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fed dry or canned commercial food, although again there was no difference in the prevalence of periodontal disease. These studies show that a natural diet or raw bones, does appear to confer some protection against dental calculus, but not against the more destructive periodontal disease. There is also the risk of fractured teeth.
Nitric oxide (NO), an important inflammatory mediator, has been shown to be increased in human periodontitis and agents blocking the production of NO or its effects might be valuable. Lactobacillus brevis (L brevis), is
a probiotic bacteria containing high levels of arginine deiminiase (AD). High levels of AD inhibit NO generation by competing with NO synthase for the same arginine substrate. In people, topical application of probiotics containing L brevis decreased inflammatory mediators involved in periodontitis. Topical L brevis CD2 in dogs showed reduction of gingival inflammatory infiltrates,
While the common idea of dry food cleaning the teeth is appealing, many dry foods do not decrease the risk of periodontitis. Similarly, feeding natural foods or raw bones may decrease dental calculus, but does not decrease the risk of periodontitis.
References available upon request
G. Segev1
1Koret School of Veterinary Medicine, Israel Introduction
The term ‘acute kidney injury’ (AKI) has been adopted
in recent years in both human and veterinary medicine and replaced the old term “acute renal failure”. The term AKI is more accurate, as not every injury is associated with a measurable failure. The new terminology
also sensitizes clinicians to early identification and intervention. Currently, an increase in serum creatinine concentration as little as 0.3 mg/dL or decreased
urine production for more than 6 hours is classified as AKI, even if concentration creatinine is still within the reference range. Yet, in many animals, the baseline creatinine concentration is unknown at presentation and urine production is not quantified. Thus any animal with acute onset of clinical signs, increased creatinine concentration, low urine specific gravity, without any evidence of previous chronic kidney disease, should
be suspected for AKI until proven otherwise. Presence of urinary markers as glucose or casts might aid in the diagnosis, however, these are present only in ~30%
of the cases, thus are insensitive. Novel sensitive and specific biomarkers are currently under investigation.
The most common etiologies for AKI in dogs can be categorized as follows:
1. Nephrotoxicity, including endogenous nephrotoxins (e.g., hemoglobin, myoglobin) and exogenous neph- rotoxins, including ethylene glycol, lilies (cats), grapes and raisins (dogs), medications (e.g., gentamicin) and contrast agents.
2. Infectious agents – leptospirosis, pyelonephritis, sepsis, and FIP in cats.
3. Ischemia / inflammatory.
Medical management
AKI is a systemic disease affecting many body organs, thus the treatment should be focused on the whole patient rather than on the kidney alone. The treatment should focus at identification and elimination of any inciting causes (if possible), controlling the ensued clinical signs and clinicopathologic abnormalities (i.e., retention of uremic toxins, acid-base and electrolyte disorders, changes in blood pressure, decreased erythropoietin production) as well as addressing complications (e.g., respiratory disorders, pancreatitis, disseminated intravascular coagulation etc.). The goal is
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