RT Book, Section A1 Butterworth IV, John F. A1 Mackey, David C. A1 Wasnick, John D. SR Print(0) ID 1161429914 T1 Kidney Physiology & Anesthesia T2 Morgan & Mikhail's Clinical Anesthesiology, 6e YR 2018 FD 2018 PB McGraw-Hill Education PP New York, NY SN 9781259834424 LK accessanesthesiology.mhmedical.com/content.aspx?aid=1161429914 RD 2024/10/03 AB KEY CONCEPTS The combined blood flow through both kidneys normally accounts for 20% to 25% of total cardiac output. Autoregulation of renal blood flow normally occurs between mean arterial blood pressures of 80 and 180 mm Hg and is principally due to intrinsic myogenic responses of the afferent glomerular arterioles to blood pressure changes. Renal synthesis of vasodilating prostaglandins (PGD2, PGE2, and PGI2) is an important protective mechanism during periods of systemic hypotension and kidney ischemia. Dopamine and fenoldopam dilate afferent and efferent arterioles via D1-receptor activation. Reversible decreases in renal blood flow, glomerular filtration rate, urinary flow, and sodium excretion occur during both neuraxial and general anesthesia. Acute kidney injury is less likely to occur if adequate intravascular volume and normal blood pressure are maintained. The endocrine response to surgery and anesthesia is at least partly responsible for the transient fluid retention often seen postoperatively. Compound A, a breakdown product of sevoflurane, causes acute kidney injury in laboratory animals. Low fresh gas flow rates promote its accumulation in the anesthesia machine breathing circuit. No clinical study has detected significant kidney injury in humans as a consequence of sevoflurane anesthesia; nonetheless, some authorities recommend a fresh gas flow of at least 2 L/min with sevoflurane to minimize the risk of this theoretical problem. Pneumoperitoneum produced during laparoscopy causes an abdominal compartment syndrome–like state. The increase in intraabdominal pressure often produces oliguria or anuria that is generally proportional to insufflation pressure. Mechanisms include vena cava and renal vein compression; kidney parenchymal compression; decreased cardiac output; and increases in plasma levels of renin, aldosterone, and antidiuretic hormone.