Congenital Kidney Malformation in Horses Tracked Across Three Decades of Cases

A congenital kidney malformation once considered a rare curiosity in equine medicine has now been systematically characterized in the largest case series of its kind, drawing on three decades of veterinary hospital records. Renal dysplasia, a disorder in which the kidneys fail to develop normally before birth, was documented in 25 horses examined at a major veterinary teaching hospital between 1991 and 2021. The findings, published in the Journal of Veterinary Internal Medicine, reveal that the condition spans an astonishing age range, from newborn foals to horses in their mid-twenties, and that two breeds in particular appear far more likely to be affected than others.

Renal dysplasia arises when the embryonic interaction between the ureteric bud and the metanephric mesenchyme goes awry. These two primitive structures must communicate precisely for nephrons, the functional filtering units of the kidney, to form. When that dialogue fails, the resulting kidney tissue is disorganized and dysfunctional, a pattern seen across mammals including humans, dogs, cats, cattle, and sheep. In human neonates, renal dysplasia is the leading cause of end-stage renal disease, and its causes are understood to involve a complex interplay of genetic, epigenetic, and environmental factors. In dogs, a familial component has been recognized, although the inheritance pattern is variable and not fully resolved. Until now, the condition had been reported in only about 14 individual horses scattered across the case-report literature, leaving veterinarians with little systematic evidence to guide diagnosis or prognosis.

The research team, working from the medical record system at the William R. Pritchard Veterinary Medical Teaching Hospital at the University of California, Davis, searched three decades of records using terms including renal dysplasia, kidney dysplasia, renal hypoplasia, and kidney hypoplasia. Only cases with histopathologic confirmation of dysplasia were included, a criterion that excluded 27 additional horses whose diagnoses could not be definitively verified under the microscope. The final cohort of 25 horses included 15 males and 10 females, with ages ranging from a single day to 24 years. Nearly half were newborn or neonatal foals aged eight days or younger, 28 percent were young horses between three and 24 months, and the remaining quarter were adults between five and 24 years old.

Perhaps the most striking result to emerge from the breed analysis is the overrepresentation of Paint horses and Miniature horses. When the researchers compared the breed distribution of affected horses against the entire equine population presented to the hospital during the same period, Paint horses showed an odds ratio of 21.3 and Miniature horses an odds ratio of 12.9, both with confidence intervals that excluded unity and P values below .0001. In practical terms, a Paint horse or a Miniature horse in this hospital population was dramatically more likely to be diagnosed with renal dysplasia than a horse of any other breed. The researchers suggest this pattern might reflect a genetic basis for the disease in these breeds, analogous to the familial clustering documented in humans and dogs, and they call for larger studies to investigate a possible heritable component in horses.

Clinically, the picture varied enormously depending on the age of the animal and the extent of the malformation. Among neonatal foals, signs were common and often severe: 64 percent had azotemia, an accumulation of nitrogenous waste products in the blood, and 37 percent had hyponatremia, a dangerously low serum sodium concentration. Neurologic signs appeared in 58 percent of neonates, including lethargy, obtundation, head pressing, facial twitching consistent with focal seizures, ataxia, and in two foals a striking inability to close the jaw, a sign previously associated with low sodium in a calf. By contrast, only 4 of 7 young horses and just 1 of 6 adult horses showed clinical or laboratory evidence of renal disease before death. Eleven of the 25 cases, or 44 percent, were discovered incidentally at necropsy, meaning the dysplasia had caused no recognizable kidney problems during life.

Laboratory findings reinforced the heterogeneity of the syndrome. Hyperkalemia was present in 41 percent of cases, hypochloremia in 55 percent, and elevated creatinine in 64 percent. The anion gap was increased in 82 percent of neonates and 73 percent of older horses, reflecting the metabolic derangements that accompany failing kidneys. Notably, in foals with hyponatremia, serum sodium concentrations fell back to pre-treatment values whenever intravenous fluids were tapered or discontinued, a pattern the authors interpret as evidence of genuinely dysfunctional renal tissue rather than a transient electrolyte disturbance. Urinalysis, available in 10 cases, revealed proteinuria in 70 percent and red blood cells in 30 percent, while ultrasonography, performed in 68 percent of cases, detected hydronephrosis, hyperechoic renal cortices, thickened cortex, hydroureter, and loss of the corticomedullary junction in a subset of examined animals.

Histopathology remained the gold standard for diagnosis, and the microscopic findings were consistent with those described in other species. Primitive mesenchyme, undifferentiated embryonic tissue trapped within the developing kidney, was identified in 32 percent of cases. Retention of fetal glomeruli, in which filtering structures fail to mature, and tubular dysplasia, in which the kidney’s microscopic tubing develops abnormally, were each found in 24 percent of cases. Tubular or cortical mineralization appeared in 16 percent, while asynchronous maturation, multifocal interstitial fibrosis, and persistent metanephric ducts were each documented once. The dysplasia was bilateral in 84 percent of cases and diffuse in 68 percent, though in the segmental cases it could be confined to the medulla, the cortex, or both. Critically, renal biopsy, often proposed as a minimally invasive diagnostic route, proved definitive in only one of three horses in which it was attempted; in the other two, the samples were suggestive but not conclusive, likely because the segmental nature of the dysplasia meant the biopsy needle missed the abnormal tissue.

Treatment in these cases was largely supportive and, in many instances, ultimately unsuccessful. Twelve horses received intravenous fluids, typically balanced isotonic solutions at rates averaging 8.5 milliliters per kilogram per hour in neonates and 6.5 in older horses. Diuretics were administered to five horses with oliguria, but they failed to increase urine output in any of them. Nine horses received antimicrobials, and one severely affected foal underwent five hemodialysis sessions, during which serum creatinine fell from 10 milligrams per deciliter to 1.9 before rebounding, ultimately prompting euthanasia. One colt underwent unilateral nephrectomy at four months of age because of persistent hematuria and marked hydronephrosis, and remarkably, the remaining kidney functioned adequately for months afterward, with the colt eventually being euthanized at 11 months for colic unrelated to renal disease.

Outcomes were sobering. The median hospitalization lasted 4.7 days. Twenty-two of the 25 horses, or 88 percent, were euthanized, with 56 percent of all cases put down because of nonresponsive renal disease. Three horses died naturally. Yet the series also demonstrates that renal dysplasia is not uniformly fatal: six adult horses, including three aged 20 to 24 years, lived with the condition subclinically, presenting for colic or other complaints rather than kidney failure. The researchers attribute this variability to whether the dysplasia is unilateral or bilateral, segmental or diffuse, and partial or complete, factors that determine how much functional renal tissue remains.

The study’s authors conclude that renal dysplasia should be considered a differential diagnosis in neonatal foals presenting with azotemia and electrolyte imbalances that fail to respond to treatment, and also in adult horses with acute or chronic kidney disease when obvious hemodynamic, toxic, or inflammatory causes have been ruled out. The overrepresentation of Paint and Miniature horses raises the possibility of breed-specific genetic risk, echoing patterns seen in humans and dogs, and the team explicitly recommends larger investigations to explore heritability. For a condition that has lingered at the margins of equine nephrology for decades, this 30-year case series provides the most comprehensive clinical, laboratory, and pathological portrait to date, and it may ultimately change how veterinarians approach unexplained kidney disease in horses of any age.

Subject of Research: Renal dysplasia in horses: a 30-year retrospective case series of 25 histopathologically confirmed cases

Article Title: Renal dysplasia in horses: 25 cases (1991-2021)

Article References: Morales, C. J., Aleman, M., Berryhill, E., & Magdesian, K. G. (2026). Renal dysplasia in horses: 25 cases (1991-2021). Journal of Veterinary Internal Medicine, 40(5), Article aalag165. https://doi.org/10.1093/jvimsj/aalag165

Image Credits: AI Generated

DOI: 10.1093/jvimsj/aalag165

Keywords: renal dysplasia, horses, congenital kidney disease, neonatal foals, Paint horses, Miniature horses, azotemia, hyponatremia, histopathology, nephrectomy, retrospective study, veterinary nephrology