UNDERSTANDING CHANGES IN PERIOPERATIVE RENAL FUNCTION

The precise mechanisms heralding the transition from compensated preserved renal function to uncompensated renal failure during the perioperative period remain poorly understood, in part because the methods used to assess renal function changes are insensitive and nonspecific. All anesthetic techniques and perioperative events that decrease blood pressure and cardiac output have the potential to alter renal function because of blood flow redistribution within the kidney and decreased glomerular filtration.

Effects of Regional Anesthesia

Regional anesthetics and the kidneys interact in a complex manner that varies according to the underlying cardiovascular, renal, fluid, and electrolyte status of the patient^[45] (see Chapter 43 , Chapter 44 , and Chapter 45 ). The combined effect of multiple factors (e.g., catecholamines, renin-angiotensin, ADH, steroids, prostaglandin) determines the consequences for renal function. The effect of sympathetic blockade depends on the level of the block and the presence of underlying disease. In a patient with global systolic ventricular dysfunction or dilated cardiomyopathy, regional anesthesia may exert the beneficial effects of an afterload-reducing and preload-reducing agent. However, the same anesthesia in a patient with hypovolemia may exacerbate hypotension and decrease renal perfusion. The interactions between regional anesthesia and renal function are different in patients with different underlying disease. In patients with ischemic heart disease, regional anesthesia may exacerbate regional myocardial dysfunction through vasodilation, hypotension, and decreased coronary perfusion pressure^[46] and may thereby decrease renal perfusion.

Spinal cord segments T4 through L1 contribute to the sympathetic innervation of the renal vasculature, which is innervated through sympathetic fibers from the celiac and renal plexus.^{[27] [47]} As long as flow is maintained and perfusion pressure does not fall below the autoregulatory range during spinal and epidural anesthesia, there is little change in GFR or renal vascular resistance. Sulerman and colleagues^[48] demonstrated in healthy volunteers that renal blood flow is unchanged during epidural anesthesia with a T6 sensory block. In their study, mean arterial pressure remained above 70 mm Hg and never decreased below 6% of the baseline level. The sympathetic innervation of the kidney affects multiple aspects of renal function, including hemodynamics, electrolyte and water reabsorption, and renin secretion.^[45] Urine volume and free water clearance may decrease during spinal anesthesia as a result of increased ADH secretion. Increased renal sympathomimetic activity decreases renal blood flow through α-adrenergic mediation and increases renin release through β-adrenergic innervation directly or by interaction with the renal tubular macula densa and the baroreceptor reflex mechanism.^[49]