Figure 1. Glomerular Filtration as a Function of Glomerular Blood Flow.

Panel A shows normal glomerular blood flow with normal glomerular filtration rate. Panel B shows reduced renal perfusion pressure within the autoregulatory range, caused by intraoperative conditions such as anesthesia and medication induced hypotension or hypovolemia. Normal glomerular filtration rate is maintained with prostaglandin-mediated afferent arteriolar vasodilation and Angiotensin II-mediated efferent arteriolar vasoconstriction. Panel C shows persistent reduction in renal perfusion pressure below the autoregulatory range. This can be seen intraoperatively with protracted systemic hypotension or severe hypovolemia due to hemorrhage and blood loss. In this state, endogenous vasoconstrictors released from the renal sympathetic nerves increase the afferent arteriolar resistance, which results in a rapid decline in glomerular filtration rate and decrease in renal blood flow. This eventually leads to tubular cell damage and cell death. Panel D shows reduced glomerular filtration rate with nonsteroidal anti-inflammatory drug use due to loss of vasodilatory prostaglandin. Panel E shows the effect of angiotensin-converting-enzyme inhibitor or angiotensin-receptor blocker. Loss of angiotensin II decreases both the afferent and efferent arteriolar resistance, relaxing the efferent arteriole significantly more. The net clinical effect is unchanged or slightly decreased glomerular filtration rate. Panel F shows the effect of chronic hypertension on the preglomerular arterial vessels, primarily the afferent arterioles. Chronic hypertension eventually leads to thickening of arteriole walls and narrowing of lumen, a process known as arteriolosclerosis. This results in inadequate blood flow through the glomeruli and may produce glomerular and tubulointerstitial ischemia. Conditions displayed in Panel D-F can contribute to the development of “normotensive” perioperative acute kidney injury.