This document provides information on various diseases of the bladder, ureters, and urethra in animals. It describes the epidemiology, pathogenesis, clinical signs, diagnosis, and treatment for conditions such as uroperitoneum in foals, urolithiasis, rupture of the bladder, cystitis, paralysis of the bladder, urethral tears in stallions and geldings, and various congenital defects of the urinary tract including renal hypoplasia, renal dysplasia, and polycystic kidneys. The document contains detailed information on each condition in a consistent format to aid veterinarians in diagnosis and clinical management.

1. Disease/
Disorder
Brief Description Epidemiology Pathogenesis Clinical Signs Lesions Diagnosis Differential
Diagnosis
Treatment Control and
Prevention
DISEASES OF THE BLADDER, URETERS AND URETHRA
UroperitoneuminFoals
Accumulation of
urine into the
peritoneal cavity. It
occurs as a result of
variety of situations:
*Congenital rupture
of the bladder
*Bladder rupture
associated with
sepsis
*Rupture of urachus
Avulsion of the
bladder from its
urachal attachment
Some studies
indicate a higher
incidence of bladder
rupture in males
than in females,
possibly because the
narrower pelvis and
the longer,
narrower urethra of
colts is a
predisposing factor.
The pathophysiology is
that of postrenal
azotemia.
Accumulation of urine
within the peritoneal
cavity results in
substantial electrolyte,
acid-base and
cardiovascular effects
in affected foals.
Foals are unable to
excrete waste products
and are unable to
maintain water and
electrolyte balance.
Lethargy, decreased
appetite, mild
abdominal
distension, and
abdominal distension
(2-4 days old)
Hypokalemia
Foals with this
condition usually
appear normal at
birth, but gradually
become ill over 1 to 2
days. They are weak,
lack energy and
interest in their
surroundings, and
have an increased
heart rate. Most of
these foals attempt
to urinate often, but
only produce a small
amount of urine.
Necropsy
examination
confirms the
presence of
uroperitoneum
and the
structural defect
allowing leakage
of urine into the
abdomen. The
defect can have
signs of healing,
which can make
it readily
confused with a
malformation,
because
affected foals
can survive for
days after the
rupture occurs-
sufficient time
for partial
healing of the
defect.
Ultrasonographi
c abdominal
examination
Physical exam
(ballottement)
Blood and
peritoneal fluid
analysis
Septicemia,
hypoxic
ischemic
encephalopathy
/neonatal
encephalopathy
Persistent
meconium
impaction or
colic
Primary renal
disease
Surgery
Peritoneal
drainage
There are no
recognized means
of prevention and
control.
Minimize the risk
of foals
developing septic
disease.

2. Urolithiasis Urolithiasis is an
obstruction to the
urinary tract. The
mechanism of urolith
formation in horses is
unknown, although
the alkaline pH and
high mineral content
of normal equine
urine may favor
crystal formation and
precipitation. Normal
equine urine also
contains large
amounts of
mucoproteins, which
may serve as a
cementing substance
to adhere crystals.
Consumption of feed
and water high in
mineral content may
increase urinary
solute concentrations
and thereby promote
crystallization and
precipitation.
Multiple nephroliths
may develop in
horses with renal
papillary necrosis
(associated with
NSAID administration
while dehydrated)
and mineralization of
the papillae.
Occurs sporadically
in horses, the
prevalence is low at
about 0.04%-0.5%
of all horse
accessions or
diagnoses. Animals
from 5-15 years of
age are most
commonly affected
and 76% males are
(27% intact, 49%
gelding) and 24%
are females.
Equine uroliths
have a diameter of
0.5–21 cm, weigh as
much as 6.5 kg, and
are found most
often within the
bladder.
Obstruction of one
ureter may cause
unilateral
hydronephrosis, with
compensation by the
contralateral kidney.
Rupture of the urethra
or bladder is more
likely to occur with a
spherical, smooth
calculus and causes
complete obstruction
of the urethra.
Most equine uroliths
are composed of
calcium carbonate, in
various hydrated
forms, with either
calcium phosphate or
struvite uroliths
occasionally noted.
Weight loss,
Anorexia, Stranguria.
Most uroliths are
located in the
bladder and cause
dysuria, pollakiuria,
and hematuria.
Hematuria is most
evident after exercise
and toward the end
of a voided urine
stream. Affected
horses frequently
stretch out to urinate
and may maintain
this posture for
variable periods
before and after
micturition.
Additional signs may
include scalding of
the perineum in
females or of the
medial aspect of the
hindlimbs in males.
Geldings and stallions
may protrude the
penis flaccidly for
prolonged periods
while intermittently
dribbling urine.
Affected horses may
occasionally exhibit
recurrent bouts of
colic or an altered
hindlimb gait.
Urethral
perforation
Hydronephrosis
Urinary bladder
rupture
Transrectalultras
onography
Urinalysis
Rectal palpation
Clinical signs,
and History
Surgical removal
of the calculus
and correction of
any defects in the
bladder.
Midline or
paramedian
laparotomy and
cystotomy,
Pararectal
cystotomy,
Subischial
urethrostomy,
Urethral
sphincterotomy
Laser or shock
wave lithotripsy
Ammonium
chloride (200
mg/kg BW) twice
daily.
Increase urinary
chloride excretion,
decrease urine pH,
and provide
calcium:
phosphorus ratio
of 2:1 in the
complete ration.
Adding sodium
chloride up to 4%
of the total ration

3. RuptureoftheBladder(Uroperitoneum) This occurs most
commonly in
castrated males as a
sequel to obstruction
of the urethra by
calculi.
Rare cases are
recorded in cows as
a sequel to a
difficult parturition
and in mares after
normal parturition,
possibly because of
compression of a
full bladder during
foaling.
After the bladder
ruptures,
uroperitoneum results
in a series of
abnormalities that
arise from failure of the
excretory process
combined with solute
and fluid redistribution
between the peritoneal
fluid and extracellular
fluid.
Bladder rupture leads
to gradual
development of ascites
from uroperitoneum,
ruminal stasis,
constipation, and
depression.
Depression, anorexia,
colic, abdominal
distension, and
uremia develop
within 1-2 days
following rupture.
Ruptured
urinary bladder
Ultrasonographi
c abdominal
examination
Physical exam
(ballottement)
Blood and
peritoneal fluid
analysis
Ascites
Urinary tract
obstruction
Surgery with a
goal of bladder
repair.
To avoid costs of
laparotomy in
feedlot animals,
urethrostomy is
created or an
indwelling
catheter is placed
and the rupture is
allowed to repair
itself.

4. Cystitis Inflammation of the
bladder usually
associated with
bacterial infection
and is characterized
clinically by frequent,
painful urination and
hematuria,
inflammatory cells
and bacteria in the
blood.
It is likely to be the
result of an
obstruction in the
urinary tract or
paralysis of the
bladder (which may
be the result of
nerve damage).
Occurs also in
mares with chronic
inflammation of the
vagina.
Bacteria frequently
gain entrance to the
bladder but are usually
removed by flushing
action of voided urine
before they invade the
mucosa.
Mucosal injury
facilitates invasion but
stagnation of urine is
the most important
predisposing cause.
Loss of control over
urination, frequent
urination, urine
dribbling, urine
scalding, and
straining to urinate.
Hyperemia,hem
orrhage and
edema of the
mucosa
Complete blood
test
Urinalysis
Rectal
examination
Based on Clinical
signs
Pyelonephritis
Presence of
calculi in the
bladder
Urethral
obstruction
Antimicrobial
therapy for 7-14
days.
Although there is
no fool-proof way
to prevent cystitis,
the environment,
diet, and on-going
attention to the
physical condition
of each horse can
help owners and
handlers to catch
the infection in its
earliest stages to
ensure proper
treatment.
Given the fact that
certain grasses can
cause cystitis,
horses should not
be pastured in
pastures where
Sudan grass,
sorghum of
sorghum-sudan
hybrid grasses are
grown, nor should
they be fed
cuttings from such
pastures.

5. Paralysisofthebladder Paralysis of the
bladder is uncommon
in large animals. This
usually occurs as a
result of neurological
diseases affecting the
lumbosacral spinal
cord such as equine
herpes myelopathy
and cauda equine
syndrome, and
particularly ascending
spinal meningitis in
lambs after tail
docking.
Spinal cord
degeneration
following
consumption of
sorghum can lead to
bladder paralysis in
horses.
Iatrogenic bladder
paralysis occurs in
horses in which
there has been
epidural injection of
excessive quantity
of alcohol.
In some horses,
idiopathic bladder
paralysis and
overflow
incontinence may
occur sporadically
in the absence of
other neurological
or systemic signs.
Compression of the
lumbar spinal cord by
neoplasia
(lymphosarcoma,
melanoma) or infected
tissue (vertebral
osteomyelitis) causes
paralysis in bladder.
Chronic distention of
the bladder leads to
accumulation of a
sludge of calcium
carbonate crystals.
Urine stasis produces
ideal conditions for
bacterial growth.
Incontinence with
constant or
intermittent dribbling
of urine. Urine flow is
often increased
during exercise.
Large bladder,
often displaced
cranioventrally,
detected on
rectal
examination.
Physical
examination
(manual bladder
compression)
Non-
neurogenic,
non-myogenic
causes of
apparent
incontinence.
Myogenic
problems of the
bladder such as
cystic calculi.
Supportive and
aimed at relieving
bladder
distension by
regular
catherization and
lavage.
Parasympathomi
metic drug (
bethanicol) and
sympatholytic (
prazosin,phenoxy
benzamine)
Regular
catheterization is
essential in
conjunction with a
prophylactic dose
of antibiotic.

6. Urethraltearsinstallionsandgeldings Urethral rents are
lesions in the convex
and surface at the
level of the ischial arc
in geldings and
stallions.
The lesions
communicate with the
corpus spongiosum and
cause hemorrhage at
the end of urination in
geldings or during
ejaculation by stallions.
The disease is
apparently caused by
contraction of the
bulbospongiosis muscle
at the end of urination,
with a consequent
increase in pressure in
the corpus spongiosum
and expulsion of blood
through the rent.
Urethral tears
typically result in
hematuria at the end
of urination, in
association with
urethral contraction.
Affected horses
generally void a
normal volume of
urine that is not
discolored. At the
end of urination,
affected geldings
have a series of
urethral contractions
resulting in squirts of
bright red blood.
Occasionally, a
smaller amount of
darker blood may be
passed at the start of
urination.
With hematuria
of several weeks
duration, the
lesion may
appear as a
fistula
communicating
with the
vasculature of
the corpus
spongiosum
penis
(cavernous
vascular tissue
surrounding the
urethra).
Endoscopic
examination of
the urethra with
visualization of
the rent in the
urethral mucosa.
Urethritis or
hemorrhage
from
"varicosities" of
the urethral
vasculature.
Breeding rest is
recommended
for stallions.
Subischial
urethrostomy or
subischial incision
into the
spongiosum penis
reduces vascular
pressure in the
corpus
spongiosum
during urination,
allowing the
defect to heal. A
buccal mucosal
graft was used to
repair the defect
in a stallion.
CONGENITAL DEFECTS OF THE URINARY TRACT
Renalhypoplasia
A decrease in total
renal parenchyma of
one-third or more,
with a
proportionately
greater loss of
medullary than
cortical tissue.
Lethargy, shivering,
depression, anorexia,
and a slow rate of
growth.
Polydipsia, polyuria,
as well as other signs
of kidney disease
such as weakness,
lack of appetite,
abdominal pain,
fever, or swelling of
the legs.
Evidence of
chronic renal
failure on
clinicopathologi
cal examination
Transrectal and
transabdominal
ultrasonography
reveal small
renal medulla
and pelves.
Renal dysplasia There is no
treatment for
renal hypoplasia.
Care for affected
dogs consists of
managing the
problems
associated with
the kidney failure
that results from
this condition.

7. Renaldysplasia It is defined as
disorganized
development of the
renal parenchyma
due to anomalous
differentiation.
This is common in
dogs but rare in
cats, lambs, and
horses. In pigs,
renal dysplasia may
be idiopathic or
associated with
nutritional
avitaminosis A.
Renal dysplasia may be
unilateral or bilateral.
When these conditions
occur, the kidneys are
usually small, firm, and
pale.
The outer portion of
the kidney that
contains glomeruli may
be smaller than normal
in size.
Renal failure,
nephromegaly and in
some instances
hematuria and colic.
Polydipsia, polyuria,
as well as other signs
of kidney disease
such as weakness,
lack of appetite,
abdominal pain,
fever, or swelling of
the legs.
Azotemia, increased
serum phosphorus
concentrations and
oliguria.
Characterized
by persistence
of abnormal
mesenchymal
structures,
including
undifferentiated
cells, cartilage,
immature
collecting
ductules, and
abnormal lobar
organization.
Animals
affected
bilaterally
generally die in
the early
neonatal period,
whereas
animals affected
unilaterally
typically
develop
hypertrophy of
the
contralateral
kidney.
Ultrasonographi
c examination of
the kidneys may
reveal a poor
distinction
between the
cortex and
medulla due to a
hyperechoic
medulla, which
was due to
fibrosis.
Renal biopsy
confirms
dysplasia
Other causes of
chronic renal
failure
including renal
hypoplasia.
Renal
neoplasia.
Other intra-
abdominal
neoplasia.
Interstitial
nephritis.
Glomeruloneph
ritis.
Pyelonephritis.
Treatment is
aimed at
managing the
associated
chronic renal
failure.

8. Polycystickidneys The kidneys are
usually grossly
enlarged on
palpation. Horses
with this condition
sometimes also have
cysts in the bile ducts
of the liver.
Polycystic kidneys
are rare in cattle
and horses and very
rare in sheep. It is
commonly recorded
in dogs.
In adult horses,
polycystic disease
may also be
acquired rather
than congenital.
Renal failure,
nephromegaly and in
some instances
hematuria and colic.
Polycystic kidneys
may cause no clinical
signs or lead to
progressive renal
failure.
If it is extensive and
bilateral the affected
animal is usually
stillborn or dies soon
after birth.
Based on
physical and
radiographic
findings,
ultrasonic
examination, or
exploratory
laparotomy.
Other causes of
chronic renal
failure ,
including renal
hypoplasia.
Pyelonephritis
Ectopicureter
The ectopic ureter
opens into the
urogenital tract at a
place Other than the
bladder such as
cervix, urethra or
vagina. The condition
may be unilateral
with urinary
incontinence from
birth as major clinical
sign
In horses, ectopic
ureter is the most
common congenital
anomaly affecting
the urinary tract; as
in dogs, it is
significantly more
common in fillies
than in colts.
Ectopic ureters
generally result from
disruption of
development of the
mesonephric and
metanephric duct
systems.
Continual dripping of
urine is the classic
sign, although
animals with
unilateral ectopic
ureter may void
normally; the
inability to void
normally suggests
bilateral ectopic
ureters. A low-grade
vaginitis or vulvitis
may also be present
due to urine scalding.
Definite
diagnosis
requires
excretory
urography or
endoscopy;
visualization of
the ureteral
openings during
endoscopy can
be assisted by
intravenous
administration
of
phenolsulfonpht
halein (0.01
mg/kg BW) or
indigo carmine
(0.25 mg/kg BW)
to impart a red
or blue color,
respectively, to
the urine being
produced.
Surgical
treatment
involving
ureterovesical
anastomosis or
unilateral
nephrectomy has
been successful.
Successful
surgical
treatments
usually involve
transplantation
of affected
ureters into the
bladder, or
ureteronephrecto
my.

9. Patenturachus The urachus is the
tube within the
umbilical cord
through which urine
from the unborn foal
travels from its
bladder to the
allantois (a fluid filled
sac surrounding the
unborn foal).
Patent urachus occurs
as three syndromes in
foals: congenital and
present at birth;
acquired and
secondary to urachal
infection or
inflammation; or
secondary to severe
systemic illness,
usually sepsis.
Failure of the
urachus to close at
birth occurs most
commonly in foals.
As a result of the
patent urachus, which
during intra-uterine life
drains urine into the
allantoic fluid, urine
leaks from the
umbilicus.
Early signs of
infection may include
an enlarged navel
that is painful to the
touch and discharge
of pus from the navel
opening.
Fever, Depression,
loss of appetite, and
signs of serious
systemic illness such
as respiratory
difficulty, lameness
and swollen joints.
Patent urachus is
typically associated
with continuous
urinary incontinence,
urine scalding of the
ventral abdomen,
and development of
bacterial urinary tract
infections.
Foals with
patent urachus
secondary to
umbilical
disease usually
have enlarged
umbilicus and
some have
purulent
discharge.
Ultrasonographi
c examination of
the umbilicus of
foals with patent
urachus is
essential to
determine the
extent of disease
and presence of
intra-abdominal
disease.
Cystitis Surgical resection
and 2–4 wks. of
appropriate
antibiotic therapy
when indicated.
Surgical resection
is the standard
treatment for
umbilical urachal
sinuses and intra-
abdominal
urachal cysts.
Bibliography
American College of Veterinary Surgeon. (n.d.). Retrieved January 8, 2014, from https://www.acvs.org/large-animal/patent-urachus-foals
II, H. C. (2009, April 1). Retrieved January 6, 2014, from dvm360.com: http://veterinarycalendar.dvm360.com/avhc/article/articleDetail.jsp?id=675274&sk=&date=&pageID=2
Moses, S. E. (n.d.). The Merck Veterinary Manual . Retrieved january 9, 2014, from The Merck Veterinary Mnual Online: http://www.merckmanuals.com/vet/index.html
O.M. Radostits, C. C. (2007). Veterinary Medicine A Textbook of the diseases in cattle, horses, sheep,pigs and goats 10th Edition. Philadelphia, USA: Elsevier Limited.

11. DISEASES OF THE KIDNEYS
DISEASE OTHER
NAME
BRIEF
DESCRIPTION
ETIOLOGY CLINICAL SIGNS LESIONS DIAGNOSIS DIFFERENTIAL
DIAGNOSIS
TREATMENT CONTROL AND
PREVENTION
GLOMERULO
NEPHRITIS
Chronic
nephritis
-can occur as
a primary
disease or as
a component
of diseases
affecting
several body
systems
-equine
infectious
anemia
-amyloidosis
-streptococci
infection
-weight loss
-anorexia
-polyuria
-kidneys are
shrunken and
fibrous
-ulceration in
the GI tract
-acute renal
failure
-pre-eclamtic
toxemia
-remove the causative agent
-restore normal fluid balance
There is no specific
prevention for
most cases of
chronic
glomerulonephritis.
Some cases may be
prevented by
avoiding or limiting
exposure to
organic solvents,
mercury, and
nonsteroidal anti-
inflammatory
analgesics.
RENAL ISCHEMIA -reduced
blood flow
through the
kidneys
-usually from
general
circulatory
failure
ACUTE
-general
circulatory
emergencies
such as shock,
dehydration,
acute
hemorrhagic
anemia, acute
heart failure
CHRONIC
-congestive
heart failure
-masked by the
clinical signs of the
primary disease
-oliguria and
azotemia will go
unnoticed in most
cases
-proteinuria-early
indication
-primary cortex
is pale and
swollen
-distinct line of
necrosis at the
corticomedullary
junction
-necrosis of
tubular
epithelium and/
or glomeruli
-urinalysis with
urea nitrogen
and creatinine
concentration
used as indices
-serum
biochemistry on
urine
-Nonoliguric
Acute Renal
Failure
-correction of fluid, electrolyte
and acid-base balance
TOXIC NEPHROSIS -direct action
of toxins
-metals
-
antimicrobials
-vit. K via IM
or IV
-vit. D2 and
D3
-NSAID
-
benzimidazole
-may not be
referable to urinary
system
-colic, stranguria
-depression,
dehydration,
anorexia,
hypothermia, slow or
elevated heart rate
and weak pulse
-diarrhea may be
present
ACUTE CASES
-kidney is
swollen and wet
on the cut
surface
-edema may be
present
-necrosis and
desquamation of
tubular
epithelium
-hyaline casts
-urinalysis with
proteinuria,
glucosuria,
enzymuria and
hematuria as
initial changes
-detection of the
proximal tubule
enzyme GGT in
urine
-pulmonary
adenomatosis
-
mycotoxicoses
-nutritional or
metabolic
disorders (eg,
selenium,
vitamin E, or
copper
deficiency)
-removal of the toxin
identified
-anti-toxins
-hemodialysis for foals with
oxytetracyclinenephrotoxicosis
-controlled
secondary diseases

12. -chlorinated
naphthalene
-oxalate in
mushrooms
-mycotoxins
are present in
the dilated
tubules
DISTAL RENAL
TUBULAR
ACIDOSIS(TYPE 1)
-
characterized
by normal
glomerular
function but
abnormal
tubular
function
-detect in the
ability to
secrete H ions
in the distal
convoluted
tubules
against a
concentration
gradient
-profound strong ion
acidosis due to
hyperchloremia
-alkaline urine pH(>8)
-increased fractional
clearance of sodium
-examining the
ability of the
distal
convoluted
tubules to
excrete H ions
by oral
administration
of ammonium
chloride
-
uroperitoneum
- renal calculi
-symptomatic
-focuses sodium bicarbonate
PO or IV administration
-The goal is to
restore the normal
pH (acid-base level)
and electrolyte
balance.
EMBOLIC NEPHRITIS -any
septicemia or
bacteremia
when bacteria
is lodged in
the renal
tissue
-toxemia
-kidney may be
enlarged on rectal
examination
-small gray spots
in cortex
-develop into
large abcesses
-extensive
scarring
-microscopic
exam of urine
-hematology
-amyloidosis
-nephritis
-antimicrobials
-avoid use of nephrotoxic
drugs
-supportive care,
including
hydrotherapy of
accessible veins,
anti-inflammatory
agents, and
systemic
antimicrobials to
control secondary
sepsis
PYELONEPHRITIS -develops by
ascending
infection
from lower
urinary tract
-secondary to
bacterial
infections of
the lower
urinary tract
-septicemia
-secondary to
anatomical
abnormalities
of the kidneys
or distal
convoluted
structures
-hematuria with
pyelonephritis
-presence of
abnormality
shaped kidneys
with loss of
corticomedullary
gradient
-hyper echoic
abnormalities in
the renal cortex
-increased
echogenicity
-erythrocytes,
leukocytes and
cell debris are
present in the
urine upon
microscopic
examination
-ultra
sonography of
the kidneys
based on the
lesions
described
-Azotemia
-Chronic Renal
Failure
-
Nephrolithiasis
-unilateral nephrectomy(only
in non-azotemic patients)
-includes longterm antibiotics
(4 to 6 weeks), sometimes at
high dosages
-alteration of the
urinary pH(reduce
the ability of the
bacteria to attach
to the epithelial
cells
HYDRONEPHROSIS -dilation of
the renal
pelvis with
-obstruction
of the ureter
-congenital or
-anuria, dysuria or
stranguria
-
ultrasonography
-unilateral
-Urinary
stones
-Urinary reflux
-hydroureter is
aimed at restoring
urine flow

13. progressive
atrophy of
the renal
parenchyma
acquired obstruction may
be detectable on
palpation per
rectum of a
grossly
distended
kidney
-UTI -restoration of fluid
balance
RENAL NEOPLASMS -primary
tumors are
uncommon
-carcinomas
occur in
horse
-unknown -enlargement of the
kidneys(characteristic
sign)
-weight loss, reduced
appetite,
intermittent bouts of
abdominal pain
-massive ascites,
hemoperitonium,
hematuria
-
ultrasunographic
examination of
the kidneys
-renal biopsy
-surgical removal of the
neoplasms
-chemotherapy
-nephrectomy