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.