Anatomy of the kidneys

The kidneys are two bean-shaped organs in the retroperitoneal spaces at the level of the twelfth thoracic to third lumbar vertebrae. The right kidney is slightly lower than the left. Each kidney weighs approximately 150 g. The notched portion of the kidney is called the hilum, which is where the ureter, the renal vein, and the renal artery enter the kidney (Fig. 13-1). The kidney is divided into an outer cortex and an inner medulla.

FIG. 13-1 Anatomy of renal and urinary systems. A, Urinary system. B, Cross section of a kidney.

Blood is supplied to each kidney by a renal artery arising from each side of the abdominal aorta. The rate of blood flow through both kidneys of a man who weighs 70 kg is approximately 1200 mL/min, or approximately 21% of the cardiac output. As the renal artery enters the kidney at the hilum, it divides into the interlobar arteries. Branches from the interlobar arteries divide into afferent arteries that supply the capillaries of the nephrons. The capillaries form the efferent arterioles and divide to form the peritubular capillaries that help to supply the nephron. (Figs. 13-2 and 13-3).

FIG. 13-2 Functional nephron.

(From Hall J: Guyton and Hall textbook of medical physiology, ed 12, Philadelphia, 2011, Saunders.)

FIG. 13-3 Arterial supply to kidney. Soon after entering the hilum of the kidney, the renal artery divides into several anterior and posterior branches. Branches divide into interlobar arteries, which give off arcuate arteries that course between cortex and medulla.

The nephron is the functional unit of the kidney. Together the kidneys contain approximately 2.4 million closely packed nephrons. Each nephron consists of a glomerulus, a proximal convoluted tubule, a loop of Henle, a distal convoluted tubule, and collecting ducts. The blood enters the afferent arteriole and goes into the glomerulus located in the cortex. The glomerulus is a compact network of capillaries encased in a double-layered capsule, the Bowman capsule. Filtered blood flows out of the glomerulus into the efferent arteriole. The portion of the blood that is filtered drains into the proximal convoluted tubule. The renal tubules begin in the Bowman capsule. The pressure gradient, caused by renal artery blood flow, forces fluid to leave the glomerulus and enter the Bowman capsule. The filtrate flows into the proximal convoluted tubule, which is still in the cortex of the kidney, and then into the loop of Henle. The proximal loop of Henle is thick walled, but becomes thin at the distal segment in the medulla of the kidney. The filtrate then flows into the distal convoluted tubule, located in the cortex of the kidney, and passes into the collecting ducts. The collecting ducts traverse the cortex to the medulla, where they merge into the renal pelvis by way of the renal calyces. In the collecting ducts, the filtrate is termed urine.

The renal pelvis is a wide, funnel-shaped structure composed of the calyces draining the kidney. The pelvis drains into the ureter, which leads to the bladder.

Kidney physiology

Urine is formed by processes of filtration, reabsorption, and secretion. Filtration occurs as the blood passes through the glomerulus. The force of filtration is a pressure gradient that pushes fluid through the glomerular membrane. Approximately 180 L of water every 24 hours along with other substances is filtered out of plasma by the glomeruli (Table 13-1). Blood cells and heavy particles including proteins are retained in the blood because they are too large to pass through the glomerular epithelium. The presence of red blood cells or protein in the urine usually indicates a pathologic process in the kidney.

Reabsorption occurs in the proximal and distal tubules. Approximately 99% of the water filtered by the glomeruli is reabsorbed. Many substances in the water are reabsorbed with active or passive transport. Active transport requires energy for movement of the substance across the membrane. Passive transport can be regarded as simple diffusion that does not require energy.

Important constituents of body fluids—substances such as glucose, amino acids, sodium, potassium, calcium, and magnesium—are almost entirely reabsorbed. Certain substances are reabsorbed in limited quantities, such as urea and phosphate, and consequently appear in the urine. In a healthy individual, creatinine is the only filtered substance not reabsorbed and entirely secreted, allowing creatinine to serve as an indicator of glomerular filtration ability. The last process in the formation of urine is secretion. Various substances, including hydrogen and potassium ions, are secreted directly into the tubular fluid through the epithelial cells that line the renal tubules. Secretion plays an important role in promoting the body’s acid-base balance.

Regulation of kidney function

The formation of urine and the reabsorption of substances needed for body function are aided by three physiologic mechanisms: the countercurrent mechanism, autoregulation, and hormonal control.

Hormonal control

Secretion of antidiuretic hormone (ADH) by the posterior pituitary gland is affected by plasma osmolality. When the blood becomes hypertonic, ADH is secreted and water is retained by the kidneys. If the blood is hypotonic, less ADH is formed, causing the kidneys to reabsorb less water and increasing urine formation. ADH acts on the distal tubules and collecting tubules by altering permeability to water.

The juxtaglomerular complex is a group of cells, located just before the glomerulus and in close proximity to the distal tubule, which contain granules of inactive renin. Renin is released in response to reduced arterial blood pressure entering the afferent arteriole of the kidney or a low concentration of sodium in the distal tubule. The released renin acts as an enzyme to convert angiotensinogen to angiotensin I. Angiotensin I is converted to angiotension II by the angiotensin-converting enzyme, which leads to angiotensin II. Angiotensin II stimulates the adrenal cortex to release aldosterone. Aldosterone signals the kidney tubules to increase the reabsorption of sodium and retention of water. Because the renin-angiotensin system causes this reabsorption of water and sodium, it plays a role in the control of arterial blood pressure and is important in the conservation of sodium and control of fluid volume in hypotensive states (Fig. 13-4).

FIG. 13-4 Renin-angiotensin-vasoconstrictor mechanism for arterial pressure control.

(From Hall J: Guyton and Hall textbook of medical physiology, ed 12, Philadelphia, 2011, Saunders.)

Regulation of body homeostasis

The kidneys play a significant role in regulation of body fluids. The kidneys adjust blood volume and influence extracellular fluid volume, extracellular fluids, electrolytes, and ions. Homeostasis is maintained when the kidneys remove waste products and toxic substances.

The kidneys regulate blood volume through ADH, aldosterone, and the renin-angiotensin mechanism. When the circulating blood volume is excessive, the cardiac output and arterial pressure increases, resulting in greater pressure in the renal artery and the kidney afferent arteriole. Water and sodium are excreted. If the patient is hypovolemic, the kidneys reabsorb fluid to return the blood volume to normal limits.

The extracellular fluid volume is controlled indirectly by the kidneys as blood volume is controlled. The relative ratio of the extracellular fluid volume to blood volume depends on the physical properties of the circulation and of the interstitial spaces, including compliances and dynamics. The kidney maintains the osmolality of the extracellular fluid mainly by regulating the extracellular sodium concentration. Extracellular sodium controls 90% to 95% of the effective osmotic pressure of extracellular fluid. The extracellular concentration of other electrolytes, including potassium, calcium, magnesium, and phosphate ions, is also under renal control.

Components of urine

The end product of filtration, absorption, and excretion is urine, composed of 95% water and 5% solids. The solids, approximately 60 g/L of urine, are listed in Table 13-2. Urea is derived from the breakdown of amino acids. Uric acid is an end product of purine metabolism, formed from purines ingested as food and from those formed in the body. Creatinine is an end product of creatine, of which 95% is found in muscle tissue. Creatinine is produced during the production of muscle energy.

Table 13-2 Principal Constituents of Urine

Creatinine is considered a nonthreshold substance because it is excreted by the kidney in its entirety. High-threshold substances are almost entirely reabsorbed in the kidney. They are an important portion of the blood and are excreted only if they are in an excess concentration. High-threshold substances include glucose, potassium, calcium, and magnesium. Low-threshold substances, such as urea, uric acid, and phosphates, are only minimally reabsorbed by the kidney.

In consideration of the substances found in urine, knowledge of the characteristics of normal urine is useful. Normal urine should be clear and transparent with an amber color, a reflection of urobilin, a byproduct of bilirubin breakdown. Urine is usually acidic because of the excretion of sodium acid phosphate, with a pH of approximately 6. The specific gravity is between 1.003 and 1.025. The volume of urine excreted every 24 hours is approximately 1500 mL.

Acid-base balance

The kidneys play a major role in acid-base balance. Although they are the most powerful acid-base regulators, they require several hours to 1 day to return the hydrogen ion concentration to a normal range. In contrast, the respiratory system can react to acid-base imbalances within 1 to 3 minutes.

The pH is an expression of the hydrogen ion concentration in the body fluids. Bicarbonate and carbon dioxide are also factors. The bicarbonate concentration is mainly under renal control, whereas the carbon dioxide is under respiratory control. Approximately 20-fold more bicarbonate than carbon dioxide is in the plasma resulting in a 20:1 ratio. Thus, any change in the 20:1 ratio affects the pH. Any change that affects kidney function affects the bicarbonate portion of the ratio and becomes a metabolic problem. Conversely, any change in the function of the lungs, which affects the carbon dioxide portion of the ratio, is a respiratory problem.

If, for example, a large amount of a bicarbonate solution is rapidly infused into a patient and ventilation does not change (Pco₂ stays constant), the result is a higher value for the bicarbonate and no change in the Pco₂. The net result is a higher pH, which indicates alkalosis, in this case metabolic alkalosis. Conversely, if an acid is infused, the ratio becomes smaller, the pH falls, indicating acidosis, which is termed metabolic acidosis.

The kidneys regulate pH by increasing or decreasing the bicarbonate ion concentration in the blood and eliminating hydrogen ions. This regulation is done with a complex series of reactions, which begins with hydrogen ions being secreted into the tubular filtrate. Carbon dioxide, an end product of tubular cell metabolism, combines with water to form carbonic acid (H₂CO₃). The carbonic acid dissociates to form hydrogen and bicarbonate (HCO₃). The hydrogen ion is taken via active transport to the renal tubule and usually exchanges in the tubule with sodium. Via active transport, the sodium moves to the extracellular fluid, where it combines with the bicarbonate that was reabsorbed into the extracellular fluid to form sodium bicarbonate (NaHCO₃). In the tubules, the hydrogen ion that was actively transported to the tubule combines with the filtrate bicarbonate to form carbonic acid. The carbonic acid dissociates to form carbon dioxide and water. The carbon dioxide is reabsorbed into the extracellular fluid and eventually excreted by the lungs; the water is excreted as part of the urine.

The kidneys correct alkalosis by decreasing the bicarbonate in the extracellular fluid, which occurs because fewer hydrogen ions enter the tubules because of a low carbon dioxide concentration and because a high bicarbonate concentration exists in the tubules. The bicarbonate cannot be reabsorbed without first combining with the hydrogen; therefore the excess bicarbonate ions are lost to the urine as are other positive ions such as sodium and hydrogen. Cellular potassium can exchange with the sodium instead of the cellular hydrogen to conserve the hydrogen, which can help to return the pH to normal limits.

Renal correction of acidosis is achieved by increasing the amount of bicarbonate in the extracellular fluid. An excess of hydrogen ions in comparison with the bicarbonate filtration into the tubules exists. The excess hydrogen ions are secreted into the tubules, where they combine with the phosphate or the ammonia buffer systems. The sodium ions in the tubules move via active transport to the extracellular fluid and combine with the bicarbonate ion to form sodium bicarbonate, which helps correct the acidosis. The urine is acidic because the kidney is excreting excess hydrogen ions.

Diuretic therapy

In the PACU, diuretics are commonly used for blood volume overload (hypervolemia), to reduce intracranial pressure, to maintain kidney function, and to determine the etiology of oliguria. The major side effects of diuretic therapy are related to the contraction of the extracellular fluid volume and alterations in potassium concentrations. Diuretics are categorized according to the site of action on renal tubules and the mechanism altering the secretion of urine. The major categories are osmotic diuretics, thiazide diuretics, potassium-sparing diuretics, loop diuretics, aldosterone antagonists, and carbonic anhydrase inhibitors. Because the use of diuretics is important in the PACU, a brief review of the major categories is provided.

Effects of anesthesia

In patients with normal renal function who receive general inhalation anesthesia, some depression of renal function occurs. All general anesthetics depress renal blood flow, glomerular filtration rate, and urinary flow. Renal function depression is the result of direct and indirect effects of anesthetic agents. Renal blood flow is depressed as a result of renal vasoconstriction or systemic hypotension. Of interest is that the antiemetic and antipsychotic drug droperidol has the smallest effect on renal function. In most instances, the renal depression caused by the anesthetic agents is reversible at the end of the operative procedure.

The stress of surgery and anesthesia trigger a physiologic stress response and release of ADH from the posterior pituitary. When ADH is released, tubular reabsorption of water occurs, which decreases urine volume and increases urine concentration. Other biochemical products of the stress response, namely epinephrine, norepinephrine, and the renin-angiotensin system, also affect the renal system. More specifically, when these amines are liberated, renal blood flow is decreased.

Renal function, as indicated by urine volume and concentration, must be carefully monitored during the emergent phase of the anesthesia. Patients who have undergone major abdominal or thoracic surgery commonly have some diuresis during the immediate postoperative period. However, the stress of surgery may result in fluid volume retention up to 48 hours postoperatively. Monitoring urine volume and concentration is critical in patients after (1) a major surgical procedure; (2) general anesthesia for more than 2 hours; or (3) a significant blood volume replacement during the preoperative or intraoperative phase of the anesthetic experience. Increased abdominal pressure during laparoscopy can compress and compromise the kidneys. Any patient with preoperative indications of compromised renal or cardiovascular function also requires careful monitoring.

Effects of drugs in patients with compromised kidney function

Kidney disease affects approximately 5% of adults in the United States. Patients with end-stage kidney disease exhibit anemia, body fluid shifts, and alterations in blood albumin and electrolyte levels. Patients may be debilitated and deconditioned. If uremia is present, the CNS may be depressed. When the renal impaired patient exhibits CNS depression, the actions of opioids are intensified and prolonged. Diazepam, which has a 24-hour half-life, is also not a good choice because of its additive effect on the CNS. Drugs that are not metabolized in the body but are typically excreted unchanged by the kidneys are avoided in patients with renal disease. Such drugs include long-acting barbiturates such as barbital and phenobarbital, skeletal muscle relaxants decamethonium and gallamine, and cardiac glycosides digoxin and lanatoside C. Because half the administered dose of the belladonna alkaloids, atropine and hyoscyamine, are excreted unchanged, the dosage of these drugs should be modified by the degree of renal impairment.

In patients with mild to moderate kidney dysfunction, all current inhalation anesthetics can be used in the usual clinical dose range. Because thiopental depends on redistribution for the termination of its action, it may be used in patients with renal impairment. The skeletal muscle relaxants succinylcholine, curare, and pancuronium can be used for patients with compromised kidney function. Vecuronium duration can be prolonged in patients with end-stage kidney disease. Neuroleptanalgesia, a combination of opioid and tranquilizer, when achieved with nitrous oxide and oxygen, is an acceptable technique for the patient with uremia. When droperidol has been administered, which is the prototype neuroleptanalgesic drug, the perianesthesia nurse should monitor the patient for prolonged depressant effects of the drug. More specifically, the tranquilizer component of droperidol has a long half-life; therefore its prolonged effects, coupled with CNS depression from the uremia, may cause the patient to be slow to arouse in the immediate postoperative emergence phase. Consequently, airway patency and cardiovascular parameters are closely monitored. Midazolam, if used as an infusion, can accumulate in patients with compromised kidney function. Propofol is metabolized in the liver and is safe for patients with kidney disease. Nonsteroidal antiinflammatory agents should be avoided because their use can exacerbate renal damage.

Acute kidney failure

A sudden decrease in renal function is the hallmark of acute kidney failure. Acute kidney failure will occur in 1 of 100 surgical patients. Patient risk factors include gender (male), age, and diabetes. Additional risk factors include a history of heart failure, hypertension, ascites or preoperative renal insufficiency.¹ Emergency surgery increases the risk of acute kidney failure by 100%, whereas intraperitoneal surgery increases risk by a factor of 3. Acute kidney failure can be due to prerenal, intrarenal, or postrenal causes.

Prerenal refers to system problems preceding blood flow to the kidney, primarily low cardiac output. Low cardiac output can be due to volume depletion, hemorrhage, or myocardial dysfunction. The lack of blood flow to the kidney is the cause of decreased urine output. Ensuring adequate hydration during and after anesthesia along with monitoring blood loss and replacement when indicated can protect renal function.

Intrarenal causes of acute renal failure include acute tubular necrosis. Nephrotoxicity damages the tubular cells of the loop of Henle with changes occurring within hours. Hypotension that results in hypoperfusion to the kidney can also lead to cell death. Patients who have prolonged hypoperfusion because of shock or sepsis and then undergo procedures with contrast dye are at extreme risk. Ensuring that the patient is well hydrated before administering potentially toxic drugs will prevent further damage. The PACU nurse should be aware of any prolonged periods of intraoperative hypotension. Surgical patients who have experienced traumatic injuries can develop rhabdomyolysis. Rhabdomyolysis is caused by the breakdown products of muscle including myoglobin, a large protein molecule. Excessive amounts of myoglobin can clog the glomerulus and the tubules. Additional infusions of isotonic intravenous fluids may be needed during recovery from traumatic muscle damage.

Postrenal failure occurs when urine is blocked from leaving the kidney. Undiagnosed kidney stones or stone movement during percutaneous kidney stone intervention can obstruct the collecting ducts in the kidney pelvis or ureters. Assessment of the free flow of urine may not reveal a blockage until renal failure has occurred.

Assessment of kidney function

Kidney function is assessed through serum and urine analysis. Because creatinine is a component of urine not reabsorbed back into the tubules it serves as an indicator of glomerular filtration. Every milliliter of glomerular filtrate or urine should contain precisely the same quantity of creatinine as 1 mL of plasma. Serum creatinine is slow to increase when glomerular filtration is impaired and cannot detect the injury in time to intervene effectively; however, serum creatinine is a marker of renal function.

Urine output, usually associated with adequate renal function, is also not a reliable marker of kidney injury. Anuria can be a sign of severe kidney dysfunction, unless the cause is postrenal obstruction. Anuria always requires further assessment. The PACU nurse is more likely to detect persistent oliguria, less than 0.5 mL/kg/h or 25 mL of urine per hour for more than 2 hours. Low urine output can have numerous causes, but constitutes a medical emergency with the surgeon notified immediately.

The urine volume may be abnormally high during emergence from anesthesia. Although intraoperative diuretic administration is a common finding, in conditions creating acute tubular necrosis the increased urine volume represents failure of the tubules to reabsorb the glomerular filtrate. The quality rather than the quantity of the urine provides useful information about the renal state of the patient. Urinalysis can reveal the amount of filtered sodium. Blood in the urine can be caused by postrenal damage.

Preexisiting kidney failure

More than 26 million people in the United States have chronic kidney disease (CKD). Many have no symptoms, whereas others require dialysis. CKD is defined by the extent of kidney damage and the level of kidney function. Damage for over 3 months with a decreased glomerular filtration rate will classify patients into five stages of CKD. Stage 1 and 2 patients are asymptomatic and are unlikely to be diagnosed until a comorbid condition occurs, such as diabetes or hypertension. Patients with stage 3 CKD experience fatigue, anemia, urine changes, and peripheral edema. Patients with stage 4 CKD have additional symptoms of uremia, anorexia, and numbness and tingling in the extremities. Stage 5 represents progress to a point that the kidneys are no longer able to function at the level needed for daily living and end-stage kidney disease has occurred. Chronic renal failure may last 10 to 20 years before end-stage kidney disease.

Patients with stage 4 or stage 5 kidney disease require creation of an arteriovenous fistula or placement of a temporary vascular shunt to allow hemodialysis. Any patient with CKD can require surgery though their morbidity and mortality risk is substantially increased. In the postoperative period they can be hemodynamically labile. Venous access is difficult because of preexisting vascular disease and the presence of a fistula or shunt. An intravenous catheter is never placed in the same extremity as the fistula or shunt; a blood pressure cuff is never placed above, on, or below the fistula or shunt. Patients with ESRD are scheduled to receive dialysis the day before surgery to optimize volume and electrolyte status. Intravenous fluids are minimized during minor surgery.² If extensive surgery is planned, intraoperative dialysis may be required. Patients with ESRD have anemia and coagulation abnormalities because of a lack of erythropoietin and altered platelet function. Bleeding during the PACU stay can be a surgical emergency.

Perianesthesia nursing care

Perianesthesia nursing care centers on recognition and care of the patient at risk for acute kidney failure. The status of the patient’s fluid volume should be calculated and evaluated during the admission assessment. Intake includes intravenous fluids and colloidal and blood products. Output includes blood loss, gastrointestinal loss, and urine output. A urine output of less than 0.5 mL/kg/h is not acceptable. The duration of NPO is considered when calculating replacement fluids (125 mL/h NPO). The possibility of third space fluids, particularly during bowel surgery, is considered. When fluid balance is determined, a plan for promoting renal perfusion is discussed with the surgical team. An indwelling urethral catheter may be needed for a patient at risk of kidney failure to monitor moment-to-moment information concerning the volume and quality of urine output. The need for the catheter must be weighed against the risk of a catheter-associated urinary tract infection. For patient safety, urinary catheters must be removed when they are no longer indicated. A bladder scanner should be readily available as a noninvasive assessment of urine production.

If acute kidney failure is apparent, immediate interventions can include larger-than-usual doses of osmotic or loop diuretics. Laboratory analysis for baseline values of serum creatinine, electrolytes, proteinuria, and urine sodium are obtained. Acute kidney failure creates hyperkalemia, which is reflected on the electrocardiogram as high-peaked T waves and depressed S-T segments. The subsequent disappearance of T waves, heart block, and cardiac arrest can occur with increasing levels of potassium.

Summary

A review of the complex anatomy and physiology of the renal system was presented to demonstrate the role the kidney plays in regulating and controlling body systems. Pharmacologic agents administered during the perioperative period must be carefully monitored to avoid kidney damage. Maintaining blood volume and renal perfusion is the key to preserving kidney function. The PACU nurse must be aware of the patient’s fluid volume status and carefully monitor the adequacy of urine output. Patients with chronic kidney failure present additional challenges for post anesthesia recovery. Care of the patient requiring genitourinary surgery including renal transplantation is presented in Chapter 41.