SAEVA Proceedings 2015 | Page 16

South African Equine Veterinary Association Congress 2015  Protea Hotel  Stellenbosch (EquioxxTM) to equine practice, it is logical to assume that use of this NSAID may be less nephrotoxic than the other non-specific NSAIDs. However, a word of caution is warranted as the new generation of more COX-2 selective NSAIDs has not really been demonstrated to be renoprotective in experimental studies in other species. Diagnosis of acute kidney injury: As mentioned above, AKI/ARF should be suspected in patients showing more lethargy and anorexia than would be expected with the primary disease process and in patients that fail to produce urine within 6-12 hours of initiating fluid therapy. Rectal palpation in horses with ARF may reveal enlarged, painful kidneys in some cases and enlargement can be confirmed by renal ultrasonography. Renal ultrasonography may also reveal perirenal oedema, increased echogenicity of the renal cortex, and/or dilation of renal pelvis. At necropsy, the renal cortex is typically pale and bulges on cut section due to oedema. The diagnosis of AKI/ARF is confirmed on the basis of history, potential exposure to nephrotoxins, clinical signs, and laboratory findings. With regard to the latter, the increase in Cr is often several-fold greater (to 5-15 mg/dl [440-1320 µmol/L]) than that for blood urea nitrogen concentration (BUN, to 50-100 mg/dl [18-36 mmol/L]) resulting in a lower than normal BUN to Cr ratio (<10, mg/dL units). Hyponatremia, hypochloremia, and hypocalcemia are usually present and, in more severe cases, hyperkalemia, hyperphosphatemia, and metabolic acidosis may also be detected. With oliguria or anuria, hyperkalemia can be severe (>7 mEq/L) and may precipitate life-threatening cardiac arrhythmias. Urinalysis should be performed on all horses in which AKI/ARF is suspected. Low urine specific gravity (<1.020) in the face of dehydration and gross or microscopic haematuria are common findings. Glucosuria may also be detected as a consequence of proximal tubular damage. Examination of urine sediment may reveal casts and increased numbers of erythrocytes and leukocytes while the amount of urine crystals may be decreased. Treatment of AKI/ARF: Initial treatment of AKI/ARF should focus on judicious fluid therapy to replace volume deficits and correct electrolyte and acid-base abnormalities. Sodium and chloride replacement are often required in horses with polyuric ARF and can be accomplished by IV administration of a polyionic replacement fluid or through electrolyte supplementation in grain feedings or as oral pastes. Serum potassium concentration in horses with nonoliguric ARF is often normal, and, except for post-renal problems (obstruction or rupture), therapy intended to lower serum potassium is usually not necessary. Next, it is important to determine if the horse is oliguric or nonoliguric (normal urine output to polyuric) because prognosis for recovery is more favourable with nonoliguric ARF. In horses with prerenal failure, rather than intrinsic ARF, Cr should decrease by at least 30-50% within the initial 24 hours of fluid therapy. In contrast, Cr remains little changed, or may increase, with ARF. In horses that remain oliguric after 12-24 hours of appropriate fluid and electrolyte replacement, furosemide (1-3 mg/kg, IV, q 2 h) should be administered. Unfortunately, furosemide treatment is often ineffective in increasing urine output in horses with ARF. If urine is not voided after the second dose, administration of mannitol (0.5-1 mg/kg as a 10-20% solution) can be instituted, although use of this osmotic diuretic is controversial. Renal arterioles contain dopamine type 1 receptors and a constant rate infusion of dopamine (3 µg/kg/min) increases RBF, GFR, and urine output by normal kidneys of several species, including horses. Consequently, this drug has been used for several decades for treatment of anuric ARF in human intensive care units and is recommended in several equine texts. However, several large studies of human patients indicated that dopamine treatment had little impact on survival while it also posed a risk of inducing or 16