD.

Aetiology/pathophysiology
Acquired disorders are the most common cause
of CKD in horses. Extensive damage to the func-
tional nephrons usually follows AKI. Potential
causes include prolonged renal hypoperfusion and
exposure to nephrotoxins such as aminoglycosides, Fig. 7.16 Anorexia and weight loss in a horse with CKD.