Signalment:  
8-month-old female thoroughbred horse,
Equus caballusThe mare showed sudden renal failure and no response to treatment. Anorexia and severe uremia were continuing and the animal was euthanized.
Gross Description:  
After formalin fixation, the surfaces of the both kidneys were slightly irregular and the cortex showed whitish to tan on the cut sections. No significant gross lesion was observed in other organs.
Histopathologic Description:
Diffuse and global, partially segmental glomerular sclerosis and enlarged glomeruli with mild to moderate proliferation of mesangial cells are remarkable. Irregularly dilated tubules are predominant in renal cortex, and papillary projections of tubular epithelium into the lumens are occasional. Immature small tubules with indistinct luminal structures and dysplastic tubules with enlarged clear nuclei are frequent. Protein cast formation, deposition of oxalate crystal and hyaline droplet degeneration are rarely in tubules/tubular epithelium. Diffuse and mild fibrosis is in interstitial tissues with mild lymphoplasmacytic infiltration, sometimes along with concentric fibrosis around renal tubules and/or Bowmans capsules and deposition of eosinophilic homogenous material. Small to mid-sized arterioles are increasing in the cortex. Rarely, abnormal large muscular arteries are in subcapsular cortex (not in all slides). Pale basophilic myxoid material depositions are rare in the interstitium.Â
Morphologic Diagnosis:  
Kidney: Equine renal dysplasia
Lab Results:  
Blood test revealed high BUN 206.7 mg/dl (normal: 9.0-20.0) and CRE: 9.69 mg/dl (normal: 0.9-1.8). Serology (antibody titer) and PCR showed no evidence of
Leptospira sp. infection.
Condition:  
Renal dysplasia
Contributor Comment:  
Based on the histopathological findings, renal dysplasia was considered most likely in the present case. Abnormal proliferation of arterioles in the renal cortex also supports a developmental anomaly of the kidneys in this mare. Variously affected glomeruli with hypercellularity and sclerosing changes suggest that the primary lesions are not located in glomeruli. However, regenerative tubules with juvenile epithelial cells, interstitial fibrosis and mild to moderate mesangial proliferation suggest a differential diagnosis of tubular nephritis following renal injury, such as toxicosis or leptospire infection. The present case was negative for leptospires. Further, plant toxicosis is unlikely because no other case of toxicosis was found in the ranch.
Renal dysplasia is rare congenital disease of developmental uni- or bilateral kidney anomaly reported in various animals.(4) Renal dysplasia in dogs is well documented; however, equine renal dysplasia is also reported. The size the affected kidney shows small and irregular surface with demonstration of immature histological structures like undifferentiated stromal tissues, immature renal tubules and glomeruli. Primitive ductal structures and cartilage and/or bone formation are sometimes found.Â
The major histological findings reported in equine renal dysplasia are papillary proliferation of tubular epithelium, immature tubules and islands of interstitial fibrosis. (1,2,7) Renal artery dysplasia is also described in one adult horse with chronic renal failure(1) and also in humans. The histopathological changes in the present case are very complicated; however, some of them, including oxalate deposition, appear to be secondary changes following renal failures. The various proposed pathogeneses of renal dysplasia, like abnormal metanephrons or vascular malformation, may be putative but clear mechanisms are still unknown.Â
JPC Diagnosis:  
Kidney: Dysplasia characterized by hypercellular glomeruli, glomerulosclerosis, tubular epithelial hyperplasia, hypertrophic arterioles and arteries, and interstitial myxoid matrix.Â
Conference Comment:  
Equine renal dysplasia is rarely reported in the horse and often has a variable histopathologic presentation. Many of the well-defined, characteristic histologic features observed in dogs, including persistent metanephric ducts, primitive mesenchyme and cartilaginous or osseous tissue, are not present in this case. Yet the clinical history and glomerular changes are consistent with the diagnosis. Some reports of equine renal dysplasia describe renal cysts, fetal glomeruli, and tubules lined by cuboidal epithelium, while others have identified normal kidney size with normal appearance and number of glomeruli but with hypoplastic nephron tubules.(5,9) Conference participants were intrigued with the aberrant arterioles and large muscular arteries present throughout the renal cortex, and speculated whether these may have played a primary role in the development of other pathologic changes in this case. Interestingly, these aberrant vascular features have been reported in human cases of segmental or complete renal dysplasia.(8) Segmental hypoplasia with renal vascular anomalies (Ask-Upmark kidney) has also been described in young Boxer dogs.(3)
A related, possibly equivalent, condition to renal dysplasia is referred to as progressive juvenile nephropathy and is associated with specific dog breeds including Lhasa Apso, Shih Tzu, and the golden retriever. These conditions share several features with dysplasia though typical presentation depends on the breed. Often a glomerulopathy resembling membranoproliferative glomerulonephritis is present and may progress to glomerulosclerosis. Overall gross and microscopic features are comparable to those of chronic renal disease with renal fibrosis in aging dogs, but this condition affects dogs under 2 years of age.(6)
References:
1. Anderson WI, Picut CA, King JM et al. Renal dysplasia in a Standard Colt. Vet Pathol. 1988;25:179-180.
2. Gull T, Schmitz DG, Bahr A et al. Renal hypoplasia and dysplasia in an American miniature foal. Vet Rec. 2001;149:199-203.Â
3. Kolbj+�-+rnsen, +�-�., M. Heggelund, and J. H. Jansen. "End-stage kidney disease probably due to reflux nephropathy with segmental hypoplasia (Ask-Upmark kidney) in young Boxer dogs in Norway. A retrospective study." Veterinary Pathology Online 45.4 (2008): 467-474.
4. Maxie MG, Newmann SJ. Urinary system. In: Maxie MG, ed. Jubb, Kennedy, and Palmers Pathology of Domestic Animals. Vol. 2. 5th ed. Philadelphia, PA: Elsevier Saunders; 2007:439-442.
5. Medina-Torres CE, Hewson J, Stampfli S, Stalker MJ. Bilateral diffuse cystic renal dysplasia in a 9-day-old thoroughbred filly. Can Vet J. 2014;55(2):141-146.
6. Newman SJ. The urinary system. In: Zachary JF, McGavin MD, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Elsevier Saunders; 2012:618,655-656.
7. Rosen N, Amstel SR, Nesbit JW et al. Renal dysplasia in two adult horses: clinical and pathological aspects. Vet Rec. 1993;132:269-270.
8. Rosenfeld, J. B., et al. "Unilateral renal hypoplasia with hypertension (Ask-Upmark kidney)." BMJ 2.5860 (1973): 217-219.
9. Zicker SC, Marty GD, Carlson GP, Madigan JE, Smith JM, Goetzman BW. Bilateral renal dysplasia with nephron hypoplasia in a foal. J Am Vet Med Assoc. 1990;196(12):2001-2005.