Disorders of the Urinary System

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Part 5  •  Medical Disorders

CHAPTER

39  Disorders of the Urinary System Christopher Cebra

Camelid kidneys are reniform and not grossly lobulated. Ure­ teral and bladder anatomy is conventional. The female urethra is also conventional and exits through the urethral tubercle on the dorsal aspect of the suburethral diverticulum. The penile urethra is long and narrow. Male camelids have a dorsal ure­ thral recess at the ischiatic arch and a sigmoid flexure near the scrotum.1 The tip of the penis is contained within fused folds of the prepuce until sexual maturity and may remain so entrapped in early castrates. In most intact male camelids, the preputial attachments break down when they are between 1 and 2 years of age. The tip of the penis develops a fibrocartilaginous pro­ jection with sexual maturity. The terminal urethra exits this projection near but not at its tip. Extrusion of the penis is near-impossible in all but sexually mature camelids, and even then, extrusion is difficult to accomplish without heavy sedation or general anesthesia. Blind catheterization of the

unextruded penis is also unlikely. In mature males, the ure­ thral diverticulum frequently catches the tip of any catheter and obstructs cranial movement. External digital pressure through the rectum or on the skin near the ischial arch may allow the catheter to pass into the pelvic urethra and bladder. The male urethra is generally too long and narrow for endos­ copy to be informative. Videoendoscopes with external diam­ eters of up to 6 mm may be passed up the urethra of adult female alpacas. Polyethylene tubing passed through the biopsy channel and into the urethral opening assists entry of the welllubricated scope. The most common blood values used to assess the kidneys are urea nitrogen and creatinine (Box 39-1). Urea nitrogen is made in the liver to detoxify the ammonia produced during amino acid catabolism. It is excreted through urine but also moves freely through most body compartments. Gastrointes­ tinal (GI) microbes may use urea as a nonprotein nitrogen

Chapter 39  •  Disorders of the Urinary System

BOX 39-1 

Reference Values for Camelid Urinalysis, Urinary Enzymes, Fractional Excretions, and Serum Values Related to the Urinary System

SERUM AND BIOCHEMICAL VALUES Urea nitrogen 13–28 milligrams per deciliter (mg/dL) Creatinine 0.9–1.7 mg/dL Urinecreatinine/Serumcreatinine 85–180 1600–2500 milliosmoles per Urineosmolality kilogram (mOsm/kg) Urineosmolality/Serumosmolality 4.5–8 Fractional Excretion of 0.1–1.3% sodium Fractional Excretion of 50–123% potassium Fractional Excretion of 0.2–1.9% chloride Fractional Excretion of 0.0–1.3% phosphorus URINALYSIS Color Clarity Specific Gravity pH Protein Glucose Ketones Blood

Light yellow to yellow Clear 1.018–1.050 7.0–8.5 Negative (trace artifact if pH = 7.5+) Negative, unless stressed or hyperglycemic Negative Negative

URINE CYTOLOGIC ANALYSIS Crystals Rare 0–3/high-power field (hpf) Epithelial cells White blood cells 0–3/hpf Erythrocytes 0–3/hpf (more if catheterized)

source, so during short periods of anorexia, blood urea may fall because of microbial consumption. During longer periods of anorexia, when a die-off of gastric microbes occurs, blood urea may rise slightly. Creatinine is a product of normal muscle turnover and is also excreted in urine. Lightly muscled camelids such as crias and chronically thin animals may have low circulating creati­ nine. High creatinine concentrations are strongly indicative of decreased renal function or urinary tract obstruction. Both creatinine and urea may increase in the blood through pre­ renal, renal, or postrenal mechanisms. Prerenal azotemia often results in increases where the blood urea nitrogen (BUN)-to-creatinine (both in milligram per deciliter [mg/dL]) is at least 20 : 1 (or >0.08 Ureammol/Creatinineµmol, or >0.16 BUNmmol/Creatinineµmol), but with acute anorexia, the micro­ bial use of urea may decrease that ratio to a certain extent. The kidneys also help maintain electrolyte and acid–base homeostasis. Camelid urine usually is alkaline and has low concentrations of sodium and chloride and a high

465

concentration of potassium (see Box 39-1). Abnormalities such as a malformation, ruptured ureter, or leaking bladder, which result in return of urine to the extracellular space, may result in systemic alkalosis, hypochloremia, and hyponatremia. Changes in blood potassium are variable because urinary dis­ orders frequently are accompanied by anorexia and decreased dietary potassium intake. Changes in calcium and phosphorus are also variable and depend on diet and vitamin D status. Azotemia is often accompanied by hypermagnesemia. Camelids tend to drink less and urinate less compared with ruminants, potentially because of greater GI conservation of water.2 Urine output ranges from about 5 to 7.5 milliliters per kilogram per day (mL/kg/day) in adults. Fractional excretions of electrolytes and activities of enzymes in urine have been determined and do not differ substantially from ruminants fed similar diets (see Box 39-1).2 However, obtaining urine may be problematic. Free-catch samples may be obtained from a distance using a cup on a stick, and females may be catheterized with practice. Narrow, semirigid tubing works best. Males may also be catheterized using a 3 to 5 French (Fr) urinary catheter, if the penis can be extruded.3 Cystocentesis is difficult unless the bladder is grossly distended and may lead to hemorrhage or urine leakage. Once obtained, urine is analyzed using conventional techniques. Camelid urinalysis values are similar to those of other species except that glycos­ uria is common (see Box 39-1). Ultrasonography of the kidney is possible through the dorsal paralumbar fossa. Camelid kidneys are more side-byside compared with ruminant kidneys; that is, each kidney is best imaged through the ipsilateral fossa. The left kidney sits dorsocaudolateral to the caudal sac of the first gastric compart­ ment and runs from the midpoint of L4 to the midpoint of L6. The right kidney is approximately halfway between the last rib and the pelvis, running from the cranial aspect of L3 to the caudal aspect of L4 in crias and partway along L5 in adults. Adult llama kidneys are approximately 5.5 to 6.5 × 8 to 10.2 centimeters (cm) in depth and length, whereas adult alpaca kidneys are approximately 4.5 to 6 × 7 to 9.5 cm. Kidneys are close to adult size by 15 months of age. Radiographically, kidneys in normal crias are approximately as long as the two adjacent lumbar vertebral bodies. Those of adults are almost as long as three adjacent lumbar vertebrae. The bladder may be imaged easily transrectally and with more difficulty transcutaneously unless it is full or distended. The urethra may be imaged through the pelvic canal transrec­ tally and for most of its length transcutaneously in males. Plain-film radiography may be used to find mineralized densities or to identify a grossly distended bladder, ureter, or kidney. Contrast material may be injected in a retrograde fashion through the tip of the penis, through the urethral tubercle, or through a cystotomy tube to highlight structures. Five to 10 mL of contrast material is sufficient to outline the normal urethra, whereas up to 50 mL in a cria and 200 mL in an adult may be necessary to highlight the entire bladder. Excretory urography may be used to examine renal uptake, the ureteral structures, and the filling of the bladder in crias and alpacas but is practically difficult in adult llamas. For the excre­ tory urogram, we have administered 75 mL of diatrizoate meglumine and diatrizoate sodium (Renocal 76) intrave­ nously (IV) to crias and 200 mL to adult alpacas and taken abdominal images at 5-minute intervals for up to 30 minutes. If the bladder or the bladder filling is the primary region of

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BOX 39-2 

Causes of Stranguria or Dysuria

Urolithiasis Bladder neoplasm Urethral stricture or malformation Ectopic ureter Intrapelvic eversion of the bladder Balanitis or posthitis Bladder rupture Spinal disorders Rabies Conditions associated with gross hematuria interest, 45- and 60-minute images may be taken as well. Computed tomography (CT), nuclear scintigraphy, and other cross-sectional imaging modalities have seen limited use in camelids, but their use is increasing as these modalities become cheaper and more widely available.4,5 Parts of the urinary tract may be visually examined by means of laparoscopy.6,7 From the right paralumbar fossa, the right kidney is usually visible, although it may be obscured by retroperitoneal fat; on one occasion, the kidney was lacerated.6 The bladder is sometimes visible from this site. From the left paralumbar fossa, the left kidney is visible about half the time.7 The kidneys and the bladder are inaccessible from a ventral approach. Direct visualization during conventional surgery is also possible. Clinical signs of urinary tract disorders vary with the nature of the disorder. Obstructive or inflammatory lesions often lead to signs of pain, including stretching, restlessness, lying in an abnormal posture, reluctance to stand, inappetence, urinating in small spurts, dribbling of urine, frequently posturing to urinate, and stranguria (Box 39-2). Lesions associated with loss of renal parenchyma or reabsorption of urine often lead to anorexia and obtundation related to the degree of azote­ mia. Inflammatory or neoplastic lesions often lead to changes in the nature of urine, with visible increases in turbidity or redness, associated with protein or blood loss in urine (Box 39-3). Disorders associated with internal urine leakage will furthermore lead to subcutaneous swelling or abdominal distension.

Congenital Lesions As with other organ systems, congenital malformations of the urinary tract appear to be more common in camelids than in most other species of domestic livestock. Although most have not been proven to have a genetic origin, the lack of viral or teratogenic etiologies and knowledge of the various bottlenecks in the camelid gene pool must suggest that at least some of these disorders are hereditary. Some occur as sole defects. Others appear to occur commonly in conjunction with other malformations. Specifically, urethral abnormalities are often linked to malformations of the genital tract, and atresia ani occurs in conjunction with pelvic abnormalities, atresia coli, and a variety of renal malformations. Malformations of the kidney include parenchymal cysts (Figure 39-1), horseshoe kidneys, dysplasia, and agenesis (Figures

BOX 39-3 

Causes of Hematuria or Proteinuria

Urolithiasis Nephritis, ureteritis, cystitis, or urethritis Renal hematuria Neoplasms of the urinary tract Prostatitis Renal malformations Intrapelvic eversion of the bladder Ruptured bladder 39-2 and 39-3).8–11 Lesions may be unilateral or bilateral. Abnormal kidneys may be absent, small, or enlarged and saclike. The more normal, contralateral kidney, if present, often undergoes compensatory hypertrophy. Agenesis and horseshoe kidneys often occur in conjunction with atresia ani or other urogenital lesions but may also occur as solitary lesions. Clinical signs depend on the amount of functional renal tissue. Unilateral abnormalities may be clinically silent and only discovered postmortem. With bilateral renal agene­ sis, signs of lethargy, anuria, and mild abdominal distention often begin within 24 hours of birth and progress over 3 to 4 days. With unilateral agenesis, signs may remain absent, unless some pathologic process affects the remaining kidney. Dyspla­ sia and cystic lesions may lead to signs in juvenile camelids or remain silent for several years. Cysts appear to grow with time and may represent a milder form of the process causing agenesis.12 Urinalysis may be normal or, in severe cases, may reflect failure to concentrate and proteinuria. Anuria is expected only with bilateral agenesis or severe bilateral disease from one of the other causes. Blood abnormalities also reflect the severity of the conditions. BUN and creatinine concentra­ tions may be normal with mild, unilateral, or early disease and show steady increases with clinical disease. As with other renal causes of azotemia, the BUN-to-creatinine ratio (in mg/ dL) is frequently much lower than the 20:1 expected with prerenal azotemia. In larger camelids, primarily with unilateral malformation, an absent or enlarged left kidney may be palpated per rectum. Ultrasonography may reveal hydronephrosis, abnormal con­ formation, the presence of cysts (see Figure 39-1), or lack of functional renal cortical tissue. The less affected or unaffected kidney is frequently grossly enlarged and may also be visible on plain abdominal radiography. Various other imaging modalities such as contrast radiography (see Figure 39-2), cross-sectional imaging studies (see Figure 39-3), or nuclear scintigraphy may reveal the lack of renal tissue or function. With bilateral disease, the bladder may remain empty and appear to be absent as well. Biopsy may be used to confirm dysplasia but is frequently unnecessary for other types of lesions. Kidneys with poor drainage also appear to be prone to developing infections, so biopsies and fluid samples may reveal bacterial inflammation and pyuria. Unilateral lesions may respond to nephrectomy of the affected kidney, which should be considered if the opposite kidney appears visibly and functionally normal and the animal displays persistent azotemia, proteinuria, hematuria, or infection associated with the abnormal kidney.4,11,13 Some camelids with unilateral renal

Chapter 39  •  Disorders of the Urinary System

A

467

B Figure 39-1  Transabdominal ultrasonographic (A) and gross (B) appearance of a renal cyst.

Figure 39-3  Computed tomography image of an adult alpaca with Figure 39-2  Excretory urogram of an alpaca cria with unilateral renal agenesis and urine dribbling. Atresia ani had been repaired previously. Note the lack of contrast uptake or any identifiable renal structure on the right side (left side of image). The left kidney appears to be func­ tioning normally.

agenesis or severe dysplasia have lived to thrifty adulthood, with the renal abnormality found incidentally after death. Similar congenital renal abnormalities have been found in closely related camelids. Congenital malformations of the ureters include ectopic ureters, atresia, and ureteral duplication.4,8,10,14 Atresia leads to rupture and retroperitoneal urine accumulation, resulting in poor growth, progressive lethargy, possible abdominal

right renal agenesis. Compare in appearance to Figures 39-9 and 39-10, which show both kidneys clearly.

discomfort with straining, and slow accumulation of abdomi­ nal fluid in young crias. Ureteral duplication is similar, with a functional and nonfunctional ureter contained within the same sheath from one kidney. Signs may progress over several weeks to months because the functional kidney is somewhat able to compensate. Signs may also wax and wane. Urinalysis is usually normal, but blood evaluation may reveal renal azo­ temia. Ultrasonography reveals diffuse edema throughout the dorsal lumbar retroperitoneal space. Megaureter and hydrone­ phrosis may develop and may be detected by ultrasonography, radiography, or other imaging studies. Excretory urograms or

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Part 5  •  Medical Disorders

scintigraphy may be used to highlight the lesions. An increased amount of abdominal fluid may be detected. Given the size of the animals affected, endoscopic examination of the bladder would be difficult but could potentially reveal a lack of urina­ tion through a dysfunctional ureter. If the lesion is unilateral, nephrectomy may be curative.4,13 Ectopic ureters frequently lead to urinary incontinence, often with associated tail, perineal, and hindlimb skin scald. Except for discomfort from the skin lesions, and mild stranguria with infections, the camelid frequently appears healthy. As such, camelids of any age may be seen with this disorder, but signs should have been noticed shortly after birth. Unless a second­ ary bacterial infection exists, which is common with lesions of this nature, blood and urine evaluation should be normal. Ectopic ureters may rejoin the urogenital tract at almost any point or enter the terminal intestinal tract, causing diarrhea. Endoscopic evaluation of the vaginal vault, suburethral diver­ ticulum, urethral tubercle, urethra, and bladder and contrastenhanced CT have been used to define the nature of the lesion.4 Ultrasonography may reveal an abnormal, hydrone­ phrotic, or infected kidney and hydroureter, but the ureter itself is difficult to follow to its final destination. Contrast radiography may be attempted in younger crias. Because of the chance for ascending infections and the persistent skin infec­ tions, unilateral nephrectomy is recommended and may be curative for unilateral lesions.4,13 A number of abnormalities of the terminal urinary tract are related to malformations of the genital tract (Figure 39-4).8,14–20 These include urethral duplication and various malformations of the penis in hermaphrodites or other sexu­ ally ambiguous animals and terminal obstruction with labial fusion or vulvar hypoplasia. These may result in anuria, dysuria, or stranguria and frequently are accompanied by visible or palpable abnormalities of the external genitalia. With complete obstruction or gross stenosis, fluid-filled cystic structures may appear at the vulvar opening in presumptive females or along the course of the penile urethra in presump­ tive males. Occasionally, signs are interpreted as tenesmus, and a history of laxative or enema administration may exist. Mild to severe azotemia and evidence of bladder, ureteral, or renal distention may be present, depending on the severity of the obstruction. In females, some urine may accumulate in the uterus as well. Contrast radiography is especially useful in defining the presence, appearance, and function of various structures. Relatively simple surgical interventions may restore the flow of urine, but the overall implications of a morpho­ logically abnormal and potentially genetically ambiguous animal should not be ignored. Vulvar fusion or hyperplasia in closely related animals has been reported in the scientific lit­ erature and anecdotally.17 A similar disorder has been reported in camels.21

Acquired Urinary Tract Obstruction Acquired urinary tract obstruction is one of the most debilitat­ ing disorders of male camelids because their anatomy compli­ cates all attempts at correction.3,14,22–26 Gelded males, especially those gelded at a young age and presumably retaining a narrow urethra, appear to be at greater risk than intact males. The long, narrow urethra of male camelids may make them even more prone to obstruction than other species under similar conditions. Camelids’ low urine output may further

Figure 39-4  Retrograde urogram of a cria with ambiguous external genitalia, stranguria, and urine dribbling. Contrast reveals poor com­ munication between the urethra and the bladder.

contribute to the obstruction. Male camels are similarly affected.27 Females, which have a wider, shorter urethra, are generally spared, although they occasionally develop obstruc­ tion from ureteroliths, pelvic displacement of the bladder, or severe cystitis.28 Uroliths and debris from cystitis or urethritis are the most common causes of acquired urethral obstruction.3,14,24–26 Other possible causes include pelvic displacement of the bladder, urethral tumors, hematoma, tumor or abscess within the pelvic canal, upper motor neuron disease, infection of accessory sex glands, cystic mucosal lesions, stricture at a previous obstruction or surgery site, congenital malformations, bladder polyps, and cystitis.14,28–31 Other factors that may contribute to obstruction include trauma to the tip of the penis, reduction in urine volume because of reductions in water intake or water content of feed, dietary mineral imbalances that promote excretion or aggrega­ tion of urinary mineral, dietary oxalates, and factors that increase the mucoproteinaceous content in urine. Birthing trauma is associated with intrapelvic hematomas and abscesses in females, and Streptococcus equi ssp. zooepidemicus may cause lymph node abscesses in any age or gender of camelid. Vitamin A deficiency, although not verified in camelids, may contribute by promoting exfoliation of the bladder mucosa. Most intraluminal obstructions occur within the last 6 cm of the penis, although not necessarily at the tip. The sigmoid flexure is the next most common site, followed by the trigone region and pelvic urethra. In rare cases related to renal disease, the lith or debris obstructs the ureter or renal pelvis. Occasion­ ally, a single, large lith causes the blockage, but more com­ monly, several centimeters of urethra are filled with small, gritlike stones and inflammatory debris. In the Pacific North­ west, the most common liths are silicates, with calcium car­ bonate, calcium oxalates, and calcium hydroxyapatite also found.3,26 Struvite stones are less common but have been seen. Stones of mixed composition are common. Silicate crystals are associated with mature forages, which contain up to 8% silicon compounds. These are concentrated and polymerize in urine, where aggregation with protein leads to liths. Calcium is also concentrated in urine when overfed or in vitamin D-deficient animals. Struvite crystals, rare in camelids, are

Chapter 39  •  Disorders of the Urinary System usually caused by overfeeding calcium, magnesium, and phos­ phorus in grains. When liths are involved, multiple animals on a farm may become affected over a period of several months. The occurrence of uroliths appears to vary regionally, with the Pacific Northwest of the United States a higher pre­ valence area than the front range of the Rocky Mountains. Uroliths have been reported in camelids as young as 3 months of age.26 In about half of the cases of intraluminal obstruction seen at our clinic, no stone is found. Some of these camelids have mucoproteinaceous plugs, consisting of fibrinonecrotic material. A case with a similar finding was reported in the literature, and as our experience with camelids grows, it is becoming more apparent that many urethral obstructions are potentially a consequence of prostatitis or cystitis.22 A variety of organisms have been cultured from the urine or urinary debris of these animals, including Escherichia coli, Klebsiella, Streptococcus, Pseudomonas, and Arcanobacter pyogenes. It is possible that cam­ elids are more prone to developing obstruction after cystitis compared with other species, most likely because of the narrow camelid urethra. Displacement or eversion of the bladder into the pelvic canal is an uncommon occurrence, reported once in the literature and twice anecdotally.28 All cases were females, but only one was of breeding age and was close to parturition. Accidental breeding was not considered likely in the other two animals. Hematuria may be present but is not marked, and catheteriza­ tion of the bladder is difficult to impossible. Transrectal palpa­ tion or ultrasonography may give the impression of the fluid-filled viscus in the canal, but excretory urography (or retrograde cystography, if the urethra is patent enough) is necessary to demonstrate the body of the bladder everted dorsocaudal to the trigone and within the pelvic canal. A congenital malformation associated with acquired urinary tract obstruction is urethral duplication.15 With this abnormality, the duplicated remnant within the pelvic canal intermittently fills with urine, physically compressing the patent urethra. Thus, signs may not be present at birth and may wax and wane over many weeks. Urethral duplication is best identified with contrast studies, which allow careful eval­ uation of multiple structures and their connections. The most common signs of urethral obstruction are stran­ guria, dysuria, oliguria, or anuria, bruxism, frequent postur­ ing, and dribbling urine. Some affected camelids will show other signs of abdominal discomfort, decreased feed intake, or blood-stained urine. Persistent straining may lead to rectal or vaginal prolapse. Occasionally, signs are interpreted as tenesmus, and a history of laxative or enema administration may exist. Blood or crystals may be found on the end of the prepuce, or the prepuce may be dry, with no evidence of recent urination. Digital rectal palpation often reveals the pulsations of urethral spasms, and a full-hand (not just digital) rectal examination may reveal a distended or displaced bladder. A full examination of the pelvic canal is helpful for identifying extraluminal obstruction and should be considered, especially in female camelids. With urine leakage into tissues or the abdomen, signs of lethargy, weakness, and anorexia begin to supercede pain signs. Visible or palpable edematous periurethral tissue or abdominal distention may be present. Transrectal or transcu­ taneous ultrasonography may reveal a distended urethra and bladder, potentially with shadowing areas around mineralized

469

densities (Figures 39-5 and 39-6). Mineral densities may be seen swirling within the bladder. In the case of intraabdomi­ nal urine leakage, increased free abdominal fluid may be imaged. Hydroureter and nephrosis may be present in came­ lids with longstanding obstruction. Transrectal ultrasonogra­ phy is also an effective means of identifying tumors, abscesses, hematomas, and prostatic or cystic abnormalities. Radiogra­ phy may reveal the larger, calcium-containing stones, but without contrast, it is not reliable for demonstrating sabulous obstructions, silicates, or mucoproteinaceous plugs (Figure 39-7). Radiography, especially with contrast in place, may reveal intrapelvic displacement of the bladder. Endoscopy of the bladder is helpful for identifying tumors, polyps, or cystitis. Urinalysis, when urine is available, reveals hematuria and proteinuria. Crystals, erythrocytes, and leukocytes may be seen on sediment examinations. Early in the course, blood work is normal. Within a few days of the onset of signs, affected cam­ elids develop progressive azotemia, with a BUN-to-creatinine ratio usually around 10 : 1, hypermagnesemia, and mild to moderate increases in serum CK and aspartate aminotransfer­ ase (AST) activities. Intraabdominal leakage of urine may result in hyponatremia and hypochloremia. Low-grade meta­ bolic alkalosis gives way to shock and lactic acidosis over a few days. Inflammatory changes, including hyperfibrinogen­ emia and alteration in the leukocyte profile, may develop after several days. If the bladder leaks or ruptures, abdominal fluid

U bladder

Figure 39-5  Transrectal ultrasonographic appearance of a lith within the urinary bladder of an alpaca. Note the acoustic shadowing beyond the hyperechoic stone.

Figure 39-6  Transcutaneous ultrasonographic appearance of a urolith obstructing the lumen of the urethra of a male llama. Note the hypoechoic urine accumulation around the lith and the acoustic shadowing beyond it.

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Part 5  •  Medical Disorders

Figure 39-7  A retrograde urethrogram of a male llama with urethral obstruction. The dye column stops at the site of obstruction.

may become grossly abnormal or may contain substantially (often 2 to 4 times) more creatinine or potassium than blood. A blood creatinine concentration greater than 4 mg/dL and complete obstruction of urine flow have been identified as factors strongly associated with a poor treatment outcome.25 A variety of options are available for treating uroliths and other intraluminal plugs. Generally, camelids with a single stone or plug near the tip of the penis are more likely to survive than those with a sabulous obstruction or an obstruction affecting the sigmoid flexure or perineal urethra. Especially if a single, distal obstruction can be identified ultra­ sonographically, radiographically, or by palpation, a brief attempt may be made to extrude the tip of the penis with the animal under heavy sedation or general anesthesia. Palpable obstructions may be milked out, or if necessary, urethrotomy directly over the obstruction may be performed. If neither is possible, a lubricated soft-tip catheter may be introduced into the urethra and gently advanced. Gentle retrograde hydropul­ sion may be used with the goals of either retropulsing the obstruction back into the bladder or breaking up a protein­ aceous or sabulous mass. Problems with this approach include failure to extrude the penis, passing the catheter past the obstruction without relieving it, trauma to the urethra, failure to relieve the obstruction, and inability to pass the catheter beyond the urethral diverticulum. Additionally, repelling the obstruction back into the diverticulum or bladder could potentially result in reobstruction unless another intervention is used to remove the obstruction. If the stone can be recov­ ered, stone analysis should be considered. Identifying the type of stone may allow for management changes to avoid further cases on the farm. Bacteriologic culture of urine or the blockage should allow better selection of an appropriate antibiotic. If the obstruction cannot be relieved by catheterization and retrograde hydropulsion, surgical intervention may be

required. The same principles apply as in small ruminants, namely, that perineal urethrostomy may initially be successful but ultimately stricture occurs and that resting the urethra may lead to relaxation of urethral spasms sufficient to pass the obstruction. Tube cystotomy is generally considered to yield the best long-term prognosis if urethral function can be restored within 7 days. Antegrade urethrography may be attempted to demonstrate patency. Celiotomy may be helpful for visual inspection of the bladder, especially if leakage or rupture is suspected. Celiotomy is also necessary to replace a displaced bladder. Camelids appear to differ from small rumi­ nants in the amount of preexisting urethral damage on admis­ sion. This is more severe with sabulous or inflammatory obstructions, which may denude several centimeters of ure­ thral epithelium. These ulcerated regions often fuse during the healing stage, obliterating the urethral lumen. If urethral function cannot be restored, the prognosis is grave. If the adhesions are confined to the distal urethra, as ascertained by ultrasonographic evidence of proximal urethral filling, a subischial urethrostomy may be necessary. Cystos­ tomy through the skin or into the prepuce provides ready drainage but is complicated by ascending infection and urine scald of the abdomen and medial thigh. Medical treatment during the acute phase includes IV fluids, antiinflammatory medications, urethral relaxants, and antibiotics. Fluids help correct azotemia and electrolyte and acid–base abnormalities and also increase urine volume to flush out debris. A rate of fluids above maintenance, use of diuretics such as furosemide (2 to 5 mg/kg, IV or intramuscu­ larly [IM], up to q6h, or 0.66 mg/kg loading dose followed by 0.66 mg/kg/hr CRI), or glucose (0.25 to 1 g/kg as an IV bolus, up to q6h) may aid in cleaning out the bladder. Force-feeding salt may increase drinking and hence urination. With cystitis or prostatitis, continuing antibiotics and antiinflammatories for at least 2 to 6 weeks may be helpful. Acepromazine (0.02 mg/kg, subcutaneously [SQ], q6h), butorphanol tartrate (0.02–0.04 mg/kg, IM, q6h), phenazopyridine (0.3–0.4 mg/ kg, orally [PO], q8h), or oxybutynin (0.1 mg/kg, PO, q8h) have been used to decrease pain and relax the bladder or urethra, and all these agents appear to offer some temporary relief. Use of specific fibrinolytic medications has not been reported but may be of value. Topical ointments may help the skin scald. If a tube has been placed into the bladder, antiinflamma­ tories and antibiotics may be instilled. Dimethyl sulfoxide (DMSO) in the flush solution may decrease inflammation and bring some debris into solution. Because most stones are sili­ cate or contain calcium, pH modification of urine has not been particularly helpful. If the obstruction can be relieved without too much diffi­ culty, the prognosis is fair. Some camelids have reobstruction in days to months later because of more liths or debris within the bladder or develop progressive narrowing of the urethra. Urethrostomy incisions may form strictures within 6 months. At least one camelid had a ruptured gastric ulcer after success­ ful resolution of the obstruction. Because of the damage to the urethra and penis, preservation of life may be easier than preservation of the breeding function in males. Preventive measures depend on the type of stone. Chang­ ing the forage may be important, especially with silicates and calcium-containing liths. Ensuring adequate salt and

Chapter 39  •  Disorders of the Urinary System fresh drinking water will help maintain urine output. Delaying castration until sexual maturity may allow maximal develop­ ment of urethral diameter and loosening of the preputial adhesions. Other types of obstruction may require specific treatments. A displaced bladder may be replaced surgically or potentially massaged back into the abdomen using gentle transrectal and transvaginal massaging. If a urinary catheter can be placed atraumatically, emptying the bladder facilitates manual replacement, and refilling it with saline subsequently may allow complete return to its normal position. If this fails, surgical replacement via celiotomy is an option. Pelvic canal hematomas regress over 1 to 4 weeks. Placement of a urethral catheter may be necessary if the obstruction is severe. Abscesses may shrink during antimicrobial treatment, or may require surgical drainage. The single reported urethral sarcoma, which occurred on the urethral tubercle of a 7-week-old alpaca, responded to local excision followed by external beam radiation.29 It had previously regrown after excision alone.

Cystitis, Urethritis, and Prostatitis Inflammatory conditions of the lower urinary tract are barely mentioned in the scientific literature but appear to be a major health concern in North American camelids.14,31 Because of size issues, identifying the immediate source of the inflamma­ tion may be difficult, especially in male and juvenile camelids, but treatment is mainly nonspecific, and a standard approach may address all the different syndromes. Clinical signs are usually similar to those seen with obstruction, namely, stran­ guria, frequent or prolonged posturing, potentially other signs of abdominal discomfort, proteinuria, and hematuria. The important difference is that camelids with nonobstructive urinary tract inflammation tend not to have a distended bladder and may excrete a reasonable stream of urine. Urinaly­ sis is abnormal, with hematuria, pyuria, crystalluria, and pro­ teinuria all possible. Blood biochemical abnormalities are mild or absent, but the leukogram and fibrinogen concentra­ tion may show evidence of inflammation. It should be noted that prostatitis particularly may cause pyuria without hematu­ ria or stranguria. Bacterial culture of urine should be attempted and may reveal a bacterial etiology. Escherichia coli, Klebsiella, Enterococcus, Streptococcus, Pseudomonas, and Arcanobacter pyogenes are common isolates. Mixed infections may occur, which supports the theory that some of these are ascending infec­ tions. Upper motor neuron disease, ectopic ureters, crystallu­ ria, and other factors may increase the risk of ascending urinary tract infection. Other possible etiologies include irrita­ tion of the mucosa by the passage of crystals or small liths, plant toxins, and high urinary pH. Ultrasonography and endoscopy offer the best methods to define the disorder. Transrectal ultrasonography may reveal thickening and irregularity of the urethral or bladder mucosa or may reveal an enlarged prostate containing both hypere­ choic and hypoechoic foci. In rare cases, the prostate or bul­ bourethral glands are grossly enlarged and contain an obvious abscess. Urethroscopy of the female adult camelid may be accomplished with a scope of up to 6 mm diameter. A smaller scope may be necessary for males and juveniles. Introducing a biopsy instrument or polyethylene tubing from the scope’s

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biopsy channel into the urethral orifice may aid in passing the scope. Digital rectal examination may be helpful in identifying an enlarged, painful prostate or urethral pulsations. With liths or chronic diseases, ultrasonography or radiography may show mineralization of the bladder mucosa. If the endoscope can be passed into the bladder, pinch biopsies may be performed for histology and culture. Friability of the inflamed bladder is a concern, however, and even a small biopsy may lead to leakage. With chronic inflammation, parts or all of the bladder mucosa undergo polypoid change. Histology of the acutely inflamed bladder may reveal evidence of bacterial infection. With chronic diseases, the bladder epithelium becomes hyperplastic and infiltrated with neutrophils, and the underlying lamina propria has zones of granulation tissue. This polypoid change may be regional or widespread in the bladder. Treatment is similar to what is used medically for urinary tract obstruction, without the surgery. IV fluids, potentially in conjunction with furosemide (2 to 5 mg/kg, IV or IM, up to q6h or continuous rate infusion [CRI]) or glucose (0.25 to 1 g/kg as an IV bolus, up to q6h) dilate and flush the urinary tract. Acepromazine (0.02 mg/kg, SQ, q6h) provides urethral relaxation. Antiinflammatory medications are also very helpful. Some suggest the use of corticosteroids for their potent antiinflammatory activity, but such agents should always been used with caution in camelids with potential infectious disease. Penicillins or ceftiofur are frequently used antibiotics. Other antibiotics that concentrate in the urine may also be useful. Enrofloxacin has been used specifically when Pseudomonas infection is suspected. Finasteride has also been used in some cases of prostatic enlargement, but no pharma­ cokinetic data for camelids are available, and GI absorption is unpredictable. Relaxants, dilators, and analgesics may also play some role. Treatment frequently must continue for 2 to 6 weeks to see positive results. Prognosis is fair to guarded. Camelids with urinary tract irritation strain frequently and for several weeks, and some of them go on to develop obstruction.

Bladder Rupture Bladder rupture occurs most commonly as a consequence of urethral obstruction but may also be caused by acute external trauma such as getting caught over a fence rail or increased friability with cystitis.22,24,32 Factors that promote urine reten­ tion such as long-term transport or handling make the bladder more susceptible to rupture. Unlike in foals, bladder rupture has not been connected to parturition in the neonate. Clinical signs may resemble those seen with urinary tract obstruction, or those signs may have been seen in the days preceding the rupture. Lethargy and progressive abdominal distention are common complaints. Signs worsen slowly over several days. Blood abnormalities include azotemia, hypochloremia, hypo­ natremia, hypernatremia, and metabolic alkalosis (initially, followed by acidosis with shock). Inflammatory changes develop with time. Other abnormalities may reflect the original disease and increased time spent in recumbency. Abdominal fluid analysis is highly suggestive. Fluid is usually recovered readily, may be proteinaceous or sanguinous, and has higher creatinine and potassium concentrations compared with peripheral blood. Ultrasonography reveals the excess

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abdominal fluid. The bladder may appear small or distended. Plain radiography may demonstrate obliteration of detail below a fluid line. Retrograde urography may demonstrate intraabdominal leakage. Correction is achieved through caudal midline celiotomy. A large tear may be readily apparent, or in the case of bladder distention secondary to urolithisis or cystitis, pin-prick–sized holes may be found. Cranial and ventral tears are reported.22,24,32 Some of the bladder wall may be necrotic and require resec­ tion. The bladder should be closed routinely, with placement of a percutaneous urethrostomy tube in the appropriate place if urethral patency is in doubt. Medical treatment is similar as for obstruction. Isotonic saline may be the fluid of choice for correction of the initial electrolyte and acid–base abnormalities, with the recognition that hyperkalemia frequently reverses to hypokalemia with the resumption of adequate urination. Prognosis is fair, based on the health of the bladder wall and the overall difficulties in reestablishing patency in camelids with urethral obstruction.

Renal Hematuria Renal hematuria is an uncommon finding, and usually linked to nephritis or neoplasia.33,34 In some cases, no clear etiology is found.35 Clinical signs include regenerative anemia and gross hematuria, occasionally with intermittent spells of stran­ guria. Urine is grossly and microscopically abnormal, with a large number of intact erythrocytes. Signs often wax and wane over several months, and anemia may become severe. Ultra­ sonography and biopsy may or may not be informative. With nephritis associated with gross hematuria, the abnormal kidney is usually grossly enlarged with homogeneous areas of pelvic dilation replacing the normal architecture. With neo­ plasia, lesions may be small and focal enough to be missed. Advanced imaging studies may reveal functional differences between the kidneys. Nephritis causing gross hematuria is usually unilateral. Neoplasia may initially appear unilateral, but it is not uncom­ mon for the second kidney to develop tumors at a later date. If the bleeding can by isolated to one kidney, usually based on endoscopic visualization of the ureters emptying into the bladder, or successful imaging of both kidneys, unilateral nephrectomy may be curative.33 If both kidneys are affected or isolation to one kidney is impossible, systemic anticoagulant treatments may help. These include δ-aminocaproic and con­ jugated estrogens. Blood transfusion may be necessary if anemia is severe.

Nephritis Nephritis and pyelonephritis are underreported but important diseases of camelids. A quick survey of 17 affected camelids necropsied at Oregon State University revealed that nephritis was associated with cryptococcosis (2), GI parasitism (2), uro­ lithiasis (2), bacterial pneumonia (2), a chronic tooth root abscess (1), chronic interstitial fibrosis suggestive of toxicosis or leptospiral infection (4), and presumptive bacteremia from an unknown source (4). Thus, in most cases, the kidneys were affected secondarily or in conjunction with other organs. As such, renal disease often represents the spread and worsening of a formerly local phenomenon.

Recovered organisms sometimes are primary pathogens capable of causing systemic illness, such as Cryptococcus. C. gatti is a relatively common problem in the Pacific Northwest and other Pacific Rim regions and is less likely to be a problem in other areas.36 An especially virulent strain associated with soil and wood is found in Oregon. Other systemic mycoses affecting the kidney, including Aspergillus and Candida have been reported elsewhere.37–39 We have not seen acute leptospi­ rosis at our clinic, but it has been reported in one guanaco with coccidiosis and could account for some of our cases of chronic glomerulonephritis and interstitial fibrosis.40 Other infectious agents represent opportunists such as the organisms of neonatal sepsis, GI or respiratory tract invaders of damaged tissue, or abscess-associated organisms gaining access to blood. Such organisms may invade the kidneys dif­ fusely or in focal colonies or emboli. The role of viruses in nephritis has yet to be defined. One of the camelids seen at Oregon State University had renal intranuclear inclusion bodies suggestive of either adenovirus infection or herpesvirus infection. It also had widespread hepatic necrosis. If renal lesions remain focal, affected camelids may show no signs beyond general ones and those arising from other affected organs. If the renal lesions become extensive, urine may become grossly or microscopically abnormal, and azote­ mia may develop. Azotemia may contribute to lethargy, obtundation, and potentially central nervous system (CNS) signs. In very rare cases, affected camelids show evidence of abdominal discomfort or stranguria. Terminal icterus was reported in the one guanaco with acute leptospirosis.40 Blood and urine analysis and ultrasonography of the kidneys may reveal abnormalities compatible with inflamma­ tion and decreased renal function. Ultrasonographically, pos­ sible changes range from small hyperechoic foci to larger areas of embolism and infarction. With chronic nephritis, contrast radiography may demonstrate decreased contrast uptake by one or both kidneys (Figure 39-8). Bacteriologic and fungal culture of blood, urine, renal tissue, or samples from other affected organs may yield the causative organism. Biopsy is especially useful for diagnosis of fungal and leptospiral disease. Special stains may be required to demonstrate the organisms. Leptospires may occasionally be found by using dark-field microscopy or fluorescent antibody staining of urine. Leptospiral titers may be helpful as well, especially in camelids with chronic inflammation in which the organism may no longer be present. Previous vaccination may also gen­ erate titers, so a complete health history is necessary for correct interpretation. In general, beyond the need for diuresis of nitrogenous wastes, treatment of acute hematogenous bacterial or fungal infections of the kidney is the same as that for infections elsewhere. In many cases, treatment for a primary disease condition is necessary as well. Nephrotoxic agents should be avoided or used with caution. Prognosis may be worse for camelids with fungal diseases, leptospirosis, or extensive bac­ terial damage than for those with relatively focal lesions caused by hematogenous bacterial infection. Chronic renal disease is less common but also less treat­ able. Affected camelids usually display the nonspecific signs of lethargy, weight loss, anorexia, and weakness and may also have peripheral edema, ascites, polyuria, and polydipsia. Often, the affected animals smell of urine. Blood analysis

Chapter 39  •  Disorders of the Urinary System

Figure 39-8  Excretory urogram of an alpaca with chronic nephritis and urinary incontinence. Note that the left kidney (right side of image) takes up little contrast, whereas the right kidney and ureter appear normal.

reveals moderate to profound azotemia, often accompanied by hypoproteinemia. Urinalysis reveals proteinuria and isos­ thenuria. Ultrasonography of the kidneys may reveal decrease in size, increased echogenicity, and loss of the corticomedul­ lary distinction. Biopsy is helpful in estimating the severity of the fibrotic changes. Treatment is mainly palliative. Erythrocy­ tosis is an uncommon finding in camelids but may be linked to chronic depletion of functional renal tissue.

Toxic Nephropathy and Acute Renal Failure Camelids appear to tolerate dehydration fairly well, and hemodynamically mediated renal failure is uncommon. However, because of their low urine output and ability to tolerate and hide relatively severe dehydration, they may be more susceptible than other domestic herbivores to iatrogenic toxic nephropathy. Agents that damage the kidneys of other species should be considered dangerous for camelids as well and should be used with caution in potentially dehydrated patients. The best-described nephrotoxic agents in camelids are gentamicin and vitamin D.41,42 Other aminoglycoside anti­ biotics, nonsteroidal antiinflammatory drugs (NSAIDs), and certain plant toxins are also suspect. For all these agents, adequate hydration and urine produc­ tion appear to be protective. Gentamicin and other aminogly­ cosides enter the renal tubular cells from urine and disrupt cellular metabolism. Inadequate recovery time between doses leads to cell death. Once-a-day administration of aminoglyco­ sides (gentamicin sulfate: 5 mg/kg, IV or IM, q24h; amikacin sulfate: 15 to 18 mg/kg, IV or IM, q24h) appears to be safer than more frequent dosing but may still affect the kidneys of dehydrated camelids.41,43 Concurrent NSAID administration may exacerbate the toxic effects. Apparently healthy camelids suspected of having decreased water intake developed evi­ dence of renal damage after 2 days of daily gentamicin admin­ istration. The same occurred after 10 days of daily treatment

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in hospitalized camelids thought to be drinking well. There­ fore, sick camelids and those that do not have access to water should be rehydrated prior to drug administration, if possible, and water intake and hydration status should be monitored carefully in camelids receiving these medications without supplemental fluids. Monitoring of trough serum gentamicin concentrations, serum creatinine concentrations, or urinary enzymes should be considered in all camelids receiving gen­ tamicin for more than 5 successive days. The dangers of aminoglycosides appear to well appreciated, but the nephrotoxic potential of NSAIDs appears to be under­ estimated. These agents are known to reduce blood flow to the renal papilla, especially when blood volume in low. Most camelids admitted to Oregon State University with evidence of acute renal failure have a history of recent NSAID admin­ istration, but aminoglycoside use is now relatively rare. Many sick camelids have vague, slowly recognized signs and are often dehydrated by the time of first recognition. As part of a broad treatment plan, they often are administered one or more doses of flunixin meglumine or a similar agent prior to being rehydrated. Such camelids are at risk of developing hemodynamically mediated acute renal failure. Vitamin D intoxication is usually caused by accidental or intentional overdosing.42 Rickets is a well-known entity in young camelids, and exogenous vitamin D is often adminis­ tered to prevent it. Although adult camelids appear relatively resistant to overdosing, crias are clearly susceptible.44 Some cases relate to preparation errors and are unintentional, but most relate to repeated, high-dose administrations. Recom­ mended doses are 1000 to 2000 units/kg as a single dose every 2 to 3 months subcutaneously or 30 to 40 units/kg/day per os.44,45 Anecdotally, some crias have received 10,000 to 15,000 units/kg at birth without noticeable adverse effects but also without evidence that this is more efficacious than the lower dose. Affected crias have received 25,000 to 65,000 units/kg over a week or less and may have serum concentrations of vitamin D in excess of 600 nanomoles per liter (nmol/L) and renal tissue concentrations greater than 250 nmol/L.42 Vitamin D promotes the absorption of calcium from the gut, its resorp­ tion from urine, and mobilization from bone. High blood ionized calcium concentrations lead to dystrophic mineraliza­ tion of tissues, including glomeruli and renal tubular cells. Levels of supplementation below the acute toxic threshold are potentially deleterious over the long run. Dystrophic renal mineralization may be linked to this and may be detected with CT (Figure 39-9). Oleander (Nerium oleander) poisoning is mainly known for its cardiac, GI, and neurologic effects but also appears to affect the kidneys in some animals.46 Camelids exposed to oleander often have azotemia, which could be prerenal and relate to cardiac output, but some also have histologic evidence of renal disease. Changes include hemorrhage or vacuolar degenera­ tion of the tubular epithelium, with diffuse evidence of min­ eralization. Oleander poisoning is one of the most common livestock poisonings in the warmer parts of the world where the plant thrives. Poisoning results from ingestion of the leaves, often when mixed with other plants or grasses in the form of clippings, when baled in hay, or as windborne dead leaves. The lethal dose for camelids is not known but is prob­ ably only a few leaves. Oleander contains oleandrin, a cardiac glycoside that inhibits the sodium–potassium pump and

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Figure 39-9  Computed tomography image showing bilateral lines of mineralization in the kidneys of an alpaca.

tri­terpenoids. The specific toxic principle affecting the kidney is unknown. Red maple (Acer rubrum) poisoning does not directly affect the kidneys, which are nonetheless damaged by the products of intravascular hemolysis. Gallic acid may be the toxic prin­ cipal. Hemoglobin is thought to damage the kidney in three ways: (1) a direct toxic effect on the proximal tubular epithe­ lium, (2) vasoconstriction caused by nitric oxide scavenging, and (3) obstruction of the distal tubules by intraluminal hemoglobin precipitation. Tubular cell hemoglobin uptake is normal, so damage only ensues when the cells are over­ whelmed. The other two mechanisms are extracellular and presumably exacerbated by low renal blood flow or urine volume. Red maple poisoning and other disorders associated with intravascular hemolysis appear to be rare in camelids.47 A variety of other plants are known to have nephrotoxic potential in other livestock species. Cestrum diurnum (day blooming jessamine, wild jasmine, day cestrum, or Chinese inkberry) contains 1,25-dihydroxyvitamin D-glycoside and is found in the warmer parts of North America. Solanum malacoxylon is similar. These plants cause mineralization of the kidneys and other tissues, similar to what is seen with iatro­ genic vitamin D intoxication. Members of the beet family (especially the tops), Chenopodium (lamb’s quarters), Kochia scorpia, Halogeton glomeratus (saltlover), Amaranthus spp. (pigweed), Sarcobatus vermiculatus (black greasewood, chico), Rheum rhaponticum (rhubarb leaves), and Rumex (curly dock) contain oxalates, which are concentrated in the kidney and may precipitate there in the presence of calcium. Quercus spp. contain gallotannins, which irritate the gut and may cause hepatic and renal necrosis. Empirically, the Oregon white oak (Quercus garryanna) appears to be less toxic than some other species. Although scientific reports are lacking, it is quite possible that camelids would not be immune to their deleteri­ ous effects. Signs of toxic renal damage are generally nonspecific and include lethargy and loss of appetite. In the acute phase, the animal may have anuria or oliguria. Occasionally, fluid accu­ mulation with anuria leads to peripheral edema, ascites, diar­ rhea, chemosis, and epiphora. In severe cases, cerebrocortical signs, including seizures, may be seen. Blood analysis reveals

azotemia with occasional hypermagnesemia, hyperphospha­ temia, hyponatremia, hypochloremia, and metabolic acidosis. The serum BUN-to-creatinine ratio (both in mg/dL) is usually well under 20 : 1. Changes in potassium are unpredictable, with hyperkalemia associated with severe, acute dysfunction and hypokalemia associated with more insidious disease. Hyperkalemia is also more common in neonates with acute renal failure because of their high potassium diets and the fact that they are often given milk by tube after voluntary intake ceases. With acute oxalate poisoning, hypocalcemia would be expected, and with acute intoxication, signs of hypocalcemia predominate over those of renal failure. Plant-based or pharmaceuticals-based vitamin D intoxication causes hyper­ calcemia and hyperphosphatemia. Urinalysis reveals isosthe­ nuria and possibly the presence of protein, casts, and increases in N-acetyl-B-D-glucosaminidase (NAG) and γ-glutamyl trans­ peptidase (GGT) activity. The fractional excretion of conserved ions (sodium) is inappropriately increased, whereas that of normally excreted ions (potassium) may be decreased. Specific findings, that is, oxalate crystals, may be indicative with spe­ cific poisonings. If oleander poisoning is suspected, urine, serum, or GI contents may be analyzed for the presence of oleandrin by liquid chromatography–electrospray tandem mass spectrometry. Ultrasonography may reveal reduction or enlargement in the size of the affected kidney and minimal urine in the bladder but is often unremarkable. Perirenal edema may be seen. Biopsy reveals nonbacterial acute tubular necrosis. With vitamin D poisoning, mineralization of the kidneys or other internal organs may be seen on biopsy, radi­ ography, or ultrasonography . Blood and tissue concentrations of vitamin D will also be well above recommended reference ranges. Tissues with dystrophic calcification, including the kidneys, may have multiple mineralized foci and a gritty feel. Anemia and hemoglobinuria are seen with red maple poisoning. Treatment consists primarily of removal from the putative source, efforts to increase urine volume, and correction of metabolic disturbances. These last two goals are usually achieved through IV fluid administration. Care must be taken not to fluid-overload oliguric or anuric patients. In such patients, peritoneal dialysis (10 to 20 mL/kg of dialysis solu­ tion with dwell times of 2 to 6 hours) may be considered to reduce azotemia and remove some toxins. Diuretics including furosemide (2 to 5 mg/kg, IV or IM, up to q6h or CRI) or glucose (0.25 to 1 g/kg as an IV bolus, up to q6h) may be administered to increase urine volume and potentially expel toxins and debris. Low-dose dopamine, previously thought to increase renal blood flow, has more recently been shown not to be useful in correcting azotemia in other species.41,48 Most toxins do not have specific antidotes. Maintaining blood potassium and calcium concentrations may decrease aminoglycoside toxicity. Calcium supplementation may be prophylactic or therapeutic for oxalate poisoning. Ascorbic acid may decrease hemolysis with red maple poisoning, and alkalinizing the urine and administering mannitol may help as well.49 If ingestion of any poisonous plant is suspected, activated charcoal (1.5 g/kg, PO, may be repeated daily) may decrease toxin absorption. Digoxin-specific Fab fragments derived from sheep are commercially available to treat olean­ der poisoning in humans, but their use in camelids has not been reported.

Chapter 39  •  Disorders of the Urinary System Prognosis depends on response to treatment. When BUN and creatinine levels return to reference ranges rapidly, the outcome is likely to be good. Halving pretreatment values every 24 hours is a good measure of progress, although we have seen one camelid that did not respond for 4 days but ultimately did well.

Postpartum Incontinence Rarely, and usually after a traumatic dystocia, camelid females develop vaginal urine pooling, with resultant dribbling and skin scald. Rather than direct trauma to the urethra, this may relate to conformational changes in the vagina related to stretching, bruising, or scarring. Diagnosis is made by specu­ lum examination or vaginoscopy, either of which will identify the urine pooling and potentially the presence of inflamed or scarred tissue. Urine may leak forward through the open cervix and affect subsequent fertility. In such cases, urometra may be detected with palpation or ultrasonography. These lesions may respond to time or treatment with anti­ inflammatory medications. In the worst case, a surgical ure­ thral extension may be performed.

Neoplasms Similar to the liver, the high blood flow and extensive capillary network of the kidneys makes them a common site for meta­ static neoplasms. Primary cancers also occur but are rarer. Primary neoplasms of the urinary system include transitional cell carcinoma and papilloma, teratoma, nephroblastoma, and sarcoma.29,33,34,50,51 Multicentric or metastatic tumors affecting the urinary tract include lymphoma, pulmonary car­ cinoma, and sarcomas.52–54 Nephroblastoma has also been reported to metastasize from the kidney to the lung and other sites. Multicentric or metastatic neoplasms outnumber primary urinary tract tumors at least 3-to-1 in the literature and in our clinic population, with approximately 40% of multicentric lymphoma cases affecting the urinary tract.52 Except for sarcoma and transitional cell tumors, the renal parenchyma appears to be the main urinary site affected. Transitional cell papilloma and carcinoma are character­ ized by lesions in the renal pelvis and ureter. Lesions may be unilateral or bilateral and are frequently multifocal. Some lesions appear more papillomatous and others carcinoma­ tous. Ingestion of bracken fern and infection with bovine papilloma virus 2 may play some role in the development of lesions.34 These tumors are most common in camelids less than 10 years old. Clinical signs include anemia, hematuria, proteinuria, and weakness, and progress over several months. With obstruction of the ureters, some evidence of abdominal discomfort may be seen. Blood evaluation reveals regenerative anemia, low serum iron, and hypoproteinemia. Azotemia is usually mild, if present. Anemia may become severe and require transfusion. Ultrasonography may reveal the masses or dilation of the renal pelvis or ureter. Both sides should be scanned. Masses may also be missed. To define whether one or both sides are affected, cystoscopy may be used to examine urine coming from each ureter. Actual sampling of urine from each ureter is superior to simply looking for macroscopic hemorrhage. If the lesions are confined to one side, the affected kidney and ureter may be removed surgically. If surgery is not

475

feasible or the lesions are bilateral, procoagulant treatments such as conjugated estrogens or δ-aminocaproic acid may be used. Nephroblastoma has been reported in one 3-month-old guanaco.51 The cria was found dead with no physical or labora­ tory evaluation. Histology revealed multiple types of neoplas­ tic tissue, including skeletal muscle, tubular structures, and mesenchymal tissue. Liver and lung metastatic lesions con­ tained skeletal muscle. Renal teratoma has been reported in a 15-month-old llama with a short history of hypoproteinemia, lethargy, mild abdominal distention, and signs of discom­ fort.50 The mass, found during exploratory surgery, involved the entire right kidney. Histology revealed cartilage, fibrous connective tissue, and cells of epithelial origin. Both these masses were found in young camelids and would probably have been detected with ultrasonography. Metastases from the nephroblastoma and infiltration around the abdominal aorta by the teratoma would have limited treatment options. Urethral sarcoma has been reported in a single case of a 2-month-old alpaca.29 The cria had stranguria, hematuria, pol­ lakiuria, and a visible mass growing out of the vagina. It appeared to arise from the terminal urethra and had prolapsed through the urethral tubercle. Histopathology and immuno­ histochemistry suggested a mesenchymal origin for the sarcoma. The mass regrew after laser excision but was subse­ quently successfully treated with vincristine and external beam radiation therapy. Metastatic and multicentric neoplasms affecting the urinary tract primarily affect the renal cortices. A single case of bladder lymphoma has been reported.52 Infiltration of the kidney may be diffuse or masslike. Affected camelids often show a variety of signs, depending on other sites of neoplastic infiltration. Renal signs are mainly nonspecific and include weight loss and lethargy, proteinuria, anemia, hypoproteinemia, and renal or prerenal azotemia. Renal function is rarely completely compromised before other effects of the tumor affect survival. Involvement of the kidney may be detected by using ultraso­ nography or CT (Figure 39-10) and confirmed through biopsy

Figure 39-10  Contrast-enhanced image of a right renal filling defect in an alpaca with metastatic sarcoma.

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and histopathology. Diffuse tumors may be recognizable through changes in tissue echogenicity compared with a healthy kidney, spleen, or liver. Unless the lesion may be treated locally, as may be the case with unilateral papillomas or a focal sarcoma, systemic chemotherapy is the treatment of choice.

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