Department of Pathology,

Faculty of Veterinary Pathology,

Zagazig University, Egypt.

Pathology of Urinary SystemBY

Prof. Dr. Mohamed Hamed Mohamedmohamedelariny@yahoo.com

+201224067373

2012

Urinary SystemGeneral Considerations:

The urinary system plays an important role in the regulation and maintenance of

fluid and electrolyte homeostasis in all higher forms of animal life. The organ primarily

responsible for these activities is the kidney. It acts as an elaborate filtration-resorption

device whose responsibilities include maintenance of a constant quality and quantity of

plasma and tissue fluids and excretion of waste products. It is also involved in the

production of such hormones as erythropoietin, renin, prostaglandin and 1, 25-

dihydroxycholecalciferol.

Anatomy:Kidneys can be classified as either unilobular or multilobular based on the presence

or absence of pyramidal areas in the renal medulla.

In unilobular kidneys, the medulla is not divided into pyramidal regions. This type

of kidney is found normally in cats, dogs, horses, and small ruminants.

In multilobular kidneys, there are distinct pyramidal subdivisions of the medulla

and this type of kidney is found normally in cattle and swine. In multilobular kidneys,

the tips of the medullary pyramids are referred to as medullary papillae and each papilla

has a corresponding portion of the collecting system called a minor calyx. Typically,

several minor calyces join to form a major calyx and the major calyces join to form the

renal pelvis which continues into the ureter.

In unilobular kidneys, the papillary ducts (found at the ends of the collecting

tubules) empty at crest-like papillae (the medullary crest) into the renal pelvis. This

structure then continues into the ureter.

Abnormalities in the urinary system can occur in various forms, including

anomalies in development, circulatory disturbances, infections, toxicosis and

immune-mediated diseases. Kidney infections have been associated with viral

and bacterial as well as parasitic organisms. The various abnormalities are

manifested in many forms such as agenesis, hypoplasia, malpositioning,

dysplasia, atrophy, cyst formation, hemorrhage, necrosis and inflammation.

Gross Examination of The Kidneys:The systematic gross examination of the kidney includes observation of its size,

shape, color, and consistency. The kidneys are usually equal in size and are

comparable in length to the length of three vertebrae. Enlargement of a kidney

may occur due to excessive blood, edema fluid, fat or urine in the tubules or the

renal pelvis or hypertrophy of the nephrons. Focal lesions in the kidney tend to

cause distortions in the shape of the kidney, whereas generalized lesions usually

do not. The normal renal color is brownish-red, except in mature cats, in which

the case tend to be yellowish due to a high lipid content. Each kidney should be

cut longitudinally and the cut surfaces of the parenchyma should be examined.

Anomalies of Development:Aplasia or Agenesis:

It is the failure of one or both kidneys to be formed. Familial tendency

for renal Aplasia has been observed in dogs.

Hypoplasia of The Kidneys:It is the failure of a kidney to develop to its normal size. It is either

unilateral or bilateral (in the unilateral there is hypertrophy of other kidney).

Macroscopical Pictures:i-The hypoplastic kidney is smaller than normal (uniform reduction in size).

ii-In cattle, the lobulated kidneys show irregular shape.

iii-The capsule is usually thickened, tense and adhered to the cortex.

iv-The parenchyma is usually grayish in color and tends to be firm.

v-On cut surface, a reduction in parenchymal size (the cortex is more

severely affected than the medulla).

Microscopical Pictures: i-There is a reduction in the number of nephrons (evident by fewer glomeruli).

ii-The remaining nephrons are usually hypertrophic.

iii-The tubules in the medulla are often dilated and their epithelial cells are flattened

iv-Interstitial fibrosis which causes separation of the tubules.

Malposition (Ectopic) of The Kidney:

The kidneys are seen in abnormal position (most commonly displaced caudally).

The swine is mostly affected animals and may be associated with Vit A def.

Horseshoe (Fused) Kidneys: (normal function)

It results from a fusion of the anterior or the posterior poles of the kidneys

and together, the fused kidneys have a shape somewhat like that of a horseshoe.

Persistence of Fetal Lobulation:Persistence of fetal lobulation occurs due to a failure of fusion of individual

renal segments (in cattle and swine).

RENAL DYSPLASIA

It is disorganized development of the renal parenchyma due to lack of

differentiation.

Macroscopical Pictures:i-The affected kidneys are usually smaller than normal. (Misdiagnosis with

hypoplasia).

ii-They are usually misshapen and fibrosed.

iii-They often contain thick-walled cysts.

iv-Their ureters are usually tortuous and dilated.

Microscopical Pictures:i-Immature tissues (glomeruli and tubules) are evident in adult kidneys.

ii-Collecting tubules are blind at its end or primitive ducts surrounded by

concentric layers of mesenchym.

RENAL CYSTSThey are thin-walled fluid filled structures which develop in the renal parenchyma.

They are mostly congenital (not caused by an obstructive lesion); vary in size, single or

multiple and can arise in any part of the nephron or in collecting tubules. In some cases,

polycystic kidney disease is also associated with cystic bile ducts, bile duct proliferation,

and cystic pancreatic ducts. In severe cases of congenital polycystic kidneys, there is

usually stillbirth or early neonatal death due to kidney failure.

Familial Renal Diseases:They include:

i-Familial glomerulonephritis (reported in numerous breeds of dogs).

ii-progressive renal fibrosis (reported in mutant Southdown sheep).

iii-Specific tubular dysfunctions (reported in dogs).

The canine familial renal diseases are characterized by renal failure, mostly

in immature or young dogs, which are not associated with renal inflammation.

Renal Failure (Azotemia / Uuremia):It means an increase of non protein nitrogenous substances in the blood as

urea, uric acid, creatinine and ammonia.

Symptoms: The characteristic features of renal failure and the symptoms include

tiredness, nausea, vomiting, pruritus, oliguria and uremic frosting. It either:

i-Acute Renal failure develops in minutes, hours, or a few days, in which

case it may be reversible.

ii-Chronic renal failure develops over a longer period of time and usually

progresses to terminal stages.

NB:Renal failure may result from decreased perfusion of the kidneys, as often

occurs in shock. (But it is not true).

Pathognomonic lesions:1-Dehydration and skin lesions as crust and eczema are seen.

2-Ulcerative and necrotic stomatitis (Uremic ulcer) with foul

smelling mucoid material on the ulcerated areas and congested mm

3-Ulcerative and hemorrhagic gastritis with secondary

mineralization of the arteriolar media and intema.

4-Fibrinous pericarditis with increase pericardial fluid.

5-Uremic aortitis with proliferative roughing of intema, besides

microscopic area of calcification (Uremic arteriosclerosis). Atrial

and aortic thrombosis are seen

6-Diffuse pulmonary edema due to vascular damage. Later, the

alveoli contain fibrin rich fluid with few macrophages and

neutrophils (Uremic pneumonia). Ascites, hydropericardium,

hydrothorax are seen.

7-Osteomalacia (in cattle): The calcium in the intestine combined

with urea and result in hypocalcemia increase activity of

parathyroid stimulate bone, calcium take out from bone

osteomalacia will established.8-Toxic injury to the bone marrow (Toxic hypoplastic or aplastic anemia).

Lesion of Uremia Mechanism

1-Pulmonary edema and Fibrinous

pericarditis

2-Ulcerative stomatitis and gastritis

3-Atrial and aortic thrombosis

4-Hypoplastic or aplastic anemia

5-Soft tissue mineralization

1-Increased vascular permeability

2-Ammonia secretion and vascular

necrosis

3-Endothelial and subendothelial damage

4-Increases erythrocytes fragility and

lack of erythropoietin production

5-Altered Ca and phosphorus

metabolism

Summary of pathognomonic lesions of uremia and its mechanisms.

Disturbances in Circulation:Renal Hyperemia:

A-Active Hyperemia: associated with inflammation (nephritis).

B-Passive Hyperemia: associated with general venous congestion.

Macroscopical Pictures:

The kidneys are swollen and uniformly dark.

Microscopical Pictures:

All blood vessels, especially capillaries are dilated and engorged with

blood

Renal Hemorrhages:

Petechial or ecchymotic hemorrhages are seen in cortex and medulla

associated with septicemic and some viral diseases. This is responsible for

the appearance that is described as a “Turkey egg kidney” in Hog

cholera.

Infarction:

It is observed as pale or red wedge shape area of ischemic necrosis

with the apex near the zone of the arcuate arteries and the base at the

capsule. Most renal infarcts involve the interlobular arteries and result in

a pyramid-shaped area of necrosis in the cortex of the kidney.

Inflammation of The Kidney (Nephritis)It is the inflammation of kidney structures.

It is due to:A-Glomerular Diseases.

B-Tubulointerstitial Diseases.

Classification of nephritisAccording to the rout of infections:

i-Hematogenic (Descending) ii-Urinogenic (Ascending)

According to the anatomy:

i-Glomerulonephritis ii- Interstititial nephritis

According to the type of exudate:

i-Suppurative nephritis ii-Non-suppurative nephritis

I-Diseases of Glomeruli:1-Amyloidosis:

Renal involvement is almost always a feature of systemic amyloidosis.

NB: In cats: amyloidosis primarily involves the medulla, with amyloid deposits

occurring in the interstitium of the medulla.

2-Inflammmation of Glomeruli (Glomerulonephritis):It is the inflammation of the glomeruli and tubules due to immune complex

deposition (Antigen-antibody reaction). Type-III hypersensitivity.

Causes:

i-Viral Diseases: as equine infectious anemia

ii-Bacterial Diseases: as strept (tonsillitis).

iii-Antisera:

iv-Damage of the skin or burns.

v-Chemical irritant and toxins.

Glomerulonephritis: It is either

I-Focal GN: (Involvement may be limited to a few glomeruli).

II-Generalized GN: (involvement of the entire glomeruli).

NB: -The term diffuse is reserved for use indicating involvement of the entire

glomerulus in contrast to segmental involvement.

-It may be Acute or Chronic stages with secondary involvement of the

tubules and interstitial tissue.

Clinically, The glomerulonephritis is manifested by

i-Hematuria ii-Proteinuria iii-Oliguria,

Iv-Hyposthenuria, and V-Azotemia (uremia)Hyposthenuria: Excretion of urine with low specific gravity due to an inability of the

tubules of the kidneys to produce concentrated urine.

Classification of Glomerulonephritis:i-Proliferative GN:

ii-Membranous GN:

iii-Membranoproliferative GN:

iv-Other Forms of GN: v-Glomeulosclerosis.

A-Proliferative Glomerulonephritis:Macroscopical Pictures:

i-The affected kidneys are enlarged, soft and pale in color with

petechial hemorrhage in the cortex and easily detached

capsule Acute.

ii-The kidneys become smaller, gray and firmer than normal

with tiny cysts in the cortex (small white granular contracted

kidney) Chronic.

Microscopical Pictures: They differed according to their types.

i-The glomeruli are swollen, avascular and edematous with

retrogressive change in renal epithelium

ii-The Bowman's capsule filled with numerous endothelial and

mesangial cells with few neutrophils infiltrations Acute.

iii-Thrombosis and necrosis of glomerular capillaries may

occur with subsequent hemorrhage into the renal corpuscle.

iv-Excessive proliferation of the endothelial cells of

glomerular capillaries and the epithelium of Bowman’s

capsule can induce adhesions between visceral and parietal

layers with the glomerular tufts in the form of epithelial

crescents Subacute.

v-Such crescents persists during the chronic stage together

with collapsed and hyalinized glomeruli, and atrophy of renal

tubules.

vi-Ultrastructurally, immune complex deposits (humps) are

seen within the lamina densa and in the subendothelial

portion of the B.M. which projected between the podocytes

(Lumpy-bumpy appearance)

NB: i-Large white Kidney: It is due to Amyloidosis

ii-Large Pale Kidney: It is subacute membranous GN due to lipid

deposition in proximal CT and interstitial edema.

Iii-White spotted kidney: It is lymphocytic interstitial nephritis.

B-Membranous Glomerulonephritis Pathogenesis: It is due to an immunologic process in which

immunoglobulins (Ig D and A) or antigen-antibody complexes are

deposited in the glomerular basement membrane. These antigens

may be exogenous, as in serum sickness, or endogenous, as in

systemic lupus erythematosis.

Macroscopical Pictures:

i-The affected kidneys are enlarged (large pale kidney).

ii-Pale in color due to lipid deposition and interstitial edema.

iii-In late stage the kidneys become contracted and fibrosed.

Microscopical Pictures:

i-Extensive thickening and reduplication of the glomerular

basement membrane and that appear as wire loop due to

deposition of immune complex.

ii-Loss of foot processes of podocytes of glomeruli.

iii-Broking and splitting of the basement membrane.

iv-Fatty change in the glomerular epithelium

v-There is no proliferation of the glomerular cells.

C-Membranoproliferative Glomerulonephritis It is characterized by thickening in the basement membranes as

well as proliferation of mesangial and parietal epithelial cells of the

Bowman's capsule.

Pathognomonic Lesions:

i-There is marked increase in mesangial cells, parietal epithelial cells

and mesangial substance.

ii-Thickening of the basement membrane with IG-deposition

NB:

The membranoproliferative GN is classified into 3 types

according to its pathogenesis:

Type I MPGN: characterized by immune complex deposition in

glomeruli.

Type II MPGN: associated with a deficiency of the third component of

complement (C3)

Type III MPGN: is rare and has not been reported in animals.

Other Forms of GlomerulonephritisThese include:

i-Rapidly progressive glomerulonephritis,

ii-Lipoid nephrosis,

iii-Focal proliferative glomerulonephritis. These forms of glomerulonephritis have been identified in humans.

GlomerulosclerosisIt refers to a condition in which glomeruli become firm or hardened and

frequently associated with diabetes mellitus.

It includes two basic forms: i-Diffuse glomerulosclerosis.

ii-Nodular glomerulosclerosis (intercapillary glomerulosclerosis ).

NB: Glomerulosclerosis is usually accompanied by secondary tubular and

interstitial changes and therefore renal failure often develops.

Macroscopical Pictures:

i-The affected kidney is contracted and small in size.

ii-It pale or mottled and firm in consistency.

iii-The surface is irregular or nodular.

iv-The capsule is not easily detached (fragmented).

Macroscopical Pictures:

i-There is diffuse (diffuse glomerulosclerosis) thickening of the

glomerular capillary membranes or segmental (nodular

glomerulosclerosis) thickening of glomerular capillary

basement membranes.

ii-These changes tend to be obscure histologically and special

stains and ultrastructural studies are often needed to

demonstrate the lesions.

NEPHROTIC SYNDROME:

The nephrotic syndrome results from excessive glomerular

permeability of plasma proteins, mainly albumin. It occurs in

most glomerular diseases including glomerulonephritis,

glomerulosclerosis, and amyloidosis.

Clinically, there is proteinuria (albuminuria), hypoproteinemia

generalized edema, hyperlipemia, and lipiduria.

II-Diseases of Renal Tubules: Hereditary Tubular Diseases:

They include hyperuricosuria, cystinuria, renal glucosuria,

hereditary Fanconi-like syndrome, and renal glycosuria.

Tubulointerstitial Diseases:In most cases, conditions which cause tubular damage also

cause alterations in the interstitium and that affecting the

interstitium usually cause glomerular damage; hence it is

possible for an interstitial problem to cause kidney failure, renal

failure, and the nephrotic syndrome.

Interstitial NephritisIt is the inflammation of interstitial tissue of kidney and characterized by

exudative and proliferative inflammation.

Types of interstitial nephritis:

i-Non-suppurative (lymphocytic) interstitial nephritis

ii-Suppurative Interstitial nephritis

A-Non-Suppurative Interstitial Nephritis:Causes: Some generalized infections as Leptospirosis.

I-Acute Non-Suppurative Interstitial Nephritis:

Macroscopical Pictures:i-The kidneys are enlarged ii-Red or gray in color

iii-Soft in consistency iv-The capsule is easily detached

v-Grayish foci or streaks at the corticomedullary junction.

Microscopical Pictures:i-Lymphocytes, few macrophages, plasma cells and neutrophils are seen

among the renal tubules.

ii-Retrogressive changes and necrosis in the renal epithelium.

iii-Hyaline and cellular casts.

II-Subacute Non-Suppurative Interstitial Nephritis

(White Spotted Kidney):

Macroscopical Pictures:i-The kidneys are slightly atrophied

ii-Firm in consistency

iii-The capsule is easily detached or not.

iv-Grayish-white nodules on the outer medulla and

adjacent cortex.

Microscopical Pictures:i-These nodules are composed from lymphocytes with

macrophages and few fibrous tissue.

ii-In more severe cases, a few neutrophils are seen.

iii-Degenerative changes and necrosis in renal tubular

epithelium.

III-Chronic Non-Suppurative Interstitial Nephritis:

Macroscopical Pictures:i-The kidneys are small and contracted.

ii-Firm in consistency.

iii-The surface is pitted or nodular.

iv-Pale in color.

v-The capsule is not easily detached.

vi-Cut surface show cystic dilation.

Microscopical Pictures:i-Connective tissue proliferation in cortex and medulla.

ii-Periglomerular fibrosis.

iii-Lymphocytes, Plasma cells and macrophages (no

neutrophils) infiltrations.

iv-Cystic dilation of the renal tubules.

v-Sometimes, degenerative changes are seen in the renal

epithelium.

B-Suppurative Interstitial Nephritis:It is usually caused by pyogenic bacteria which may reach the

kidney via hematogenous routes (Embolic Suppurative Nephritis) or

urogenous routes (Pyelonephritis).

I-Embolic or Pyemic Suppurative Nephritis:

Macroscopical Pictures:i-Both kidneys are affected due to hematogenic route.

ii-The kidneys are large and congested with small hemorrhagic areas.

iii-Multiple grayish abscesses under the capsule and surrounded by

hyperemic zone.

iv-Cut surface show pus.

Microscopical Pictures:i-Intense collection of neutrophils in the areas of glomeruli or among and

inside the renal tubules.

ii-Liquefactive necrosis (pus) of basophilic substance, surrounded by line

of defense.

iii-The adjacent renal tubules are either collapsed or show cystic dilation.

iv-Lymphocytes and plasma cells can be seen.

v-Hyaline casts are seen inside the renal tubules.

NB: The abscesses originated in glomeruli are rounded in shape while,

these originated from intertubular capillaries are linear in shape. The

linear may extent to medulla inducing “pyelonephritis”.

II-Pyelonephritis:It is the inflammation of the renal pelvis and kidney-tissue

characterized by the formation of a purulent exudate in those areas.

(Urinogenic route and caused by Corynebactium renalis).

Macroscopical Pictures:i-One or both kidneys are involved (Urinogenic).

ii-The capsule is easily detached.

iii-Multiple grayish foci are seen on the surface surrounded by

hyperemic zone.

iv-Cut surface showed absent or necrotic papillae leaving “ulcer

like depression” in the pyramids

v-The renal pelvis may filled with pus (greenish) extend to

ureters.

vi-The whole kidney may be replaced by pus (Pyonephrosis).

Microscopical Pictures:i-Necrotic or sloughing papillae surrounded by hyperemic zone.

ii-Such zone is replaced by fibrous connective tissue Later on.

iii-Neutrophils infiltrations or aggregations on the papillae.

iv-Leukocytic infiltrations inside and around the glomeruli.

v-Basophilic material (liquefactive necrosis) are seen in the

renal pelvis surrounded by line of defense.

vi-Interlobular inflammatory edema.

vii-Cystic dilation and hyaline casts are also seen.

NB:

Nephrosis: It is non-inflammatory conditions (cloudy

swelling, vacuolar and hydropic degenerations, fatty change,

gouts, hemosiderosis,…..)

HydronephrosisIt is gradual accumulation of urine inside the renal pelvis which extend

gradually to the renal parenchyma. It may be uni- or bi-lateral types.

Causes: Incomplete (partial) or intermittent obstruction of the following:

i-One or two ureters by calculi.

ii-Urinary bladder by stones or tumors.

iii-Urethera by enlarged prostate or stones.

Macroscopical Pictures:i-The renal pelvis is distended with urine (early stage).

ii-The kidney become sac-like filled with urine (late stage).

iii-Tiny cysts appear in the medulla.

iv-Necrosis or ulceration of the wall of the renal pelvis.

Microscopical Pictures:i-Atrophy of renal tubular epithelium.

ii-The glomeruli are compressed or collapsed.

iii-Fibrous connective tissue proliferation (may be hyalinized).

iv-Cystic dilation of the renal tubules.

v-Few lymphocytes infiltrations with plasma cells and macrophages

Fate: i-Bilateral Uremia Death.

ii-Unilateral Hydronephrosis and hypertrophy of the other.

Nephrotoxic Tubular necrosis:There are many toxic substances which have some specificity for causing

damage in renal tubules. The proximal tubules are more frequently affected

because of their increased metabolic activity and their earlier exposure to

these toxins. Nephrotoxic tubular necrosis is characterized histologically by

extensive damage to proximal tubules, but with preservation of the tubular

basement membranes. In less severe cases, this allows for some regeneration

of the damaged cells.

NB:i-In severe cases, nephrotoxic tubular necrosis will lead to

glomerulonephritis or interstitial nephritis and subsequently renal

failure or kidney failure.

ii-Ischemic necrosis may accompany nephrotoxic tubular necrosis in

severe cases due to tubular swelling resulting in impaired circulation.

Examples for Nephrotoxic Substances:1-Organomercurials (Fungicide): It causes severe necrosis in proximal

tubules.

2-Chlorinated Naphthalenes: It causes necrosis of renal tubular

epithelial cells and hyperkeratosis in esophagus of cattle.

3-Aminoglycosides (Drugs): It excreted by glomerular filtration and

they tend to accumulate in proximal tubular epithelial cells inducing its

damage. Polyuria, proteinuria, hematuria and azotemia are clinically seen.

4-Tetracyclines: It causes acute renal tubular necrosis has been reported

due to overdoses of tetracycline.

5-Sulfonamides: Excessive intake of sulfonamide medication may cause

nephrotoxic tubular necrosis. Animal on sulfonamide therapy should have

unlimited access to drinking water.

6-Mycotoxins: Aspergillus and Penicillium produce a variety of

nephrotoxic mycotoxins, including ochratoxins, citrinin, oxalate, and

viridicatum toxin.

7-Oak Poisoning: It has been reported in ruminants and horses and

develops following ingestion of acorns, leaves, or buds of oak shrubs.

Gross findings include perirenal edema and hemorrhage, swollen pale

kidneys, and petechial hemorrhages throughout the renal cortex.

8- Heavy metal toxicity : Heavy metal toxicity causes glucosuria and

aminoaciduria due to tubular degeneration.

Urolithiasis (Nephrolithiasis): Lith = Stone.

Factors important in formation of calculi:i-Presence of nidus (desquamated epithelium, leukocytes or organic ppt).

ii-Presence of crystals in urine as oxalate, phosphate and magnesium.

iii-Vitamin A deficiency epithelial metaplasia nidus formation

iv-Metabolic defect in uric acid metabolism uric acid calculi

v-Grazing on estrogenic plants causing calculi (epithelial

metaplasia)

vi-Hyperparathyroidism (increase calcium and phosphorus)

vii-Urinary pH, reduced water intake, bacterial infection.

Characters and nature of calculi:i-Calculi are a visible aggregation of precipitated urinary solutes, mainly

minerals mixed with urinary proteins and proteinaceous debris

ii-They are hard spheres or ovoid with central nidus surrounded with

concentric laminate.

iii-Large renal pelvic calculi take the shape of staghorn appearance

because it takes the shape of renal calyces.

iv-Urinary bladder calculi can be single or multiple, variable in size

and some time composed of sand like material.

v-Calculi may have smooth or rough surface; and may be solid, soft

or friable. Their color may be gray, white, brown and yellow depend

on their composition.

vi-Small calculi may be voided in the urine, but typically calculi

cause urinary obstruction which is more common in male due to

long and narrow diameter urethra.

vii-The chemical composition of calculi are varies greatly according

to animal species.

In herbivorous animals, the calculi mainly formed from silicate

which is rarely conjugated with phosphates, carbonate or oxalates of

calcium and magnesium due to the alkaline pH of urine. Because of

the acidic urine in carnivorous and omnivorous animals, the calculi

is chiefly formed from calcium oxalate which is very hard and sharp

edges causing damage to urinary epithelium.

Effect of calculi:Calculi produce mechanical irritation to the urinary epithelium, partial

obstruction lead to hydronephrosis and complete obstruction leading to

uremia.

Organ : Kidney.

Disease : Nephrolithiasis.

Macro : Irregular hard stone in the renal pelvis.

Organ : Kidney.

Disease : Nephrolithiasis.

Macro : Staghorn Calculus.

Inflammation of The Lower Urinary Tract:Pyelitis: It is the inflammation of the renal pelvis.

Ureteritis: It is the inflammation of the ureter.

Cystitis: It is the inflammation of the urinary bladder.

Uretheritis: It is the inflammation of the urethera.

Types of Cystitis: I-Acute Cystitis: it includes

Catarrhal

Fibrinous

Purulent

Hemorrhagic

II-Chronic Cystitis: it includes

Catarrhal

Polypoid (in cattle).

Follicular (in dogs)

Parasitic Lesions:Stephanurus Dentatus: Adult worms are found encysted in the perirenal fat

and their cysts communicate with the renal pelvis of swine.

Dioctophyma Renale: It is reported in dogs, mink, cats, and other fish eating

mammals (giant kidney worm).

Capillaria Spp.: It reports in renal pelvis, ureters and urinary bladder of dog,

cat and mink.

Klossiella Equi: Klossiella equi is a sporozoan parasite of the kidneys of

equidae.

Renal Neoplasia:I-Primary Neoplasm: They are rare and include renal adenomas, renal

carcinomas, nephroblastoma, transitional cell papilloma, transitional cell

carcinoma, fibroma, fibrosarcoma, hemangioma, and hemangiosarcoma.

II-Secondary Neoplasm: They are due to spread of some malignant tumors as

lymphosarcoma.

Neoplasms of bladder

Secondary tumors: are rare.

Primary tumors are frequent.

Epithelial tumors are common either benign or malignant and

leiomyomas is also recorded.