Renal function and anesthesia

1

Describe the anatomy of the kidney.

The kidneys are paired organs lying retroperitoneally against the posterior abdominal wall. Although their combined weight is only 300 g (about 0.5% of total body weight), they receive 20% to 25% of the total cardiac output. That means that within 5 minutes, the body’s entire blood volume has circulated through the kidneys. This exceeds skeletal muscle perfusion, even during heavy exercise by 8-fold and makes the kidney the most highly perfused major organ in the body. The renal arteries are branches of the aorta and originate just inferior to the superior mesenteric artery. The renal veins drain directly into the inferior vena cava. Nerve supply is abundant; sympathetic constrictor fibers are distributed via celiac and renal plexuses. Pain fibers, mostly from the renal pelvis and upper ureter, enter the spinal cord via splanchnic nerves.

The kidney can be divided into two zones: cortex and medulla. The medulla can further be subdivided into the outer and inner medulla ( Fig. 42.1 ). Each kidney contains about 1 million nephrons, which can be categorized as short, cortical nephrons or long, juxtamedullary nephrons. The short, cortical nephrons predominate and make up 85% of all nephrons in the kidney. All nephrons originate within the cortex with their loop of Henle contained in the medulla.

The glomerulus and Bowman capsule are known collectively as the renal corpuscle. Each Bowman capsule connects to a proximal convoluted tubule within the renal cortex which, as the name suggests, takes on the form of a “convoluted” structure, before it straightens and descends into the outer medulla, where it becomes the loop of Henle. The loop of Henle, for cortical nephrons, is short in that it only descends to the intermedullary junction where it makes a hairpin turn, becomes thick limbed, and ascends back into the cortex, where it becomes the distal convoluted tubule and comes into contact with the glomerulus and other cellular structures, known as the juxtaglomerular apparatus . Distal convoluted tubules then merge together to form collecting tubules within the cortex. The juxtamedullary nephrons (remaining ~ 15% of nephrons) are different from cortical nephrons in that they have a longer loop of Henle that descend deep into the medullary tissue. Juxtamedullary nephrons, in part because of their longer loop of Henle, play a significant role in the conservation of water.

About 5000 tubules join to form collecting ducts. Collecting ducts merge to form minor calyces, which then merge to form major calyces. The major calyces join and form the renal pelvis, the most cephalic aspect of the ureter.

2

List the major functions of the kidney.

• Regulation of body fluid volume and its composition

• Acid-base balance

• Detoxification and excretion of waste products, including drugs

• Secretion of renin (involved in extrarenal regulatory mechanisms)

• Endocrine and metabolic functions, such as erythropoietin secretion, vitamin D conversion, and calcium and phosphate homeostasis

3

Discuss glomerular and tubular function.

Glomerular filtration results in production of about 180 L of glomerular fluid each day. Filtration does not require the expenditure of metabolic energy and is mediated by a balance of hydrostatic and oncotic forces. The glomerular filtration rate (GFR) is the most important index of intrinsic renal function. A normal GFR is 125 mL/min in males and is slightly less in females.

Normal tubular function reduces 180 L/day of filtered fluid to about 1 L/day of excreted fluid, altering its composition through active and passive transport. Transport is passive when it is the result of physical forces, such as electrical or concentration gradients. When transport is undertaken against an electrical or concentration gradient, metabolic energy is required, and the process is termed active.

Substances may be reabsorbed or secreted from the tubules and may move bidirectionally, taking advantage of both active and passive transport. The direction of transit for reabsorbed substances is from tubule to interstitium to blood, whereas the direction for secreted substances is from blood to interstitium to tubule. Secretion is the major route of elimination for drugs and toxins, especially when they are plasma protein bound.

4

Review the site of action and significant effects of commonly used diuretics.

See Table 42.1 .

5

Describe the unique aspects of renal blood flow and control.

The renal blood flow (RBF) is about 1200 mL/min and is maintained at a constant flow for a mean arterial pressure ranging from 80 to 180 mm Hg because of autoregulation. The cortex requires about 85% of RBF to achieve its excretory and regulatory functions, the outer medulla about 15%, and the inner medulla about 1% of total RBF. The inner medulla only needs a small percentage of blood flow, as a higher flow would wash out the solutes that are needed to maintain the high tonicity (1200 mOsm/kg) of the inner medulla. Without this hypertonicity, urinary concentration would not be possible.

The principal goal of RBF autoregulation is to maintain a normal GFR, which is mediated by afferent and efferent arterioles, sympathetic tone, and hormonal influences. The euvolemic, nonstressed state has little baseline sympathetic tone. Under mild to moderate stress, RBF decreases slightly, but efferent arterioles constrict, maintaining GFR. During periods of severe stress (e.g., hemorrhage, hypoxia, major surgical procedures), both RBF and GFR decrease secondary to sympathetic stimulation.

The renin-angiotensin-aldosterone axis also affects RBF. At the juxtaglomerular apparatus, the macula densa can sense a decrease in sodium chloride delivery, causing the juxtaglomerular cells to release renin, which catalyzes the conversion of angiotensinogen to angiotensin I. Enzymes, primarily within the lung, convert angiotensin I to angiotensin II. Angiotensin II is a potent renal vasoconstrictor (especially on the efferent arteriole) and any increase (in addition to increased sympathetic tone) will cause a decrease in RBF.

6

Describe the sequence of events associated with decreased RBF.

The high perfusion to mass ratio of the kidney makes them highly susceptible to injury from decreased RBF. The initial response to decreased RBF is to preserve ultrafiltration by redistributing blood flow to the kidneys, selective afferent arteriolar vasodilation, and efferent arteriolar vasoconstriction. Renal hypoperfusion results in active absorption of sodium and passive absorption of water in the ascending loop of Henle. Although afferent vasodilation and efferent vasoconstriction can initially help maintain GFR, if these compensatory mechanisms are exhausted, GFR will decrease, leading to oliguria. However, the kidney is attempting to maintain intravascular volume, and from the kidney’s perspective, the process described is renal success .

Oliguria, itself, is a poor measure of renal function, because other factors, aside from hypovolemia or acute kidney injury (AKI), can decrease urine output, such as stress because of surgery or acute illness. For example, one physiological response to stress is to secrete antidiuretic hormone and increased sympathetic tone, where both can decrease urine output despite euvolemia, normal RBF, and normal functioning kidneys.

7

What is the equation that describes renal perfusion pressure?

Renal perfusion pressure can be calculated using the subsequent equation:

RPP, renal perfusion pressure; MAP, mean arterial pressure; CVP, central venous pressure; IAP, intrabdominal pressure

Note that only the higher of CVP or IAP should be used. This equation (and concept) is similar to the equations for cerebral and coronary perfusion pressure, as discussed in other chapters.

8

How is the renal perfusion equation clinically relevant?

Any disturbance in physiology that reduces renal perfusion can cause AKI. For example, any decrease in mean arterial pressure (MAP) can decrease renal perfusion, causing decreased oxygen delivery and AKI. Similar to the cerebral vasculature, the renal vasculature is also autoregulated and can shift to the right in patients who have uncontrolled, chronic hypertension, leading to poor renal perfusion despite a normal blood pressure. Further, in the setting of advanced heart failure or cardiogenic shock, the central venous pressure (CVP) rises, which decreases renal perfusion, which is exacerbated in the setting of hypotension. Administering diuretics to patients with heart failure can reduce the CVP (and renal congestion) and improve renal perfusion and oxygen delivery. Lastly, disease states that increase intraabdominal pressure, such as abdominal compartment syndrome or excessively high intraabdominal pressure during laparoscopic surgery, can also impair renal perfusion, leading to a decrease in urine output and subsequent AKI.

9