- Developmental Physiology
- Congenital and Hereditary Disorders of the Kidney
- Congenital and Hereditary Anomalies of the Ureters
- Congenital And Hereditary Anomalies Of The Urinary Bladder
- Agenesis and Hypoplasia
- Anomalies of the Urachus
- Colourocystic Fistula
- Ectopic Uterine Horns Entering the Urinary Bladder
- Primary Neoplasia
- Congenital And Hereditary Anomalies Of The Urethra
- Aplasia and Hypoplasia
- Urethrorectal Fistula
- Urethrogenital Malformations
- Acquired Disorders of the Urinary Tract
Urinary tract disorders of puppies and kittens may result from heritable (genetic) or acquired disease processes affecting differentiation and growth of the developing urinary tract or from similar processes that eventually affect the structure or function of the mature urinary system. Successful management of urinary tract disorders depends on familiarity with the structure and functions of the kidneys, ureters, urinary bladder, and urethra.
Although the embryonic kidneys produce urine, maintenance of fetal homeostasis is primarily the responsibility of the placenta. Varying quantities of urine formed by the fetal kidneys pass from the developing urinary bladder through the urachus to the placenta, where unwanted waste products are absorbed by the maternal circulation and subsequently excreted in the mother’s urine (). Fetal urine also passes through the urethra into the amniotic cavity, where urine forms a major constituent of amniotic fluid. The latter part of gestation is characterized by rapid increases in nephron number and size and by maturation of glomerular and renal tubular functions (). Prenatal development of glomerular filtration and renal blood flow appears to parallel increases in fetal kidney size. Parturition is accompanied by dramatic increases in glomerular filtration rate (GFR) mediated largely by hemodynamic changes (increased cardiac output, increased systemic arterial blood pressure, and decreased renal vascular resistance) and by changes in intrinsic morphologic and functional characteristics of glomeruli (increased glomerular permeability and increased filtration surface area) (). Inulin clearance studies in puppies have demonstrated that glomerular filtration rate increases sevenfold over the first month of life (). Similarly, renal blood flow (RBF) increases nearly fourfold during the same time period (). Both glomerular filtration rate and renal blood flow continue to increase after 4 weeks of age, reaching adult values approximately 10 weeks after birth (). Similarly, endogenous creatinine clearance studies suggest that glomerular filtration rate in kittens increases rapidly after birth, reaching adult values by 9 weeks of age ().
The rate of maturation of intrinsic renal mechanisms regulating GFR, RBF, and distal delivery of water and solutes appears to vary in puppies (). Limited studies suggest that puppies are able to adequately increase proximal tubular resorption of at least water, sodium, and glucose in response to elevations in glomerular filtration rate (glomerulotubular balance) (). Autoregulation of renal blood flow and glomerular filtration rate in neonatal puppies appears to be relatively inefficient in response to rapid changes in systemic arterial blood pressures (). Maturity of renal tubular functions varies considerably with age. Newborn puppies have a limited ability to concentrate or dilute urine in response to changes in extracellular fluid volume (). The urine/ plasma osmolality ratio (U/P Osm) in puppies rose from 2.0 at 2 weeks of age to 7.0 at 11 weeks of age; normal U/P Osm values for adult dogs range from 3.3 to 8.4 (). The U/P Osm values in kittens rose from 4.6 at 4 to 6 weeks of age to 8.9 at 13 to 19 weeks of age (). Sodium balance appears to be relatively stable in newborn puppies. Whole kidney fractional resorption of sodium was constant in 2-to 77-day-old puppies and similar to values in mature dogs (less than 0.7%) (). Puppies younger than 3 weeks of age appear to have an impaired ability to excrete excess sodium compared with adult dogs. Puppies were able to excrete only 10% of an isotonic saline load within 2 hours of administration, whereas adult dogs were able to excrete up to 500% ().
Significant differences in acid-base balance exist between puppies/kittens and adults. In vitro studies of kidney slices revealed that neonatal puppies, but not kittens, have an impaired ability to increase renal ammoniagenesis in response to an acid environment compared with adults (). Puppies challenged with ammonium chloride or sulfate developed more severe acidosis and were less able to increase renal ammoniagenesis, secrete protons, and acidify urine compared with adult dogs (). Renal tubular resorption of amino acids is incomplete in 5-day-old puppies (). By 3 weeks of age, most amino acids are resorbed in puppies, and by 7 weeks of age adult patterns of amino acid resorption are evident. Incomplete tubular resorption of glucose is commonly observed in puppies. Glucosuria was detected in 50% of urinalyses obtained from 5-day-old puppies; glucosuria was not detected in puppies 21 days of age or older (). Although renal transport mechanisms for glucose appear to be relatively mature in puppies, transient glucosuria may be related to a greater proportion of immature nephrons and increased splay in puppies younger than 14 days of age ().
The immaturity of glomerular and renal tubular function has significant clinical implications with regard to therapeutic management of puppies and kittens. Puppies and kittens are predisposed to rapid dehydration as a result of their higher water requirements and their decreased ability to maximally concentrate urine and resist osmotic diuresis (). Conversely, they are inherently more susceptible to fluid volume and solute overload (). Although this paradox poses unique therapeutic challenges, use of conservative rates of fluid administration and careful monitoring during the course of fluid therapy may prove beneficial in managing immature animals. Puppies and kittens may be more susceptible to drug toxicity because of their limited capacity to eliminate those drugs and drug metabolites dependent on renal excretory mechanisms ().
Congenital And Hereditary Anomalies Of The Urinary Bladder
Agenesis and Hypoplasia
Complete agenesis of the urinary bladder is extremely rare and has been reported in a 4-month-old mixed-breed female dog with a lifelong history of urinary incontinence (). Hypoplasia of the urinary bladder has been typically associated with bilateral and, occasionally, unilateral ectopic ureters (). Small urinary bladder capacity may contribute to postoperative urinary incontinence occasionally observed after surgical correction of ectopic ureters. Bladder capacity may, however, increase substantially over a period of several months after correction of ureteral ec-topia.
The term exstrophy encompasses a number of congenital anomalies characterized by ventral midline defects in the ventral abdominal wall, urinary bladder, intestines, and external genitalia. Life-long urinary incontinence, ascending urinary tract infection, and pyelonephritis are the predominant clinical features of exstrophy of the urinary bladder and ventral abdominal wall (). Correction of exstrophy requires reconstructive surgery, and success depends on the severity of the defect and the presence of other urinary tract abnormalities.
Anomalies of the Urachus
The urachus is a fetal conduit that allows urine to pass from the developing urinary bladder to the placenta (). The urachus usually undergoes complete atrophy and is nonfunctional at birth. If the urachus fails to undergo complete atrophy, macroscopic or microscopic remnants may remain and result in persistent urachal patency or in formation of urachal cysts or diverticula (). A persistent (or patent) urachus exists when the entire urachal canal remains functionally patent between the bladder and the umbilicus (). A persistent urachus is associated with inappropriate loss of urine through the umbilicus and is often accompanied by omphalitis, ventral dermatitis, and a urinary tract infection. Rarely, a persistent urachus may terminate in the abdomen cavity, resulting in uroabdomen. Urachal cysts may develop if secreting urachal epithelium persists in isolated segments of a persistent urachus (). Vesicourachal diverticula occur when that portion of urachus located at the bladder vertex fails to close (). Microscopic urachal remnants persisting in the urinary bladder vertex after birth are usually clinically silent; however, macroscopic diverticula may develop at the bladder vertex of cats (and possibly dogs) with microscopic urachal remnants following the onset of concurrent but unrelated acquired diseases of the lower urinary tract (i.e., bacterial cystitis, urolithiasis, crystalline-matrix urethral plugs, and idiopathic disease) (). Vesicourachal diverticula are best identified by positive-contrast or double-contrast cystography or by excretory urography. Survey abdominal radiographs and pneumocystography are inconsistent in identifying diverticula. Surgical management may be indicated for any of the urachal anomalies. Many macroscopic diverticula of cats (and possibly dogs) are, however, self-limiting after amelioration of clinical signs of lower urinary tract disease.
Complete or partial duplication of the urinary bladder, with or without concomitant duplication of the urethra, is a rare congenital disorder of dogs (). Similar anomalies have not been reported in cats. Clinical signs usually develop early in life and include dysuria, urinary incontinence, and abdominal distention. Anomalies involving duplication of the urinary bladder are amenable to surgical correction; however, prognosis is guarded and depends on the degree of malformation and the presence of other concurrent anomalies.
Communication between the urinary bladder and colon is a rare congenital defect that has been observed in a 5-week-old male domestic short-haired cat (). Colourocystic fistulas potentially predispose animals to urinary tract infections and urinary incontinence. Surgery design to obliterate the fistula without compromising the urinary bladder and colonic function would be of potential benefit.
Ectopic Uterine Horns Entering the Urinary Bladder
A 9-month-old female domestic short-haired cat with both uterine horns terminating into the urinary bladder has been reported (). Clinical signs relating to this anomaly included dysuria, hematuria, and urinary incontinence.
Neoplasms of the urinary bladder are uncommon in puppies and kittens (). Botryoid rhabdomyosarcomas are, however, commonly seen in young large-breed dogs younger than 18 months of age (). Botryoid rhabdomyosarcomas are embryonic mesenchymal tumors believed to arise from pluripotent stem cells originating from primitive urogenital ridge remnants (). These neoplasms are infiltrating tumors that arise from the trigone and project into the bladder lumen as botryoid (resembling a cluster of grapes) masses. Primary clinical signs of botryoid rhabdomyosarcomas include hematuria, dysuria, and stranguria and may be accompanied by secondary signs associated with urethral obstruction and/or hypertrophic osteoarthropathy. In dogs, botryoid rhabdomyosarcomas are locally invasive; however, distant metastases appear to be uncommon. Surgical resection alone has been reported to result in only short-term remissions of 3 months or younger (). We observed long-term (greater than 5-year) remission in an 8-month-old male golden retriever, however, after radical surgical excision and ureteral transplantation. A partial response to combination chemotherapy utilizing doxorubicin, cyclophosphamide, and vincristine sulfate was observed in a female Doberman with local recurrence and distant metastases after surgical excision ().
Congenital And Hereditary Anomalies Of The Urethra
Aplasia and Hypoplasia
Urethral aplasia is a rare congenital anomaly characterized by complete absence of a patent urethra. Urethral aplasia and urinary bladder aplasia have been reported in a 4-month-old female mixed-breed dog with a life-long history of urinary incontinence (). In this case, both ureters were ectopic and terminated on the floor of the vagina. Urethral hypoplasia resulting in urinary incontinence has been described in immature female domestic short-haired cats (). Early in life, cats with urethral hypoplasia typically develop severe urinary incontinence, which is most pronounced when the animal is recumbent or sleeping. Diagnosis is based on clinical signs and retrograde contrast vaginourethrography. Radiographic features include marked urethral shortening and vaginal aplasia. Urethral hypoplasia may be accompanied by other urogenital anomalies and is frequently complicated by urinary tract infection. Urinary incontinence may be resolved by surgical reconstruction of the bladder neck.
Most urethrorectal fistulas in puppies and kittens appear to be congenital (). Male puppies appear to be affected more frequently than female puppies, and there is an apparent breed predilection for English bulldogs. Breed or sex predispositions have not been reported in kittens. Abnormal urination patterns, usually observed early in life, are characterized by simultaneous passage of urine from the anus and the penis (male) or vulva (female) during micturition. Diagnosis is based on clinical signs and identification of a urethrorectal fistula by antegrade or retrograde contrast urethrography or retrograde colonography. Clinical signs are usually controlled by fistulectomy and eradication of secondary urinary tract infections.
Urinary incontinence is a common clinical manifestation of urethrogenital malformations in puppies and kittens associated with diseases of intersexuality, especially pseudohermaphroditism (). Urinary incontinence most likely is due to retention of urine in anomalous communications between the urethra and the genital tract and subsequent passive leakage of urine to the exterior. Diagnosis is based on history, physical examination, and contrast radiography (retrograde contrast urethrography and excretory urography). Urinary incontinence and pseudohermaphroditism may be reversible after surgical correction of urethrovaginal malformations.
Hypospadias is an uncommon anomaly affecting predominantly male puppies and is characterized by ventral malposition of the urethral meatus (). Etiologic factors in puppies with hypospadias are unknown; however, the high prevalence of hypospadias in Boston terriers may suggest a genetic basis in some cases. Affected dogs are of variable age and may be asymptomatic or develop clinical signs of urinary incontinence, periurethral dermatitis, or recurrent urinary tract infection. Diagnosis is based on physical examination. The presence of an os penis in male dogs precludes surgical reconstruction in most cases; however, scrotal or perineal urethrostomy, combined with castration and removal of vestigial preputial and penile tissues, may be of cosmetic value.
Duplication of the urethra is an uncommon congenital anomaly that has been encountered in puppies, but not kittens (). Complete urethral duplication occurs in both males and females and may be associated with concurrent duplication of descending colon, rectum, urinary bladder, vagina, and vulva in females and penis in males and with other urogenital anomalies (unilateral renal hypoplasia, bilateral cryptorchidism). Diagnosis is based on physical examination, contrast radiography, and exploratory celiotomy. Anomalies of urethral duplication may, in some cases, be amenable to surgical excerptation of the duplicated structure. Surgical reconstruction has rarely, however, been attempted in cases involving extensive duplication.
Urethral ectopia is a rare congenital anomaly characterized by abnormal position of the external urethral orifice. Clinical signs depend on the site of termination of the abnormal urethra and other urogenital anomalies. Life-long urinary incontinence was the predominant clinical feature in a 21-month-old female English bulldog with an ectopic urethra terminating in the cranial vagina and concurrent unilateral ectopia (). In contrast, a 2-month-old female domestic short-haired cat with an ectopic urethra terminating in the ventral rectum did not have urinary incontinence but did void urine through the anus ().
Prolapse of the mucosal lining of the distal portion of the urethra through the external urethral orifice occurs primarily in young male dogs 4 months to 5 years of age (). There is an apparent predilection for brachycephalic breeds, especially English bulldogs and Boston terriers. Diagnosis of urethral prolapse is based on characteristic historical and physical examination findings. The condition is usually recognized because of bleeding from the prolapsed urethra independent of micturition and intermittent or persistent licking of the penis. Treatment of urethral prolapse has traditionally involved surgery (). Clinical observations, however, suggest that, in some cases, urethral prolapse may be associated with only minor clinical signs or may be asymptomatic.
Selections from the book: “Veterinary pediatrics: dogs and cats from birth to six months”. Johnny D. Hoskins. (2001)