Page 715 - Small Animal Internal Medicine, 6th Edition

CHAPTER 41 Acute Kidney Injury and Chronic Kidney Disease 687

TABLE 41.1 BOX 41.1
VetBooks.ir Clinical Differentiation of Acute Kidney Injury and Some Causes of AKI in Dogs and Cats
Chronic Kidney Disease
ACUTE KIDNEY CHRONIC Nephrotoxins
• Ethylene glycol
CLINICAL FEATURE INJURY KIDNEY DISEASE
• Aminoglycosides
• Amphotericin B
Renal size Normal or Small and
mildly irregular or • Easter lily (cats)
enlarged normal • Grape or raisin toxicity (dogs)
• Hypercalcemia
Previous history of Absent Present or absent • Cholecalciferol rodenticide
polyuria and • Calcipotriene (Dovonex)
polydipsia • Anticancer drugs
Nonregenerative Absent Present or absent • Cisplatin
anemia • Radiocontrast dyes administered intravenously
Weight loss Absent Present or absent • Heavy metals (e.g., thiacetarsamide)
Poor body condition Absent Present or absent • Tainted food (melamine, cyanuric acid)
• Hydroxyethyl starch (increased risk with 10% solution
Poor hair coat Absent Present or absent but not 6%)
Ultrasound Normal-sized Enlarged
appearance of Renal Ischemia
parathyroid • Dehydration
glands • Trauma
• Anesthesia
• Sepsis
• Heat stroke
• Pigment nephropathy
• Myoglobinuria
• Shock
• Hemorrhage
• Surgery
• Nonsteroidal antiinflammatory drugs (NSAIDs)

Other
• Leptospirosis—acute tubulointerstitial nephritis
• Borrelia—rapidly progressive glomerulonephritis
• Cutaneous and renal glomerular vasculopathy—renal
thrombotic microangiopathy (especially Greyhounds)

Acute Hyperphosphatemia
• Tumor lysis syndrome

FIG 41.1
Photomicrograph of acute tubular necrosis showing normal which can contribute to additional ischemic damage. Causes
glomerulus with areas of tubular necrosis. Note some
tubules with loss of tubular epithelium, some with flattened of AKI in dogs and cats are presented in Box 41.1.
epithelium, and tubular lumens filled with necrotic debris AKI passes through three clinical phases (Fig. 41.3). The
(200×). (Courtesy Dr. Steve Weisbrode.) latent phase represents the time after exposure to a nephro-
toxin or renal ischemia before the onset of azotemia. It is
associated with an increasing number and severity of renal
to tubular cell membranes. The term nephrotoxicant refers to tubular lesions over time if the renal insult is not removed.
a chemical or drug that can result in renal injury regardless The latent phase often is not detected because clinical signs
of whether it is caused by direct nephrotoxic injury (e.g., are absent or minimal. Prompt removal of the inciting cause
aminoglycosides) or renal ischemia (e.g., NSAIDs). Patients will result in rapid return to normal renal function.
with underlying renal disease may develop AKI more readily Entry into the maintenance phase signifies that a critical
than patients with kidneys that were normal before the amount of lethal injury has occurred in the renal tubules,
insult. Concurrent dehydration also may increase the sever- and a course of 1 to 3 weeks of AKI is expected before res-
ity of AKI after renal ischemia or exposure to nephrotoxins, toration of renal function can occur. Removal of the inciting
in part because dehydration activates renal vasoconstriction, cause during the maintenance phase will not result in