Department of Pathology, Faculty of Veterinary Pathology, Zagazig University, Egypt.
Pathology of Urinary System BY Prof. Dr. Mohamed Hamed Mohamed mohamedelariny@yahoo.com +201224067373
2012
Urinary System General 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, 25dihydroxycholecalciferol.
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 CYSTS They 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).
Summary of pathognomonic lesions of uremia and its mechanisms.
Lesion of Uremia
Mechanism
1-Pulmonary edema and Fibrinous 1-Increased vascular permeability pericarditis 2-Ulcerative stomatitis and gastritis 2-Ammonia secretion and vascular
necrosis 3-Atrial and aortic thrombosis
3-Endothelial and subendothelial damage
4-Hypoplastic or aplastic anemia
4-Increases erythrocytes fragility and lack of erythropoietin production
5-Soft tissue mineralization
5-Altered Ca and phosphorus
metabolism
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 nephritis According 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 Glomerulonephritis These include: i-Rapidly progressive glomerulonephritis, ii-Lipoid nephrosis, iii-Focal proliferative glomerulonephritis. These forms of glomerulonephritis have been identified in humans.
Glomerulosclerosis It 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 Nephritis It 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,‌..)
Hydronephrosis It 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 ii-Unilateral
Uremia Death. 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.