Physiologic changes resulting from CPB that are potentially damaging to the kidneys include reduced renal perfusion, loss of the renal blood flow autoregulatory reflexes, and inflammatory responses. Consequently, one of the greatest predictors of post-CPB renal dysfunction is CPB duration.
Acute renal failure occurs in approximately 7-8% of adult cardiac patients and is more common with increased age, low EF, diabetes, and preop renal dysfunction. Measures taken to elevate cardiac output intraoperatively generally improve renal blood flow (with the exception of high doses of epinephrine and dopamine which cause renal vasoconstriction and reduce renal blood flow).
The differential diagnosis of post-CPB creatinine increase is:
- Acute tubular necrosis, the result of prolonged hypotension leading to nephron ischemia
- Renal vascular diseases (either embolic or thrombotic)
- Obstructive disease (kidney stone) — very rare
- Transfusion related hemolysis reaction — more likely when large amount of blood products given
Potential preventative measures therefore include maintaining adequate renal perfusion, hemodilution, diuresis during bypass, and maintenance of alkaline urine (so hemoglobin doesn’t precipitate in the renal tubules).