Prevention of ARF and Acute Decompensation of Patients with CRF
Identify patients at risk such as older animals,
dehydrated animals, or those with known renal disease. Avoid known
nephrotoxins in these patients if other drugs are available.
Ensure normal fluid balance prior to administration of potentially
nephrotoxic agents (e.g., radiographic contrast agents) and prior to
anesthesia. You may assume subclinical dehydration is present and deliver a
volume of isotonic fluid equivalent to 3-5% body weight over several hours
prior to induction of anesthesia.
Example: 10 kg dog
3% x 10 kg = 0.3 kg x 1000 ml/kg = 300 ml
5% x 10 kg = 0.5 kg x 1000 ml/kg = 500 ml
Monitor urine output during anesthesia. The normal is > 1/2 ml/lb/hr. If
less, patient may be in the initiation stages of ARF. One may prevent
progression of ARF by increasing fluid rate, diuretic administration if
normotensive, or dopamine.
Monitor early indicators of injury or blood levels of potentially
nephrotoxic drugs in patients at high risk for nephrotoxicity.
Monitoring for renal injury caused by aminoglycosides is a good example.
Aminoglycoside toxicity: Since the
availability of quinolone antibiotics for treatment of pseudomonas
infections, there is less use of the aminoglycosides. In fact few reports of
aminoglycoside toxicity have been reported since the 1980s. Nonetheless
aminoglycosides serve as an example of drug induced renal injury.
Aminoglycosides are still in use for treatment of serious gram negative
infections. Renal injury results from the accumulation of aminoglycosides in
the proximal tubular epithelial cells. Neomycin is most toxic, streptomycin
the least and gentamicin, amikacin and Kanamycin are in between. Most
patients which develop gentamicin toxicity are polyuric but oliguria can
occur. In an experimental model of gentamicin toxicity in which dogs were
given 15 mg/kg SQ. x 10 days the following parameters were first detected as
being abnormal in the order listed: (Brown ACVIM 1990)
- cylindruria
- increased fractional sodium excretion
- increased urine protein/creatinine ratio
- increased fractional potassium excretion
- reduced urine specific gravity
- proteinuria measured by dipstick
- increased serum creatinine
- increased BUN
- increased fractional glucose excretion
- glucosuria by dipstick
This study demonstrates that early toxicity can be detected as changes in
the urinalysis but azotemia is a late development.
Aminoglycoside toxicity may occur up to seven days following cessation of
treatment. Risk factors that may perpetuate aminoglycoside toxicity include
dehydration, pre-existing renal disease, pyelonephritis, low K+, concurrent
use of other nephrotoxic drugs, concurrent use of antiprostaglandin drugs
that reduce vasodilator renal prostaglandin's resulting in reduced renal
blood flow, and treatments that exceed 5 days. Serum levels of gentamicin
can be measured to reduce the potential for toxicity. The goal is to achieve
peak levels of 8- 10 ug/ml and trough levels of <2 ug/ml. Human laboratories
provide opportunities to monitor blood levels of other potentially
nephrotoxic drugs as well.
Last Edited: Jul 26, 2007 2:22 PM
