Renal agenesis or dysplasia has been reported in dogs, cats, and people.1-3 Although unilateral agenesis as occurred in this case is rarely noted, it can cause compensatory hypertrophy in the existing
kidney; bilateral agenesis is fatal. Invariably, renal agenesis leads to genital tract malformation.
During embryonic development, the kidneys, urinary tract, and most of the reproductive organs arise in the intermediate mesoderm
between the somites and the lateral plate. Three stages of renal development recapitulate evolution of the kidney: pronephros,
mesonephros, and metanephros. Urogenital system development in mammals requires the coordinated differentiation of two distinct
tissues—the ductal epithelium and the nephrogenic mesenchyme—both derived from the intermediate mesoderm of the early embryo.
The former gives rise to the genital tracts, ureters, and kidney collecting duct system, whereas mesenchymal components undergo
epithelial transformation to form nephrons in both the mesonephric (embryonic) and metanephric (definitive) kidney.4
Pax-2 is a transcriptional regulator gene of the paired-box family and is widely expressed during the development of both
ductal and mesenchymal components of the urogenital system. If the Pax-2 gene is dysfunctional, the ureters, inducers of the
metanephros, are absent, so kidney development does not occur.4 Mesenchyme of the nephrogenic cord fails to undergo epithelial transformation and is unable to form tubules in the mesonephros.4
In people, unilateral renal agenesis may have a noncystic fibrosis-mediated genetic basis that leads to abnormal development
of the entire mesonephric duct at around seven weeks of embryonic development. Unilateral renal agenesis is compatible with
normal life if the other kidney is normal; however, if contralateral dysplasia or hypoplasia is present, renal failure ultimately
The etiopathogenesis of renal agenesis in small animals is uncertain. A familial genetic predisposition for the condition
has been reported in Shetland sheepdogs and Doberman pinschers.2 Because of close associations in the development of the urogenital system, findings of abnormal or absent vas deferens,
epididymal tails, or uterine horns at the time of castration or ovariohysterectomy should arouse suspicion of concurrent unilateral
renal agenesis. Because unilateral renal agenesis is compatible with normal life, specific therapy is not indicated unless
reduced renal function ensues.
To our knowledge, only a few reports of aplasia of a uterine horn and ipsilateral renal agenesis occur in the literature.6,7 One cat with renal agenesis and segmental aplasia of the right uterine horn had initially been presented for evaluation
of acute vomiting, depression, and constant shivering.7 The authors of the report did not observe any functional or anatomical defects in the existing left kidney except enlargement.
High-volume spay and neuter facilities may encounter reproductive organ development anomalies more frequently than traditional
veterinary practices. Monitoring kidney and urinary tract function after adoption is necessary to ensure a good quality of
life in organ- (kidney-) deficient animals. Breeding such animals is discouraged as the offspring may be predisposed to genetic
disorders. The baseline information collected is of benefit for future therapeutic considerations. An incidental finding of
renal aplasia also suggests that a thorough exploration of the abdominal cavity be done to avoid leaving functional ovaries,
which postoperatively may result in the animal developing estrous cycles, ectopic pregnancy, or pyometra.
We are grateful to John E. Ledoux, VMD, in Atkinson, N.H., for performing and interpreting the abdominal ultrasonographic
examination. We are also grateful for the assistance of technicians Shelby Page, Melanie Norman, Nicole Willis, and Lori Wyatt
at Main Street Animal Hospital in Bradford, Mass. The help of Sarah Ingram, DVM, in preparing the manuscript is highly appreciated.
We thank Barbara Cusick, president of the Animal Rescue Merrimack Valley in Bradford, Mass., for providing foster care to
Gracie, the cat featured in this case.
Tumkur Narasimhan, DVM, MS, PhD
Yassine Absar, DVM
Main Street Animal Hospital
839 South Main St.
Bradford, MA 01835
1. McCallum TJ, Milunsky JM, Munarizz R, et al. Unilateral renal agenesis associated with congenital bilateral vas deferens:
phenotypic findings and genetic consideration. Hum Reprod 2001;16(2):282-288.
2. Hoskins JD. The urinary system. In: Veterinary pediatrics: dogs and cats from birth to six months. 3rd ed. Philadelphia, Pa.: WB Saunders Co, 2001; 371-395.
3. Morita T, Michimae Y, Sawada M, et al. Renal dysplasia with unilateral renal agenesis in a dog. J Comp Pathol 2005;133(1):64-67.
4. Torres M, Gomez-Pardo E, Dressler GR, et al. Pax-2 controls multiple steps of urogenital development. Development 1995;12 (12); 4057-4065.
5. Maxie MG. The urinary system. In: Jubb KVF, Kennedy PC, Palmer N, eds. Pathology of domestic animals. 4th ed. San Diego, Calif.: Academic Press, 1993;447-538.
6. Aiello SE. Urinary system. In: The Merck veterinary manual. 8th ed. Whitehouse Station, N.J.: Merck and Co Inc, 1998; 1130-1157.
7. Chang J, Jung JH, Yoon J. et al. Segmental aplasia of the uterine horn with ipsilateral renal agenesis in a cat. J Vet Med Sci 2008;70(6):641-643.