Vessels

The renal arteries arise directly off of the abdominal aorta (Figure 114-3). Although most kidneys are supplied by a single renal artery, multiple renal arteries are reportedly seen in 13% of canine kidneys and in 10% of feline kidneys.²³ The left kidney is more likely to have multiple renal arteries than the right kidney. Some single renal arteries branch immediately after leaving the aorta, making it appear that the kidney has two renal arteries. This is primarily of significance during nephrectomy, when severe hemorrhage can be encountered if one of these renal artery branches is not identified and ligated before transection.

The renal arteries split into dorsal and ventral branches as they reach the renal hilus. These arteries further branch into three to seven interlobar arteries and then into arcuate arteries at the corticomedullary junction. The arcuate arteries radiate outward toward the periphery of the kidney and further split into interlobar arteries, from which afferent glomerular arteries arise. Efferent glomerular arteries return blood from the glomerular tufts and drain into the venous system.

Small “capsular” arteries may enter the kidney from the capsular surface. These secondary arteries anastomose to the primary renal arteries and create a renal “arterial circle” that permits some arterial flow to a kidney even when a renal artery is obstructed. Capsular arteries most commonly arise from the phrenicoabdominal artery and adrenal arteries²³ and appear to be more prominent in diseased kidneys.

The vasa recta is composed of long, unbranched capillaries that extend alongside the nephron from the cortex into the renal medulla. Through these capillaries, water reabsorbed from the collecting tubules is returned back into the circulatory system, helping to maintain hypertonicity of the renal medulla through a countercurrent exchange system.14,15,23,39

The venous circulation of the kidney arises from deep and superficial veins within the renal parenchyma. Veins in the outer cortex drain toward the capsular surface. These veins converge to form the stellate veins, interlobar veins, arcuate veins, and renal vein. The renal vein returns blood back into the caudal vena cava. The left renal vein also receives blood from the left ovarian or testicular veins. Capsular and parenchymal lymphatics converge to make lymphatic trunks, which exit at the renal hilus.23,27

Innervation

The kidney receives innervation from the sympathetic ganglion and parasympathetic sources. These fibers are myelinated and unmyelinated from sympathetic and parasympathetic (vagus) trunks. There are numerous plexuses around the renal vessels.23,26,27

Functional Unit of the Kidney

The basic functional unit of the kidney is the nephron (Figure 114-4). Dogs have an estimated 500,000 nephrons per kidney. The nephron consists of the renal corpuscle and the renal tubules, which end at the collecting duct. The renal corpuscle, which is found only in the renal cortex, is composed of the glomerulus and the glomerular capsule (also referred to as Bowman’s capsule). The glomerulus is a tuft of capillaries enclosed within the glomerular capsule. Between the glomerulus and the afferent arterioles is a group of cells called the macula densa. These cells help maintain autoregulation of renal blood flow.

The glomerular capsule is the beginning of the tubular system that is responsible for the formation and transport of urine. It is composed of highly specialized epithelial cells called podocytes, which rest on the glomerular basement membrane. Interdigitation of podocyte appendages creates filtration slits, or pores, between the cells. The size of these filtration slits is the primary determinant of which particles can filter out of the blood and into the renal collecting tubules. Water and small particles (<60,000 daltons) can freely pass through these filtration slits, but particles larger than 60,000 daltons have very limited ability to pass through. Most cellular components of blood exceed this size; thus, the presence of these components in the urine may be an indication of significant glomerular damage. An inherent negative charge to the glomerular basement membrane may also help to repel other negatively charged molecules, such as albumin, enhancing the selective nature of glomerular filtration.⁹²

Injury to the glomeruli (glomerulitis) can result in a loss of podocytes, resulting in an inefficient and indiscriminate filtration mechanism. Glomerular disease may result in edema formation, systemic hypertension, thromboembolism, hyperlipidemia, protein malnutrition, immunosuppression, changed pharmacokinetics of excreted drugs, and endocrine abnormalities.⁹²

Urine Formation

Normal urine production in dogs and cats varies between 20 and 45 mL/kg/d.² Urine begins as a filtrate that is created as water and small particles move through the filtration slits. Glomerular filtrate is roughly 300 mOs/L (roughly equal to plasma). The filtrate then drains into the tubular system that begins with the proximal convoluted tubule (see Figure 114-4). From this point, the filtrate moves into the descending loop of Henle as it crosses from the renal cortex into the medullary region. The loop of Henle makes a hairpin turn in the medulla, becoming the ascending loop of Henle. The tubule system crosses again into the cortical region, becoming the distal convoluted tubule. Filtrate in the distal convoluted tubule drains into the collecting tubule and moves into the papillary duct and the collecting system. Creation of dilute urine requires the resorption of solutes from filtrate, while the formation of concentrated urine requires the resorption of water from the filtrate. These processes are accomplished in the various portions of the nephron.

Renal Blood Flow

The kidneys are estimated to receive around 25% of an animal’s cardiac output, or roughly 4 mL/min/g of renal tissue. This high blood flow—the greatest of any capillary bed in the body—is required for production of urine, which is an active process that is blood flow dependent. Blood flow varies throughout the kidney: the cortical blood flow is highest, at 4 mL/min/g of tissue, and the flow rates of the outer and inner medulla are 0.7 mL/min/g of tissue and 0.1 mL/min/g of tissue, respectively.

Renal blood flow is calculated as [Renal perfusion pressure ÷ Renal vascular resistance], where renal perfusion pressure is approximately equal to mean systemic blood pressure. Vasoconstriction and vasodilation of the afferent and efferent renal arterioles are primarily responsible for renal vascular resistance. These vessels are therefore the targets of vasoconstrictive and vasodilative signals needed for renal autoregulation. Autoregulation allows the kidneys to maintain an adequate blood flow during times of systemic hypotension or hypertension. Any loss in autoregulatory ability makes the kidney more susceptible to hypertensive or hypotensive injury. Furthermore, a diseased or insufficient kidney itself has decreased autoregulatory ability and may be more susceptible to ischemic injury during times of hypotension (e.g., anesthesia, hemorrhage, sepsis).

The glomerular filtration rate is roughly 20% of renal plasma flow. The glomerular filtration rate is determined by the balance of hydrostatic and colloid osmotic forces acting across the capillary membrane and the permeability and filtering surface area of the capillaries. Changes in tone of the afferent and efferent arterioles affect glomerular filtration rate: glomerular filtration rate decreases with increased vascular constriction of the afferent arterioles and increases with vasodilation of the efferent arterioles.

Urine Concentration

The concentrating ability of kidneys varies among species, depending on the environmental requirements of the animal. For instance, animals in aquatic environments have limited concentrating ability (beavers, 500 mOs/L), but desert creatures have the ability to produce extremely concentrated urine (desert mice, 10,000 mOs/L).³⁹ Healthy humans can produce urine between 1200 and 1400 mOs/L.

The concentrating ability is based on renal medullary hyperosmolarity, which is maintained by the vasa recta through a counter-current mechanism. Because of increased osmolarity of blood leaving the renal medulla, particles such as urea transfer from blood exiting the medulla into blood entering the medulla. This counter-current exchange permits the medullary interstitium surrounding the collecting ducts to maintain a high osmolarity. Concentrating ability is decreased by increased blood flow through the vasa recta secondary to vasodilation, increased arterial pressure, or increased fluid volume. Increased medullary blood flow is the basis for the loss of renal concentrating ability known as “medullary wash-out.” This condition is most commonly associated with aggressive or long-term fluid administration in hospitalized patients.

Osmolarity of renal medullary interstitial fluid is 1200 to 1400 mOs/L compared with roughly 300 mOs/L for nonmedullary interstitial fluid. Medullary interstitial hypertonicity is created by several mechanisms, including facilitative diffusion of large molecules (urea) into the interstitium; limited ability of water to diffuse into the interstitium; and active transport of sodium, potassium, chloride, and other electrolytes into the interstitium from the thick portion of the proximal loop of Henle. This last mechanism is the most important because it can create a gradient of greater than 200 mOs/L across tubule membranes.

Urea contributes 40% to 50% of the osmolarity found in the renal medulla. In the medullary collecting ducts, water is continually reabsorbed. Urea is pulled along with the water or helped to cross through specific urea transport molecules (UT-A1) that are stimulated by the presence of antidiuretic hormone. Water moves out with the urea, maintaining high osmolarity of the urine. High-protein diets result in greater production of nitrogenous waste, leading to more effective concentrating ability. On the other hand, malnutrition and other conditions that decrease urea production (e.g., portosystemic shunts) result in decreased concentrating ability. Urea is recycled within the renal medulla as it moves from the medullary collecting ducts into the interstitium and then into the loop of Henle. The thick loop of Henle, distal tubules, and cortical collecting ducts are impermeable to urea. The medullary collecting tubules, however, are permeable to urea, which moves back into the medullary interstitium. Recirculation of urea helps produce maximally concentrated urine during times of water deprivation.

Healing of the Upper Urinary Tract

When vascular injury is minimal, connective tissue and collagen rapidly repair renal parenchymal wounds. Inflammation and infarction occur with parenchymal ischemia secondary to compression, electrocoagulation, vascular transection, or inflammation and delay wound healing.⁸ Intraparenchymal hemorrhage increases the amount of fibrosis and renal damage, resulting in obliteration of local nephrons and dilatation and obstruction of renal tubules in the area of the hematoma.^34,86 Use of transparenchymal horizontal mattress sutures to stem hemorrhage, however, causes parenchymal necrosis, fibrosis, scarring, and atrophy.³⁴ Healing is more rapid when intraparenchymal vessels are individually ligated.

Diagnostic Tests

In general, a complete blood count, biochemistry and coagulation panels, urinalysis, urine culture, and blood pressure should be evaluated in any animal undergoing renal surgery.72,90 Systolic blood pressure greater than 180 mm Hg is considered abnormal.⁹⁴ The risk of hemorrhage during or after surgery is increased in patients with azotemia, hypertension, or thrombocytopenia.¹⁰ Buccal mucosal bleeding time is recommended in animals with uremia, which impairs platelet adhesion and aggregation.¹⁰ A cross-match should be performed in any animal with coagulopathy or anemia or in which excessive bleeding is expected. In one study, coagulation panels were abnormal in 39.8% of dogs and 51.9% of cats tested before renal biopsy.⁹⁴

Thoracic radiographs should be performed in any animal in which neoplasia is suspected. At the time of diagnosis, pulmonary metastases are detected on thoracic radiographs in 16% to 48% of dogs with primary renal tumors; 77% have metastatic disease at the time of death.17,49 In cats with nonlymphomatous primary renal neoplasia, pulmonary metastases are diagnosed preoperatively in 43%.⁴² Thoracic radiographs are also recommended in patients that are dyspneic or have undergone trauma. Hydrothorax and urothorax have been reported in animals with perirenal cysts and diaphragmatic renal herniation, respectively.^77,87

Renal Imaging

Abdominal radiographs and renal ultrasonography are performed in most affected animals to evaluate renal structure, identify and locate calculi, examine the kidneys and other organs for primary or metastatic neoplasia, and obtain fluid or tissue samples. Renal function of the contralateral kidney should be evaluated before unilateral nephroureterectomy.⁵²

Preoperative Considerations

When possible, uremia, blood pressure irregularities, anemia, coagulopathies, and electrolyte imbalances should be corrected before anesthesia.^72,90 Patients with hypoproteinemia require oncotic support (e.g., hetastarch). An indwelling urinary catheter is placed to monitor urine production before and after surgery. Patients with erythrocytosis secondary to renal neoplasia may require phlebotomy (removal of 10 to 20 mL/kg of blood) and intravenous fluids to normalize hematocrits and decrease the risk of intraoperative hemorrhage and postoperative thromboembolism. Because complication rates are high after renal surgery, medical management of nephric or ureteral calculi is usually attempted before considering surgery. Surgery is recommended for animals with complete obstruction, worsening azotemia, or unresponsive pyelonephritis.⁶³

Maintenance of renal perfusion under anesthesia is critical; therefore, pre- and intraoperative hypotension should be corrected or prevented.32,90 Drugs that cause hypotension (e.g., acepromazine) or nephrotoxicity (e.g., aminoglycosides or nonsteroidal antiinflammatory drugs [NSAIDs]) should be avoided.³¹ Animals with renal dysfunction are often premedicated with an anticholinergic drug and opioids and induced with IV propofol or an inhalant anesthetic delivered by mask. Anesthesia is maintained with isoflurane or sevoflurane, and blood pressure and urine output should be monitored during the procedure. Dopamine or dobutamine may be required intraoperatively in hypotensive animals that do not respond to fluids or oncotic support. Epidural administration can reduce intraoperative anesthetic requirements and provide preemptive and postoperative analgesia.

The abdomen should be prepped from the midthorax to the pubis. If the incision is to be extended to the pubis or the urethra catheterized, the clip and prep should include the perivulvar or peripreputial region. Wide lateral preps are performed in patients that may require feeding tubes or nephrostomy tube placement.

Postoperative Care

Intravenous fluids are continued after surgery to maintain renal perfusion and prevent blood clot formation within the urinary tract. Postoperative analgesia can be delivered by intermittent intravenous injections or a constant rate infusion of opioids. Animals should be monitored for anemia, oliguria or anuria, and evidence of urinary tract obstruction, and physical activity should be severely restricted for at least 24 hours. Depending on the surgery and the patient’s condition, early postoperative follow-up may include serial red blood cell and platelet counts, biochemistry panels, weight and blood pressure measurement, and quantification of urine output.

Developmental Anomalies