68
Polycystic kidneys / Morales, A. y col.
FIGURE 5.- HISTOPATHOLOGY OF KIDNEY. The renal
cortices contained numerous round cysts ranging in size
from 150 mm to 2.5 mm in diameter, lined by low cuboidal to
attened epithelium (Hematoxilin & Eosin 20x)
FIGURE 6.- HISTOPATHOLOGY OF KIDNEY. The renal
cortices contained round cyst range of 2.5 mm diameter,
lined by low cuboidal to attened epithelium with sediment
and renal cysts consistent mineralization is observed with
calcium oxalate (Hematoxilin & Eosin 20x)
Polycystic Kidney Disease (PKD) is an inherited disorder in
which clusters of cysts develop primarily within of kidneys. Cysts
are round sacs containing water-like uid. The cysts vary in size
and, as they accumulate more uid, they can grow very large.
Although kidneys usually are the most severely aected organs,
PKD can cause cysts to develop in liver, ovary and elsewhere
in the body. The presentation of cysts in kidneys and ovaries
coincide with some reports in the literature [10]. The disease
causes a variety of serious complications. A common complication
of polycystic kidney disease is high blood pressure, laminitis and
others pathologies. Kidney failure is another common problem
for animals with polycystic kidney disease. Polycystic kidney
disease varies greatly in its severity, and some complications
are preventable but its diagnosis can be confused. Some studies
the major inherited types are autosomal dominant (AD) and
autosomal recessive (AR) [8]. ADPKD is caused by at least two
(and possibly three) genes located on separate chromosomes,
while ADPKD-1 is due to a 14 kb transcript in a duplicated region
on the short arm of chromosome 16 very near the alpha-globin
gene cluster and the gene for one form of tuberous sclerosis.
ADPKD-2 has been assigned to the long arm of chromosome 4.
ARPKD is due to a mutated gene on both copies of the long arm
of chromosome 6 [8]. Cysts originate in renal tubules. Proliferation
of tubule epithelial cells modulated by endocrine, paracrine, and
autocrine factors is a major element in the pathogenesis of renal
cystic diseases. In addition, uid that is abnormally accumulated
within the cysts is derived from glomerular ltrate and, to a greater
extent, by transepithelial uid secretion. Abnormal synthesis and
degradation of matrix components associated with interstitial
inammation are additional features in the pathogenesis of renal
cystic diseases [8]. The ADPKD genotypes are characterized by
bilateral kidney cysts, hypertension, hematuria, renal infection,
stones, and renal insuciency. ADPKD is a systemic disorder;
cysts appear with decreasing frequency in the kidneys, liver,
pancreas, brain, spleen, ovaries, and testis. Cardiac valvular
disorders, abdominal and inguinal hernias, and aneurysms of
cerebral and coronary arteries and aorta are also associated with
ADPKD [8]. Although there have been cases of polycystic kidney
disease in horses and donkeys, secondary clinical complications
have been described recently as the reports have been like nding
occasional necropsy or slaughter inspections. Unfortunately,
this case has the limitation of not conducting a genetic study
to determine polycystic familial kidney disease in donkeys, to
consider a hereditary origin. However, the observed lesions show
severe pathological changes of the kidneys associated with a
polycystic kidney disease, they may be associated with recurrent
infections although secondary bacterial infection was ruled out,
or a previous obstruction of the urinary tract is not described
in the history of this donkey. In this case, although a unilateral
polycystic kidney deterioration of the conditions of the patient,
the secondary complications and chronic liver injury and chronic
obstructive pulmonary disease ultimately led to euthanasia.
CONCLUSION
In conclusion it was reported a case of severed PKD and
ovarian cyst in a donkey. Future studies are needed to elucidate
the pathogenesis of polycystic kidneys in a donkey as well as its
etiology considering the similarity between the observed clinical
signs in animals.
BIBLIOGRAPHICS REFERENCES
[1] AGUILERA-TEJERO, E.; ESTEPA, J.C.; LOPEZ, I.; BAS, S.;
RODRIGUEZ, M. Polycystic kidneys as a cause of chronic
renal failure and secondary hypoparathyroidism in a horse.
Equine Vet. J. 32:167–169. 2000.
[2] BADIOLA-DÍEZ, J.; CAMÓN-URGEL, J.; HIDALGO-CHA-
PADO, JM. Renal cystic involvement in equidae. Arch. Esp.
Urol. 33(1):77-104. 1980.