Urologic Disorders of Immature Cats

Pediatrics

0195-5616/87

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Urologic Disorders of Immature Cats

]odyP. Lulich, D.V.M.,* CarlA. Osborne, D.V.M., Ph.D.,t Dennis F. Lawler, D. V.M .,:t Tirrwthy D. O'Brien, D.V.M., Ph.D.,§ Gary R. johnston, D.V.M., M.S .,II and Terrance P. O'Leary, D.V.M., Ph.D. 1!

CONGENITAL ANOMALIES OF THE FELINE URINARY TRACT Development of the urinary system requires a phenomenal degree of coordinated interaction between embryonic precursors of the adult kidney, ureters, urinary bladder, and urethra. It is, therefore, truly phenomenal that congenital anomalies of these components are an infrequent cause of clinical disease. The urinary tract is more than a waste disposal system . It plays a major role in fluid, electrolyte, and acid-base regulation. In addition, the kidneys influence hemodynamics via: (1) erythropoietin-mediated red blood cell production, (2) renin-angiotensin-mediated blood pressure control, and (3) vasopressin- and aldosterone-mediated blood volume. Therefore, aberrations in normal development, whether acquired or from genetic defects, may threaten survival. Many urinary tract anomalies are asymptomatic, whereas others are the cause of perinatal deaths, progressive renal failure, urinary incontinence, *Veterinary Medical Associate and Teaching Assistant, Department of Small Animal Clinical Sciences, University of Minnesota College of Veterinary Medicine, St. Paul, Minnesota tDiplomate, American College of Veterinary Internal Medicine; Professor, Department of Small Animal Clinical Sciences, University of Minnesota College of Veterinary Medicine, St. Paul, Minnesota tDepartment of Pet Nutrition and Care Research, Ralston Purina Company, St. Louis, Missouri §Diplomate, American College of Veterinary Pathologists; Assistant Professor, Department of Veterinary Pathobiology, University of Minnesota College of Veterinary Medicine, St. Paul, Minnesota IIDiplomate, American College of Veterinary Radiology; Associate Professor, Department of Small Animal Clinical Sciences, University of Minnesota College of Veterinary Medicine, St. Paul, Minnesota ~Associate Professor, Department of Veterinary Pathobiology, University of Minnesota College of Veterinary Medicine, St. Paul, Minnesota

Veterinary Clinics of North America: Small Animal Practice-Vol. 17, No. 3, May 1987

663

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Table 1. DISORDER ANOMALY

Summary of Abnormalities Associated with Feline Urinary Tract Anomalies ASSOCIATED ABNORMALITIES•

-RENAL

NO.

URETERAL

UROCYSTIC

MISCELLANEOUS

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I. Renal structure A. Agenesis 1. Bilateral 2. Unilateral B. Aplasia 1. Bilateral 2. Unilateral C. Dysplasia 1. Bilateral 2. Unilateral D. Hypoplasia 1. Bilateral 2. Unilateral E. Polycystic 1. Bilateral 2. Unilateral

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II. Renal ectopia A. Not crossed 1. Bilateral 2. Unilateral B. Crossed III. Ureteral ectopia A. Both in to urethra B. One into urethra c. Both into vagina D. One into vagina E. Termination unknown IV. Urocyst A. Colourocystic fistula B. Ectopic uterine horns (into urocyst) c. Patent urachus D. Urachal diverticulum V. Urethra A. Ectopic urethra (into rectum) B. Myelodysplasia (altering urethral function) c. Urethrorectal fistula Total

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*Abnormalities not identified in this summary reflect either instances in which the authors did not mention them or instances where they were not detected.

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and/or persistent infection (Table 1). Early detection and proper management of some anomalies may result in restoration of adequate function, or at least prevent progressive dysfunction. ANOMALIES OF FELINE RENAL STRUCTURE Renal Agenesis

Clinical Importance. Bilateral renal agenesis has not been commonly recognized in cats. We cannot determine whether the infrequency of observation accurately reflects an infrequency of occurrence because this lethal anomaly may be associated with stillborn fetuses and neonatal mortalities. 24 Since veterinarians are rarely supplied with specimens for evaluation, the reported disease occurrence may not reflect disease incidence. In contrast to bilateral renal agenesis, unilateral renal agenesis has been more frequently observed in cats. 43 ·47 •67 •94-96 • 100· 105 However, in one necropsy study of 1000 cats, unilateral renal agenesis was only diagnosed twice. 95 In humans, a higher incidence has been reported in males, the right kidney being more commonly affected. 23 Although review of available literature indicates that female cats with unilateral renal agenesis have been identified more frequently than males, it would be inaccurate to infer a sex predilection, owing to the small number of cases evaluated. In cats, as with humans , the right kidney was usually affected. The clinically silent nature of unilateral renal agenesis often precludes antemortem diagnosis. In our survey, seven cases were diagnosed at necropsy, whereas two were discovered incidentally during celiotomy (Table 2). In four of the nine aforementioned cases, contralateral renal enlargement was present. One patient with concomitant cleft palate and syndactylia died shortly after birth. A diagnosis of unilateral renal agenesis should prompt questions designed to detect putative causes that may affect future offspring (see Addendum, l. Problem-Specific Database for Feline Perinatal Death). Because unilateral renal agenesis is irreversible, control of this disorder lies in its prevention. There have been no in-depth studies designed to evaluate renal function of nonaffected kidneys. If a persistent degree of renal dysfunction is discovered, appropriate diagnostic and therapeutic steps may be considered. Applied Embryology. The development of the adult renal parenchyma requires coordinated interaction between the ureteral bud (developing ureter) and the metanephric blastema (the developing embryonic kidney that persists in the adult). Three different renal systems develop in the embryo: the pronephros, the mesonephros, and the metanephros. However, only the metanephros persists to become the kidneys . The first system, the pronephros, is apparently nonfunctional in terms of urine formation. It is replaced by the mesonephros, which begins to form fetal urine. The mesonephric kidney degenerates. However, several of its tubules (the mesonephric, paramesonephric, and metanephric ducts) are retained in the caudal portion of the developing embryo. These ducts subsequently differentiate into: (l) seminal vesicles, prostate gland, and vas deferens in

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Feline Renal Agenesis and Associated Abnormalities VAS

AGE (MO)

AFFECTED KIDNEY

F

7

L

+

+

+

NR

+

Normal

NR

M

A

R

+

NR

NR

NR

+

NR

Necropsy 6nding; partial ureter present

47

NR

F

NR

R

NR

+

+

NR

Necropsy 6nding

67

F

42

R

+

NR

+ +

NR

Him

NR

-

Palpable abdominal mass (uterine remnant pyometra)

DSH

F

(1 day)

L

NR

NR

NR

NR

NR

NR

F

A

R

-

NR

M

A

R

+

+ +

+

NR

NR

+

NR

NR

NR

NR

NR

NR

NR

NR

NR

NR

NR

NR

NR

NR

NR

NR

Unilat- DSH era!

URETERAL

UTERUS UNICORNIS

DEFERENS

AGENESIS

AGENESIS

ENLARGEMENT

t'1

SEX

BREED

CONTRALATERAL RENAL

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NORMAL IPSILATERAL GONAD

CLINICAL SIGNS

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COMMENTS

REFERENCE

96

43

Neonatal death; cleft palate; syndactylia

Necropsy 6nding

-

NR

Necropsy 6nding

94

+

NR

Necropsy 6nding

105

NR

NR

Necropsy 6nding

95

NR

NR

Necropsy 6nding

95

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A = adult; DSH = domestic shorthair; F = female; Him = Himalayan; M = male; NR = not reported.

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males; (2) oviducts, uterine horns, and a portion of the uterine body in females; and (3) ureters in both sexes. The metanephros lies adjacent to the developing ureter. Once the developing ureter contacts the metanephros, the embryonic kidney begins to differentiate into its adult form . 38 •64 Renal agenesis can result from at least three defects: (1) failure in development of the ureteral bud, (2) failure in development of the metanephros, and (3) failure of coordinated interaction between the ureteral bud and metanephros. There is a general consensus of opinion that unilateral renal agenesis most commonly results from failure in development of the ureteral bud. 91 If accurate, this hypothesis would provide a plausible explanation as to why concomitant ureteral agenesis has been a common finding in affected cats. It is of interest that abnormalities of the vas deferens and uterus (structures derived from adjacent ducts) have also been observed. Other abnormalities may also cause renal agenesis, as evidenced by one cat with gonadal agenesis, but persistence of the ureter. 94 ·96 The primordial gonad is located adjacent to the embryonic kidney. Therefore, it has been postulated that primary defects that affect the embryonic kidney may also alter gonadal development. 94 Because of the close association between the development of genital and urinary systems, genital anomalies commonly occur with renal agenesis. Although it is possible that renal agenesis could occur as a result of a genetic defect, no breed predispositions to bilateral or unilateral renal agenesis have been identified to date. Therefore, it is likely that developmental aberrations are a more common cause of this anomaly. The fact that renal agenesis was induced in offspring of pregnant rats given intraperitoneal injections of sodium arsenate supports this hypothesis. 29 No etiologic agents have been identified in cats with renal agenesis. Clinical Findings and Diagnostic Considerations. Perinatal death is the only known clinical finding associated with bilateral renal agenesis in cats. Clinical findings that should arouse suspicion of unilateral agenesis include inability to palpate both kidneys and/or detection of deformed or absent vas deferens, epididymal tails, or uterine horns during neutering. Inability to detect the right or left kidney by contrast urography or ultrasonography provides further support for a diagnosis of unilateral renal agenesis. However, a definitive diagnosis is dependent on confirmation during celiotomy or necropsy. Prognosis. Bilateral renal agenesis typically is associated with perinatal death. Unilateral renal agenesis is apparently compatible with normal life, provided that the contralateral kidney undergoes compensatory hypertrophy and hyperplasia of sufficient magnitude to maintain homeostasis. However, recent studies have examined the long-term consequences of compensatory hypertrophy of viable nephrons in rats, dogs, and humans with irreversible nephron damage. Results of these studies have prompted questions about long-term progressive deterioration in renal function. Studies have also suggested that compensatory glomerular hyperfiltration may result in glomerulosclerosis and a subsequent decline in renal function . 46 •60 Thus, it is possible that the life span of an otherwise normal cat with unilateral renal agenesis

669

UROLOGIC DISORDERS OF IMMATURE CATS

may be shortened (that is, living for 12 instead of 15 years). Bowever, further studies are needed before meaningful generalities can be established. · Therapeutic Consideratio.ns. Currently, treatment of patients with renal agenesis is limited to those with unilateral involvement. J)ietary Factors. A direct correlation has been established between the quantity of dietary protein consumed and glomerular filtration rate (GFR) (for example, increased protein consumption is associated with an increase in GFR). Furthermore, studies in rats and hum~J1S with renal insufficiency suggest that dietary protein restriction may prevent or minimize glomerulosclerosis. 46 Based on these observations, it is logical to ask whether a moderate degree of protein restriction might be of long-term benefit in cats with unilateral renal agenesis. · Concomitant Disease. It is probable that cats with unilateral renal agenesis will develop a variety of unrelated diseases throughout their lifespan. If such diseases prompt veterinary care, appropriate caution should be used to preserve remaining renal function. For example, invasive procedures, urinary catheterization, anq renal biopsy should be undertaken with caution. Prompt recognition and correction of nonrenal disorders assocjated with reduced renal perfusion (for example, dehydration, cardiac failure, hypoalbuminemia) or obstruction to urine outflow (for example, urolithiasis) may prove beneficial, if not requirements, for patient survival. 109 Likewise, use of nephrotoxic drugs an<~ anesthetic agents that markedly depress renal function should be avoided. 19· 57 RENAL DYSPLASIA AND

APLA~IA

Renal dysplasia is characterized by disorganized parenchymal development resulting from arrested or anomalous cellular differentiation. Microscopically, the kidneys consist of segmental or focal areas of primitive nephrons and adjacent fibrous connective tissue (Figs. 1 and 2). Renal aplasia is a severe form of renal dysplasia affecting the entire kidney. Renal dysplasia may occur if developing nephrons are exposed to noxious stimuli. For example, in utero inoculation of feline fetuses with panleukopenia virus resulted in developmental arrest of maturing nephrons located in the peripheralcortex. 59 · In humans, urinary tract obstructjon is a common cause of renal dysplasia. 9 The severity of dysplasia often parallels the severity of obstruction. A similar phenomenon may occur in cats, as evidenced by one case in which complete ureteral obstn~ction was associated wjth unilateral renal aplasia. 92 It is conceivable that increases in hydrostatic pressures during nephrogenesis may result in altered development qr even destruction of nephrons. However, since experimental methods other than induced obstruction are more consistent in reproducing renal dysplasia, obstruction to urine outflow may not represent the primary defect. 68 Specific therapy for renal dysplasia is dependent on detection and timely elimination of the underlying cause. Since nephrogenesjs continues after birth in dogs, and presumably cats, early identification and correction of abnormal outflow resistance may prove advantageous. 45 Once present, renal

670

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LULICH ET AL.

Figure 1. Photomicrograph of a dysp,)astic kidney from a 4-month-old Persian cat illustrating a segmental area of interstitial fibrosis, tubular cell atrophy, and immature glomeruli. Hematoxylin and eosin stain; 13 x = original magnification.

dysplasia is irreversible. If a sufficient population of nephrons have been affected to cause primary renal failure, the latter may be progressive (see the preceding section on diagnosis of renal agenesis). In this circumstance, only supportive and symptomatic treatment is available. 81

RENAL HYPOPLASIA A hypoplastic kidney is a miniature replica of a normal kidney. Initially, it consists of normal renal parenchyma without marked evidence of fibrosis or inflammatory reaction. Renal hypoplasia can result from a decrease in the number of developing cells or failure of cellular maturation. Clinical signs, therapy, and prognosis are dependent on the severity of the condition and the extent ofkidney involvement (one or both kidneys) (Table 3). Mild disease may remain undetected, whereas severe bilateral disease is commonly associated with renal failure.

POLYCYSTIC RENAL DISEASE Feline polycystic renal disease is characterized by formation of multiple cysts throughout the renal medulla and cortex (Fig. 3). Affected kidneys may become enlarged and lobulated. In cats, cysts vary from several mil-

UROLOGIC DISORDERS OF IMMATURE CATS

671

Figure 2. Photomicrograph of the kidney described in Figure 1. Note the cellularity of the immature glomerulus. Hematoxylin and eosin stain; 128 x = original magnification.

limeters to several centimeters in diameter. Renal cysts are typically lined by cuboidal epithelium and may contain up to 10 ml of a clear urinelike fluid of low cellularity. In humans, polycystic renal disease is inherited as an autosomal dominant or recessive trait. 110 The fact that most cats with polycystic kidneys are of the longhaired variety suggests a familial tendency (see Table 3). A report of polycystic kidneys in several generations of a family of longhaired cats in South Carolina supports this hypothesis. 21 Precise etiologic mechanisms causing the formation of multiple cysts in both kidneys of cats are unknown . In man, it has been popular to incriminate hypertrophy and hyperplasia of renal tubular epithelium as the initiating events. 110 According to this line of reasoning, the proliferating epithelium eventually causes outflow obstruction, leading to progressive dilatation of tubular lumens. An alternative hypothesis is that there is an intrinsic defect in the tubular basement membrane, allowing "blow-outs" of the tubular walls. In this sense, polycystic disease may be t.he renal equivalent of pulmonary emphysema associated with alpha 1-antitrypsin deficiency. 35 Irrespective of its etiology, polycystic renal disease is characterized by progressive cyst enlargement and compression of adjacent parenchyma, leading to progressive, irreversible renal failure.

Table 3. Anomalies of F e lineRe nal Structure and Associated Abnormalities ANOMALY

Aplasia Unilateral

BREED

NR

SEX

AGE (MO)

F

NR

AFFECTED KIDNEY

Left

GROSS PATHOLOGY

Renal ectopia (caudal abdomen); extreme reduction in size

Dysplasia Bilateral

Hypoplasia Bilateral

Unilateral

Polycystic Bilateral

CLINICAL FINDINGS

Reduced nephron numbers; generalized fibrosis

Ectopic, atretic ure ter of reduced length

NR

Stunted growth

REFERENCE

93

NR

4

Both

Irregular contour; adherent capsule

Small hypercellular glomeruli; segmental areas of interstitial fibrosis and tubular cell atrophy

NR

NR

NR

K

Both

Reduced size

Segmental areas of small hypercellular glomeruli

Cerebellar hypoplasia associated with panleukopenia virus

DSH

M

0

Both

NR

NR

Cleft palate; contracted hindlimb tendons

Stillborn; renal hypoplasia of litte rmate (see below)

62

DSH

F

(3 days) Left

NR

NR

Cleft palate; contracted hindlimb tendons

Neonatal death; renal hypoplasia of littermate (see above)

62

DSH

F

6

Right

Reduced size

Moderate glomerular hypercellularity; mineralized collecting duct and TBM

Ectopic ureter; Streptococcus spp. (> 10'/ml) isolated from urine

Urinary incontinence

DLH

F

K

Both

Multiple cysts in cortex and me dulla; mild dilatation of renal pelves

Dilated cysts lined by cuboidal epithelium; reduced glomerular number; many atrophic glomeruli

Dilated and cystic bile ducts

E nlarged abdomen; neonatal deaths of related kittens

Dilated cysts lined by cuboidal epithelium; reduced glomerular number; many atrophic glomeruli

Dilated and cystic bile ducts

Fluid-filled cysts distributed throughout kidney

NR

Kinked tail; bilateral pate llar luxation

None

Multiple 2-4 mm cysts within cortex and medulla

NR

Cardiomegaly; hydrothorax;

Cardiac murmur

Him

Him

NR

K

F

F

doxnes~i.c s h orthairo F

Both

Both

7

2.5

-

Both

f emaleo K -

Multiple cysts in cortex and medulla; mild dilatation of renal pelves

kittens; M

-

m a le; NR -

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DLH

DSH -

ASSOCIATED ABNORMALITIES

MICROSCOPIC PATHOLOGY

This report

59

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Enlarged abdomen; neonatal deaths of related kittens

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UROLOGIC DISORDERS OF IMMATURE CATS

673

Figure 3. Photograph of a bisected polycystic kidney from a 10-year-old female domestic longhaired cat.

ANOMALIES OF FELINE RENAL POSITION Renal Ectopia Definitions. Renal ectopia (with and \\jthout fusion) is a term used to describe the congenital malposition of one or both kidneys. 25 Simple renal ectopia occurs when the ectopic kidney, ureter, and ureteral entrance into the urinary bladder reside on the same side of the abdomen. In contrast, crossed renal ectopia is characterized by transposition of kidney or kidneys to the opposite side of the abdomen. Therefore, the associated ureter or ureters must cross the midline before entering the urinary bladder. The following classification is based on the retroperitoneal location of the ectopic kidney or kidneys: (1) a pelvic ectopic kidney lies within the pelvic canal, bounded dorsally by the sacrum; (2) an iliac ectopic kidney lies within the iliac fossa, bounded laterally by the wings of the ilia; and (3) an abdominal ectopic kidney lies cranial to the ilia and caudal to the diaphragm. Renal fusion represents the congenital union of normally lateralized kidneys. The attachment may be limited to the renal capsule or it may also involve the parenchyma. Fused kidneys assume a variety of shapes. Horseshoe kidneys are symmetrically fused along the medial borders of either their caudal or cranial poles. The name is derived from their resemblance to the shape of a horseshoe. Clinical Importance. Kidneys in the cat normally lie ventral to the first to fifth lumbar transverse proc~sses; the right kidney is typically more cranial than the left. 74 Both kidneys are located lateral to the median plane, and their pelves face medially. Renal ectopia occurs when the mature kidney fails to reach its normal location and orientation within the abdomen. The

674

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LULICH ET AL.

prevalence of renal ectopia in humans has been reported to vary from 1 in 500 to 1 in 1200. 2 · 17· 106 In a study of 400 cats used for dissection within a 7year period, two cases of renal ectopia were detected. 54 Review of available literature indicates that feline renal ectopia was reported more often in males than in females (6 of 10) and was diagnosed in patients ranging from neonates to adult cats (Table 4). No breed predilections were identified. In cats with bilateral renal ectopia, renal fusion (horseshoe kidney) was a common finding. Applied Embryology. Paired metanephric blastemas (structures destined to become the kidneys) and ureteral buds develop in the caudal embryo. Each ureteral bud grows cranially until it becomes capped by its corresponding embryonic kidney. This interaction immediately precedes the initiation of renal ascent and ureteral elongation. During their ascent, the kidneys reorient themselves so that the initial ventrally directed renal pelves face medially. Renal migration and rotation are complete by the time the feline embryo is 16 mm in length (recall that at birth, a kitten is approximately 145 mm in length). 14 •104 It is unclear whether the embryonic kidney migrates oil its own and/or is forcibly advanced from its initial location within the pelvic canal. Irrespective of the driving forces, potential mechanisms disturbing normal renal migration include: (1) failure in growth or development of the ureteral bud, (2) failure in growth or development of the metanephric blastema, and/or (3) mechanical impedance of renal ascent by neighboring nonrenal structures (retained vasculature from the metanephric blastema, anomalies of other organs, renal fusion, incomplete embryonic extension, and so on). Congenital fusion of the kidneys is thought to occur prior to their rotation and ascent. 70 •104 It is conceivable that renal fusion may result from unsuccessful or delayed migration, followed by subsequent enlargement and fusion within the pelvic cavity. Because of their fusion , such kidneys seldom attain their normal orientation within the abdominal cavity. Etiologic Possibilities. Does an ectopic kidney represent the consequence of altered orientation and development of neighboring structures, or does it represent an intrinsic property of damaged primordial renal tissue? The right kidney of a 10-year-old domestic shorthaired cat submitted to the Veterinary Diagnostic Laboratory at the University of Minnesota was buried within the caudate lobe of the liver (Figs. 4 and 5). In this instance, the kidney ascended beyond its normal location. Since intrinsic disease of this kidney would not be expected to cause migration beyond that recognized as normal, displacement by some other abnormal structure may have occurred. The relationship between fused kidneys and renal ectopia is poorly understood. Is fusion the consequence of enlargement of kidneys that have failed to ascend from within the pelvic cavity, or are fused kidneys impeded from their cranial migration because of their attachment? In our survey of six fused ectopic kidneys, three remained in the pelvic cavity or iliac fossa. The other three were located in an almost normal position (Figs. 6 and 7). Do genetic abnormalities, maternal illnesses, and/or teratogens contribute to development of renal ectopia and fusion in cats? The answer is unknown. However, offspring offemale rats fed diets with either a deficiency

Table 4. 1YPE

DSH

F

2

Both

Abdominal

Horseshoe shape; fusion at caudal poles

Diffuse nephrosis; inflammatory cell infiltration

Mild renal failure

Palpable abdominal mass

NR

M

Adult

·Both

Abdominal

Horseshoe shape; fusion at caudal poles; lobulation; cranial poles surrounded by separate capsules

NR

Renal vascular anomalies

Necropsy finding

Horseshoe shape; fusion at caudal poles; incomplete rotation

Normal; fusion of cortical parenchyma without a distinct separation

Multiple vascular anomalies

Horseshoe shape; fused at cranial poles; incomplete rotation

Normal; fusion of cortical parenchyma without a distinct separation

Reduced ureteral length

Horseshoe shape; fusion of renal parenchyma

Normal

Reduced ureteral length

Pelvic

Horseshoe shape; fusion at caudal poles

NR

Pelvic

Right kidney smaller than left; kidneys are not fused

NR

LOCATION

MICROSCOPIC PATHOLOGY

GROSS PATHOLOGY

ASSOCIATED ABNORMALITIES

CLINICAL SIGNS

REFERENCE

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NR

DSH

DSH

.Unilateral

Feline Renal Ectopia and Associated Abnormalities

SEX

BREED

Not crossed Bilateral

AFFECTED · KIDNEY

AGE (YR)

F

M(N)

M(N)

DSH

M

DSH

NR

Adult

4

2

Both

Both

Both

(3 days) Both

0

Both

Abdominal

Iliac

·Pelvic

This report

0 C'l

54

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Necropsy finding

104

0

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Necropsy finding

70

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Palpable abdominal

99

mass

Cleft palate

Neonatal death; renal hypoplasia in two littermates

Atresia ani;

Stillborn

This report

This report

62

contracted hindlimb tendons; tail absent

DSH

F

10

Right

Abdominal; intrahepatic

Three quarters of kidney buried within caudate lobe of liver

Renal tubules interdigital with hepatic cords

NR

Necropsy finding

DSH

M(N)

0.75

Right

Iliac

Oval shape; reduced size; incomple te rotation

NR

Reduced ureteral length

Palpable abdominal mass

53

NR

F

NR

Left

Iliac

Extreme reduction in size

Renal aplasia

Atretic, ectopic ureter

Necropsy finding

93

NR

M

Adult

Right

Pelvic

Laterally flattened; reduced size

NR

Reduced ureteral length

Necropsy finding

54

DSH = domestic shorthair; F = female; M = male; N = neutered; NR = not reported.

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Figure 4. Intrahepatic ectopic kidney of a 10-year-old female cat. The kidney was partially embedded within the caudate lobe of the liver. (From J Am Vet Med Assoc 190:76, 1987.)

Figure 5. Photomicrograph of the union between the liver and ectopic kidney of the cat described in Figure 4. Note that renal tubules interdigitate with hepatic cords without interposition of a capsule of fibrous connective tissue. Hematoxylin and eosin stain; 40 x = original magnification.

UROLOGIC DISORDERS OF IMMATURE CATS

677

Figure 6. Lateral ventrodorsal view of an excretory urogram of a 2-year-old female domestic shorthair cat with renal fusion (horseshoe kidney). Both ureters, urinary bladder, and urethra were normal. Note opacification of both renal pelves, and fusion of the caudal poles of the kidneys (arrow).

or excess of vitamin A developed renal fusion and other urologic abnormalities. 86·m Clinical Findings and Diagnostic Considerations. The following generalities concerning the spectrum of clinical findings associated with congenital renal ectopia (with and without fusion) are based on our survey of 11 cases. Clinical information was only reported for five of these cases. A palpable abdominal mass was the most commonly reported finding (three of five) . Perinatal death was observed twice, and was associated with nonrenal anomalies (cleft palate, atresia ani, and contracted hindlimb tendons). Renal disease was not suspected in six cases diagnosed at necropsy. Since renal ectopia is not an abnormality that causes damage to renal parenchyma, it may not be recognized. A high index of suspicion of ectopic kidneys is warranted in a cat with an abnormal abdominal mass, particularly if the kidneys cannot be identified in their normal location (see Addendum, 2. Problem-Specific Database for an Abdominal Mass in Immature Cats). Radiography and ultrasonography may be used to differentiate renal ectopia from other abnormalities such as nonrenal neoplasia, foreign bodies, and pregnancy. Prognosis. Renal ectopia and/or fusion apparently do not affect survival. However, if abnormal position and/or rotation of the kidneys distort their ureters, varying degrees of obstructive uropathy may develop. In our

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P.

LULICH ET AL.

Figure 7. Photograph of the horseshoe kidney of the cat described in Figure 6. The kidneys were fused along the medial border of their caudal poles. The connecting isthmus consisted of normal renal parenchyma with cortex interposed between two layers of medulla.

survey, hydronephrosis and hydroureter were not observed. In humans, a higher prevalence of renal neoplasia has been associated with fused kidneys; the majority of neoplasias originated from the connecting isthmus. Renal neoplasia was not recognized in our survey.

ANOMALIES OF THE FELINE URETER Ureteral Ectopia

Clinical Importance. Ureteral ectopia is a congenital anomaly in which one or both ureters do not terminate normally in the urinary bladder. Most affected cats have urinary incontinence. Of the literature reviewed, unilateral and bilateral ureteral ectopia occurred with equal frequency. In most instances, the ectopic ureter or ureters terminated in the urethra. 8 •11 ·36· 61 •93 •98. 103 The majority of cases were diagnosed by 6 months of age; females were identified more often than males. Urinary incontinence, ureteroectasia, hydronephrosis, and urinary tract infection were common sequelae to this disorder (Table 5). Applied Embryology. The metanephric duct (embryonic ureter) develops as a branch from the mesonephric duct (precursor of the epididymus and vas deferens). The pathogenesis · of ectopic ureters is related to the abnormal origin and/or sustained migration of the embryonic ureter before inserting into the urogenital tract. 85 In cats, ureteral ectopia may be associated with other abnormalities such as renal ectopia, renal hypoplasia, and renal aplasia (see Table 1). 93 In dogs, agenesis of the urinary bladder and urethra, urethral abnormalities (ectopic urethra), and persistent hymen have been associated with ureteral

Table 5. TERMINATION

Both into urethra

BREED

DSH Prsn

SEX

AGE (MO)

F(N)

72

M

3

Feline Ureteral Ectopia, Associated Abnormalities, and Response to Treatment

AFFECTED

ASSOCIATED

URETER

ABNORMALITIES

Both Both

Recurrent cystitis Small right kidney

CLINICAL SIGNS

None Urinary incontinence; hematuria

TREATMENT

RESPONSE TO TREATMENT REFERENn;

None Bilateral transposition into urocyst

98

11

None

Urinary incontinence; inflamed perineal skin

Bilateral transposition into urocyst

Incontinence resolved

DSH

M

4

Both

Constricted preputial opening; left hydronephrosis; right hydroureter

Urinary incontinence

Right ureteronephrectomy

Nocturnal urinary

Bilateral hydronephrosis; right hydroureter

Urinary incontinence

NR

F

NR

Left

Ectopic kidney in caudal abdomen; atretic ureter

Prsn

F

6

Left

Tuft of hair protruding from vulva; left hydronephrosis and hydroureter

DSH One into vagina

F

Burmese f(N)

DSH Termination unknown (distal to urocyst)

F

incontinence

c::

Bilateral transposition into urocyst

Resolution of urinary

l03

incontinence;

DSH

F

Necropsy finding

NR

NR

93

Urinary incontinence;

Transposition into urocyst

Transitory pollakiuria; resolution of hydronephrosis; hydroureter and perivulvar inflammation

30

inflamed perivulvar skin

Left

None

Hematuria; dysuria

None

None given

61

Small left kidney; irregular contour; left hydroureter

Urinary incontinence;

Left ureteronephrectomy

Incontinence resolved

27

Left ureteronephrectomy

Incontinence resolved

76

Right ureteronephrectomy

Incontinence resolved

This report

6

Right

Streptococcus spp. (> lOS/ml) isolated

"' t'l

(")

~

Left

Left hydronephrosis; hydroureter

:s:: :s::

> >-j

6

Left

"'1

8

24

2

0

t'l

hydronephrosis and hydroureter One into urethra

c=i

"'0 "'"'0

Both

Both

C'l

11

4

24

0

Incontinence resolved; bilateral renal pelvic dilatation; right hydroureter

F

M(N)

"'0t""

0 c;;

NR

DSH

c::

vaginal discharge; vulvar inflammation Urinary incontinence;

vaginal prolapse; distended abdomen Urinary incontinence

DSH = domestic shorthair; F = female; M = male; N = neutered; NR = not reported; Prsn = Persian.

Q')

-4

cc

680

]ODY P. LULICH ET AL.

ectopia. 91 However, to date, such abnormalities have not been reported in cats. The underlying etiology of ureteral ectopia in cats is unknown. Although familial occurrences have been reported in dogs, no familial predisposition has been identified in cats. 44 •52 Clinical Findings. Clinical signs associated with ectopic ureters vary, depending on their site of ureteral termination and concurrent urologic abnormalities. Ureters that terminated in the proximal urethra were not typically associated with urinary incontinence. 98 Apparently, sufficient urethral sphincter function remained to maintain urinary continence. Urinary incontinence has been the most frequent clinical sign leading to the diagnosis of ectopic ureters in cats (see Addendum, 3. ProblemSpecific Database for Urinary Incontinence in Immature Cats). Continuous urine dribbling has been characteristic of ureters that terminated in the distal urethra in males. In females, urine may accumulate within the vagina, resulting in intermittent incontinence. Discoloration of the perineal hair and urine-scald dermatitis may also occur. Cats with unilateral ureteral ectopia and urinary incontinence maintain a normal micturition pattern. Signs related to concurrent urinary tract infection or renal failure may also be present. Diagnostic Considerations. The termination of ectopic ureters is best visualized by retrograde contrast radiography (urethrography or vaginography). 44 •56 Although intravenous urography may reveal the affected ureter or ureters, accumulation of contrast medium in the bladder lumen often obscures visualization of the site or ureteral ectopia. However, intravenous urography is useful inasmuch that it provides information concerning the size, shape, and position of the kidneys and proximal ureters. 66 Hemograms, serum chemistry profiles, urinalyses, and quantitative urine cultures are also recommended to evaluate the integrity and function of the urogenital tract. Therapeutic Considerations. An effective medical protocol to eliminate urinary incontinence associated with ectopic ureters has not been developed. Surgery has been the time-honored treatment of choice. The surgical procedure selected is dependent on the number and location of ectopic ureters, status of renal function, and concomitant urogenital anomalies. Ureterocystostomy and ureteronephrectomy have been the surgical procedures most commonly performed. Ureterocystostomy (transposition of the ureter into the urinary bladder) should be considered with (1) bilateral ureteral ectopia, (2) normal ipsilateral renal function, or (3) evidence of renal failure. In patients affected with concomitant severe and generalized renal disease, a single affected kidney and its associated ureter · may be removed. Ureteronephrectomy should also be considered when unilateral disease is accompanied by intractable infection. In general, an asymptomatic ectopic ureter requires no therapy. However, owners should be forewarned of ureteral structures leading to obstructive uropathy and/or the possibility of ascending urinary tract infection. Prognosis. Successful transplantation of an ectopic ureter into the urinary bladder is typically associated with immediate cessation of urinary incontinence. However, in dogs, it is possible that a reduced degree of urinary incontinence may persist following surgery in patients with ectopic ureters

681

UROLOGIC DISORDERS OF IMMATURE CATS

Table 6. ANOMALY

BREED

SEX

Anomalies of Feline Urocyst AGE (MO)

ASSOCIATED ABNORMALITIES

Colourocystic fistula Ectopic uterine horns (entering urocyst) Patent urachus

DSH

M

1.3 NR

DSH

F

9

DSH

M

4

Urachal diverticulum

DSH

F

DSH

M

DSH

Cystitis; agenesis of uterine body

Patent urachus leaking urine into abdominal cavity 4 Staphylococcal spp. (> lOS/ml) isolated from urine; urocystoliths 0.3 Urethral obstruction

= domestic shorthair; F = female;

M

CLINICAL SIGNS

Cystitis; neonatal death Urinary incontinence Enlarged abdomen

REFERENCE

61 51 41

Pollakiuria; hematuria

This report

Neonatal death

This report

= male; NR = not reported.

terminating in the urethra. In this situation, an abnormality of urethral function may be present. In dogs with this type of abnormality, phenylpropanolamine (an alpha-adrenergic stimulator) has been successfully used to eliminate the incontinence.97 Similar clinical experience has not yet been reported in cats. Cats with ureterocystostomies have an increased risk for ascending urinary tract infection. However, ureteroectasia and pyeloectasia present prior to surgery typically subside.

ANOMALIES OF THE FELINE UROCYST Overview Primary anomalies of the urinary bladder are apparently rare in cats. In humans, failure of the cloacal membrane to become reinforced by an overgrowth of mesoderm often leads to exstrophy and epispadias. 50 In cats, these anomalies have not been documented. To date, only three anomalies have been documented in cats: connections between the colon or uterus, and the urinary bladder and urachal disorders (Table 6). Applied Embryology The urinary bladder is formed by subdivision of the cloaca, a vesicle in the caudal embryo. The cloaca serves as a common termination for the alimentary and urogenital systems. Wastes are transported from the cloaca through the allantoic duct into the allantoic sac. During embryogenesis, caudal migration of the urorectal septum divides the cloaca into a dorsal alimentary portion and a ventral urogenital portion. Incomplete division of the cloaca will result in anomalous connections between the digestive and urogenital systems. The allantoic duct normally maintains its connection with the urinary bladder at the level of the umbilicus. As the embryo elongates, the bladder

682

]ODY

P. LULICH ET AL.

is pulled caudally into the pelvic canal. During the bladder's migration, the attached apical portion progressively narrows to form the urachus. 72 The urachus is nonfunctional at the time of birth. Therefore, urine retained in the bladder is voided through the urethra. Colourocystic Fistula Apparently, only one case of a fistula between the urinary bladder and colon has been reported in cats. 62 This anomaly may have resulted from incomplete or imperfect division of the embryonic cloaca, or it could have been acquired after birth. Colourocystic fistulas predispose to urinary tract infections and urinary incontinence. Although there have been no reports of treatment in cats, we presume that surgery designed to obliterate the fistula without altering function of the bladder and colon would be required. Ectopic Uterine Horns Entering the Urinary Bladder The close association between the development of the urinary and genital systems might be expected to result in anomalies shared by the two systems. However, such anomalies are rare. We know of only one case of a 9-month-old female domestic shorthaired cat with both uterine horns terminating into the urinary bladder. 51 Surprisingly, the signs related to this disorder were limited to dysuria and hematuria (see Addendum, 4. ProblemSpecific Database for Hematuria and/or Dysuria in Immature Cats). Patent Urachus and Urachal Diverticula In the mammalian embryo, the urinary bladder is attached to the umbilicus. As the bladder descends into the pelvic canal, the attached apical portion progressively narrows, forming the urachus. At birth, the urachal lumen is nonfunctinal. Factors responsible for urachal closure remain unclear. Muscle tissue within the walls of the urachus, as well as stretching of this structure caused by caudal migration of the bladder, may be involved. In humans, patency of the urachus has commonly been attributed to distal outflow obstruction. 72 The implication is that abnormal increases in intraurocystic pressures during urachal development delay or prevent complete closure of its lumen. Interestingly, obstruction to urine outflow was not detected in a 4-month-old domestic shorthaired cat with a patent urachus. 41 Vesicourachal diverticula result from incomplete obliteration of the urachal lumen. During micturition, urine may become trapped within the diverticula, promoting adherence and colonization of the urothelium with microorganisms. Depending on the type of pathogen(s) involved, affected cats may develop hematuria, dysuria, and/or struvite urothlithiasis (see Table 6). It is not clear whether diverticula are the cause and/or result of urinary tract disease (refer to article entitled "Etiopathogenesis and Biological Behavior of Feline Vesicourachal Diverticula").

UROLOGIC DISORDERS OF IMMATURE CATS

683

ANOMALIES OF THE FELINE URETHRA Overview The urethra develops from the most ventral portion of the urogenital sinus. If there is incomplete distal division of the embryonic cloaca by the urorectal septum, an abnormal connection between the rectum and urethra will occur. In addition, if there is persistence of the urogenital membrane, the urethral orifice may improperly develop. To date, primary anomalies of the urethra in cats have consisted of ectopic urethra and urethrorectal fistula (Table 7). Functional abnormalities of the urethra are common in Manx cats with sacrococcygeal hypoplasia. In this instance, anomalous development of the spinal cord disrupts neurologic pathways to the urethra and urinary bladder. Ectopic Urethra We have encountered a 2-month-old domestic short hair cat with an ectopic urethra. The cat did not have urinary incontinence, but voided urine through the anus. Intravenous urography revealed that contrast agent entering the urinary bladder ultimately accumulated in the rectum. At necropsy, the urethra was found to terminate in the ventral portion of the rectum (Fig. 8). We postulate that this anomaly was caused by an incomplete distal division of the embryonic cloaca by the urorectal septum and persistence of the urogenital membrane. Myelodysplasia Myelodysplasia (abnormal development of the spinal cord) is a genetically transmitted disease commonly encountered in Manx cats. There has been one report of this disorder in a Maltese cat. 31 The disease usually affects the caudal, lumbar, and sacral cord segments and is characterized by hydromyelia, syringomyelia, meningocele, demyelination, and neuronal necrosis (Fig. 9). 69 •79 The resulting disruption in nerve pathways results in abnormalities of bladder and urethral function. Myelodysplasia disrupts nerve pathways responsible for normal micturition, including pelvic and pudendal nerves (which originate from sacral spinal cord segments that innervate the urinary bladder and urethra). Abnormal development of the caudal spinal cord disrupts normal sacral reflexes, resulting in loss of (1) perception of bladder fullness, (2) initiation of bladder contraction, and (3) urethral sphincter control. Affected cats often develop urinary incontinence. Lack of a normal micturition reflex may result in abnormal intraluminal pressure and overdistension of the bladder (Fig. 10). Non urinary signs may also occur, including fecal incontinence, fecal retention, plantigrade stance, and hopping gait. Therapy should be directed at relieving urinary incontinence and preventing secondary infection. Provided intraluminal pressure in the urethra is not excessive, manual compression may be utilized to minimize overdistension of the urinary bladder.

0')

00

""" Table 7. ANOMALY

BREED

Anomalies of the Feline Urethra and Associated Abnormalities AGE

ASSOCIATED

CLINICAL

SEX

(MO)

ABNORMALITIES

SIGNS

REFERENCE

This report

Ectopic urethra (into rectum)

DSH

M

2

Atresia coli

Urinating through anus

Myelodysplasia (altering urethral function)

Manx

M

K

Hydromyelia; syringomyelia

Fecal and urinary incontinence; no sensation to anal, preputial, and penile skin; plantigrade stance; hopping gait; no tail

65

Manx

M

K

Hydromyelia; syringomyelia

65

Manx

M

8

Urachal diverticulum; sacral spinal cord demyelination; motor neuron necrosis; myelocele

Fecal and. urinary incontinence; no sensation to anal, preputial, and penile skin; plantigrade stance; hopping gait; no tail Urinary incontinence; dysuria

Manx

NR

8

Rudimentary sacrum

Fecal and urinary incontinence; no tail

49

· Manx

NR

6

Sacrococcygeal agenesis

Fecal and urinary incontinence; hopping gait; no tail

49

Manx

NR

NR

Normal sacrum; imperfecta coccygeal vertebral

Fecal and urinary incontinence

49

F

2

Sacrococcygeal agenesis; incomplete fusion of dorsal laminae L6-7

Fecal and urinary incontinence; plantigrade stance; no tail

31

Maltese Urethrorectal fistula DSH

=

Tnis report

NR

domestic shorthair; F

=

F(N)

120

female; K

=

male; N

neutered; NR

0 t:l

Dysuria; pollakiuria; hematuria

Thickened urocyst wall

kitten; M

=

._

not reported.

108

-< ~

t"'

c:

c (")

::I: 1'1 ...,)

>

r

UROLOGIC DISORDERS OF IMMATURE CATS

685

Figure 8. Photograph of an ectopic urethra entering the rectum of an 8-week-old male domestic shorthaired cat.

Figure 9. Photomicrograph of a section of sacral spinal cord obtained from an 8-monthold male Manx cat with urinary incontinence. Note the severe dilation of the central canal. Hematoxylin and eosin stain; 5x = original magnification.

686

JODY

P.

LULICH ET AL.

Figure 10. Lateral view of a retrograde positive contrast urethrocystogram of the cat described in Figure 9. Note the narrowed prostatic urethra, dilated preprostatic urethra and urinary bladder, and vesicourachal diverticula.

Urethrorectal Fistula In man, urethrorectal fistulas may result from failure of the urorectal septum to completely separate the cloaca into the ventral urogenital sinus and dorsal rectum. 72 In addition, urethrorectal fistulas may develop secondary to traumatic, inflammatory, and/or neoplastic disorders. Urethrorectal fistulas predispose to abnormal micturition and recurrent urinary tract infection.108 Diagnosis is confirmed by retrograde contrast urethrocystography or retrograde rectocolonography. Treatment is limited to surgical resection of the fistula, or transection of the urethra and extrapelvic urethral anastomosis.84

ACQUIRED RENAL DYSFUNCTION IN IMMATURE CATS Observations Acquired renal disease has been reported less frequently in immature cats than in adults (Table 8). Although renal failure has been identified in cats as young as 5 months of age, reported mean ages of cats in two retrospective clinical studies offeline renal failure ranged from 7.42 to 10.2 years at the time of initial diagnosis. 1·6 •20 .Coronavirus-induced feline infectious peritonitis has been suggested as one etiologic agent of renal disease in young cats. 3.42.59.77 Speculations

If, in fact, young cats have a lower incidence of acquired renal failure than adults, what plausible factors could account for this difference? One

c::

"'00

t"'

G"l

Table 8.

SEX

PROBABLE ETIOLOGY

1

Unknown

Membranoproliferative glomerulopathy; interstitial nephritis

This report

11 10 6

Unknown

Renal failure; nephrotic syndrome

Inorganic mercury

Renal failure; nephrotic syndrome

Unknown

Chronic inflammation; cell infiltration of kidney cortex

73 101 This report

Unknown

Renal papillary necrosis

This report

Unknown Escherichia coli

Acute tubular necrosis; renal failure

6 This report

Feline infectious peritonitis

Multifocal pyogranulomatous inflammation of multiple organ systems

This report

Multiple organ involvement

77 3 This report

BREED

Glomerular

DSH

F

DSH

F M(N)

NR

Vascular

Unknown DSH

=

S?

AGE (MO)

LOCATION

Tubulointerstitial

n

Summary of Acquired Renal Disease Identified in Cats Less than 1 Year of Age

DSH

F

DSH

M

DSH DSH

M F(N)

Prsn

M

3 5 9 4

C/l

COMMENTS

REFERENCE

F M

1 9

Feline infectious peritonitis

NR DSH

M

7

Associated with hypertrophic cardiomyopathy

Acute renal tubular necrosis

NR

NR

3

Migrating Toxocara larvae

Glomerular ischemia resulting from thromboembolism

DSH

F

9

Unknown

Oliguric renal failure

This report

DSH

M

4

Trauma

Renal hemorrhage

This report

domestic shorthair;. F

=

female; K

=

kitten; M

=

male; N

=

neutered; NR

not reported; Prsn

=

"' 1:'1

"'0

C/l

Himalayan

Feline infectious peritonitis

0 0

"l

f5: f5:

...,> c:

1:'1 "'()

...,>

C/l

40

Persian. O'l

00 -l

~

00

Table 9.

Age-Related Changes in Serum and Urine Values in Normal Young Cats SERUM

URINE

UREA

TOTAL

AGE (WK)

NO. OF

CREATININE

NITROGEN

PROTEIN

SPECIFIC

OSMOLALITY

CATS

(MG/DL)

(MG/DL)

(GM/DL)

GRAVITY

(MOSM/KG)

pH

(GM)

6-8 8-10 10-12 12-16 16-20

6 6 9 7 6

0.40±0.13 0.30±0.11 0.50±0.13 0.90±0.11 0.80±0.18

24.6±2.5 24.4±4.2 31.9 ±4.3 28.4±2.9 22.4±3.3

5.10±0.24 5.13±0.16 5.18±0.28 6.10±0.47 6.30±0.34

1.030±0.01 1.030±0.03 1.030±0.05 1.030±0.01 > 1.035

1111±224 1055±139 1286±332 1318±328 1631±268

6.51±0.14 6.44±0.12 6.64±0.11 6.63±0.11 6.62±0.32

616±94 803± 122 839± 165 1199±286 2386±229

BODY WEIGHT

Values represent mean ± 1 standard deviation.

-0 0

-<

~

!:""

c:

c (")

::c

~

>

r

UROLOGIC DISORDERS OF IMMATURE CATS

689

possibility is that the regenerative potential of developing kidneys exceeds that of kidneys after maturation. Consequently, a single insult to the kidney may be followed by complete regeneration of nephrons. In addition to the capacity of immature kidneys to heal by regeneration, they have a large functional reserve. The combination of these two phenomena may allow mild renal disease to remain undetected. Inherent age-related protective mechanisms may also render the kidneys less susceptible to disease. The kidneys of human infants (and possibly of kittens) are initially unable to concentrate urine maximally (Table 9).39 Therefore, it is possible that ingested nephrotoxic substances may be inhibited from attaining maximal concentrations within proximal segments of the nephron. Consideration of normal serum creatinine concentration is also pertinent to this discussion. In one pilot study of kittens ranging in age from 6 to 12 weeks, the serum creatinine concentration was approximately half that normally seen in adults (see Table 9). These data should be considered when interpreting serum creatinine concentrations in the evaluation of young cats suspected of mild decreases in glomerular filtration rate. Certain forms of renal disease may be influenced by age-related phenomena. For example, enzymes involved in carbohydrate metabolism were found to be elevated in aging feline kidneys as compared with immature feline kidneys. 58 In addition, renal lipids accumulate in greater quantities in the kidneys of adult cats than in immature cats. 33 •102 Further study is necessary to evaluate the relationship (if any) between these observations and the cause and effects of renal failure.

ADDENDUM 1. Problem-Specific Database for Feline Perinatal Death History Maternal history-Health status?_ _ , Vaccination status?_ _ , Nutritional status?_ _ , Previous disorders?_ _ . Reproductive history-Previous reproductive disorders (especially gestational)?_ _ , Parturition difficulties?_ _ , Maternal behavior?_ _ . Litter history-Size?_ _ , Health status (respiration?_ _ ; feces?_, urine?_ _ , alertness?_ _ , activity?_ _ , growth rate?_ _ , other?_ _). Patient-Health status (respiration?_ _ , feces? _ _ , · urine?_ _ , alertness?_ _ , activity?_ _ , growth rate?_ _ , etc.?_ _), Time of death?_ _ , Number born within litter?_ _ . Physical Examination Crown-rump length?_ _ . Weight?_ _ .

690

JODY

P

LULICH ET AL.

Physical examination (especially mouth, anus, feces, limbs, digits, tail, umbilicus, and placenta). Laboratory Evaluation Whole body survey radiology (if bladder contains urine, establish patency of lower urinary tract by manual compression of urinary bladder). Complete necropsy, including placenta. Further Diagnostic Considerations Bacterial, fungal, and!or viral cultures of selected tissues and body cavities.

2. Problem-Specific Database for an Abdominal Mass in Immature Cats History Checklist Age?_ _ , Breed?_ _ , Sex?_ _ . Duration and!or changes in degree of abdominal distension if present? Changes in micturition? Changes in defecation? Physical Examination Temperature?_ _ , Pulse?_ _ , Respiratory rate?_ _ , Nonlocalizing abdominal pain?_ _ . Peritoneal fluid? _ _ (if yes, consider palpation after removal). Abdominal mass(es)-Position(s)?_ _ , Size(s)?_ _ , Shape(s)?_ _ , Consistency?_ _ , Contour(s)?_ _ , Attachment(s)_ _ , Pain?__ . Palpable liver abnormalities?_ _ . Abnormalities of the spleen?_ _ . Kidney-Position?_ _ , Number?_ _ , Size?_ _ , Shape?_ _ , Consistency?_ _ , Pain?_ _ . Abnormalities of the intestinal tract?_ _ . Abnormalities of the genital tract?_ _ . Urinary bladder-Position?_ _ , Size?_ _ , Shape?_ _ , Consistency?_ _ , Pain?_ _ . Laboratory Evaluation Survey abdominal radiography Abdominal ultrasonography Further Diagnostic Considerations Biopsy (aspiration, punch, or surgical) Localizing contrast radiographic or ultrasonographic procedures Exploratory celiotomy

691

UROLOGIC DISORDERS OF IMMATURE CATS

3. Problem-Specific Database for Urinary Incontinence in Immature Cats History Age_ _ , Sex__, Breed (especially Manx)?_ _ . Owrier's definition of incontinence? Characterize incontinence-Time of onset?_ _ , Duration?_ _ , Severity?_ _ . Urine Color?_ _ , Odor?_ _ , Volume?_ _ . Characterize micturition-Present?_ _ , Frequency?_ _ , Urine color?_ _ . , Odor?_ _ , Volume?_ _ . Previous or present urologic disorders?_ _ , Reproductive disorders?_ _ , Neurologic disorders?_ _ . Physical Examination Kidney-Position?_ _ , Number?_ _ , Size?_ _ , Shape?_ _ , Consistency?_ _ , Contour?_ _ , Pain?_ _ . Urinary bladder-Position?_ _ , Size (before and after micturition)?_ _ , Shape?_ _ , Consistency?_ _ , Wall thickness?_, Intraluminal masses? (consistency?_ _ , attached?_ _ , grating sensation?_ _), Ease with which urine is expressed via manual compression?_ _ , Pain?_ _. . Urethra (if possible)-Position?_ _ , Size?_ _ , Shape?_ _ , Consistency?_.__ , Intraluminal masses? (consistency?_ _ , attached?_ _ , grating sensation?_ _), Pain?_ _ . Penis/Prepuce/Vulva-Size?_ _ , Shape?_ _ , Consistency?_ _ , Pain?_ _ . Observe micturition. Verify incontinence. Locate origin of incontinence (urogenital tract, anus, umbilicus?). Neurologic exam (gait?, stance?, perineal reflex?). Laboratory Evaluation Urine (compare voluntary voided sample with that collected by cystocentesis). l. Complete urinalysis 2. Quantitative urine culture Renal function profile (serum urea nitrogen and creatinine minim~.

Further Diagnostic Considerations Survey abdominal radiography Contrast radiography l. Antegrade cystourethrography 2. Retrograde urethrocystography 3. Retrograde vaginography 4. Intravenous urography

.

692

}ODY

P

LULICH ET AL.

4. Problem-Specific Database for Hematuria and/or Dysuria in Immature Cats History Age_ _ , Sex.___, Breed_. Is hematuria associated with dysuria?_ _ . Time of onset and duration of hematuria?_ _ . Is hematuria/dysuria constant?_ _ , Intermittent?_ _ . Changes in micturition frequency? _ _ , Velocity_ _ , Stream size?_ _ , Location?_ _ . Urine color?_ _ , Odor?_ _ , Volume?_ _ . Is hematuria independent of__, at beginning__, end_ or throughout_ micturition? Treatment?_ _. , Type?_ _ , Dose?_ _ , Response?_ _ . Physical Examination Kidney-Position?_ _ , Number?_ _ , Size?_ _ , Shape?_ _ , Consistency?_ _ , Contour?_ _ , Pain?_ _ . Urinary bladder-Position?_ _ , Size?_ _ , Shape?_ _ , Consistency?_ _ , Wall thickness?_ _ , Intraluminal masses? (consistency?_ _ , attached?_ _ , grating sensation?_ _ ), Pain?_ _ . Urethra (if possible)-Position?_ _ , Size?_ _ , Shape?_ _ , Consistency?_ _ , Intraluminal masses? (consistency?_ _ , . __), Pain?_ _ . attached?_ _ , grating sensation?_ Penis/PrepuceNulva-Size?_ _ , Shape?_ _ , Consistency?_ _ , Pain?___ . Locate additional sites of hemorrhage and/or petechiation?_ _ . Observe micturition (normal?_ _ , abnormal?_ _). Laboratory Evaluation Complete blood count Complete urinalysis (midstream sample*) Quantitative bacterial culture of urine (cystocentesis) Activating clotting time Serum chemistry profile (serum urea nitrogen and creatinine mum) Survey abdominal radiography Further Diagnostic Considerations

mini-

Contrast radiography (one or more of the following) 1. Intravenous urography 2. Retrograde urethrocystography (positive, double contrast) 3. Ultrasonography *Cystocentesis is a valuable alternative provided the technique does not lead to substantial microscopic hematuria. Comparison of results of midstream urinalysis and cystocentesis urinalysis may aid in localization of urethral or genital lesions. ACKNOWLEDGMENTS

The authors gratefully acknowledge the editorial assistance of Lori Schultz.

UROLOGIC DISORDERS OF IMMATURE CATS

693

REFERENCES l. Abdullahi S, Osborne CA, Polzin DJ, et al: Some clinical manifestations of naturally

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