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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.
Abnormalities in the urinary system can occur in various forms, including anomalies in development, hereditary problems, circulatory disturbances, infections, toxicoses and immune-mediated diseases. Kidney infections have been associated with viral and bacterial as well as parasitic organisms. Also, various toxins have been incriminated as the cause of nephrotoxicoses. The various abnormalities are manifested in many forms such as agenesis, hypoplasia, malpositioning, dysplasia, atrophy, cyst formation, hemorrhage, necrosis and inflammation.
Kidneys are retroperitoneal abdominal organs and, as with many other organs in the body, they have an outer cortical region and an inner medullary region. They 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 cattle, this lobulation also affects the cortex and causes a distinct external lobular appearance of the entire kidney. This has been referred to as persistence of fetal lobulation and is also seen normally in a few other mammalian species, including polar bears and otters. Kidneys in sub-mammalian species of animals, including birds, tend to be less distinctly structured and can also be described as being lobulated. In multilobular kidneys, the tips of the medullary pyramids are referred to as medullary papillae and each papillae 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 a crest-like papillae (the medullary crest) into one structure which is probably best considered to be the renal pelvis. This structure then continues into the ureter.
There are a few other species related idiosyncracies that need be considered. Cats have subcapsular blood vessels which are quite obvious grossly. Compound papillae are found at the poles of the kidneys in swine, and theoretically, compound papillae are more susceptible to ascending infections. In cattle, the major calyces join directly to the ureter without forming a pelvis.
The basic functional unit of the kidney is the nephron. It consists of the renal corpuscle, the proximal tubule, the loop of Henle, and the distal tubule. The renal corpuscle is comprised of the Bowman's Capsule and the glomerulus. There are usually about 400,000 nephrons in the average canine kidney.
An arteriolar portal system exists in the kidneys, consisting of the glomeruli being situated between the afferent and the efferent arterioles. The glomeruli function as primary filters through which an ultrafiltrate of plasma, containing only trace amounts of proteins, passes into the Bowman's space. The proximal tubules are responsible for reabsorption of nutrients and other substances which the body needs to retain. The loops of Henle serve as a countercurrent multiplier system which concentrates and then dilutes the filtrate and in doing so creates a hyperosmotic state in the medulla. The distal convoluted tubule, influenced by the presence or lack of antidiuretic hormone, either allows the filtrate to pass from the nephron in its diluted state or concentrates the filtrate by allowing water to be reabsorbed. The collecting tubules are not a part of the nephron but they (also under the influence of ADH) continue to either concentrate the urine or allow for its passage in a dilute form.
Renal circulation begins at the renal artery which enters the kidney at the hilus. The renal artery divides, within the region corresponding to the renal pelvis, in to interlobar arteries which then give rise to the arcuate arteries at the corticomedullary junction. Branches of the arcuate arteries radiate into the cortex giving rise to branches called the interlobular arteries which then arborize to form the afferent arterioles. The afferent arterioles enter the renal corpuscle emptying blood into the glomerulus. The efferent arteriole carries blood away from the glomerulus and to the peritubular capillaries. Venules from the peritubular capillaries join to eventually form the renal vein which leaves the kidney at the hilus.
The remainder of the urinary system serves for transport and/or storage of urine and include the ureters, the urinary bladder, and the urethra. The ureter is a fibromuscular tube which conveys urine from the kidney to the bladder. Normally, there is one ureter for each kidney and it too has a retroperitoneal disposition. The urinary bladder is a muscular, membranous, distensible reservoir for urine which it receives via the ureters and which it expels via the urethra.
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 case the they 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. Except in cattle and in cats the subcapsular cortical surface should be relatively smooth. In cattle, the overall surface of the kidney is irregular due to the persistence of fetal lobulation; however, the subcapsular surface of individual lobules is relatively smooth. In cats, the subcapsular blood vessels are responsible for a somewhat irregular surface in the kidneys. The ratio of the thickness of the cortex to the medulla is usually 1:2 or 1:3; however, the cortex is actually a far greater overall percentage of the kidney parenchyma. Removal of the capsule is essential in an examination of the kidney. It should pull away from the cortex with minimal resistance. In cattle, again due to the lobulation of the kidney, this procedure tends to be more difficult; however, removing the capsule from individual lobes should offer minimal resistance. If while removing the capsule, there is a tendency for cortical parenchyma to also tear away, this may be indicative of fibrous adhesions except in the horse, in which case trabeculae are normally present attaching the cortical parenchyma to the capsule.
A complete lack of renal tissue is referred to as agenesis or aplasia. It may be unilateral or bilateral but bilateral renal aplasia is inconsistent with postnatal life and is only found in aborted fetuses or stillborn animals. Unilateral renal aplasia is compatible with normal life if the other kidney is normal. There is usually a compensatory hypertrophy of the contralateral kidney in these cases. Often, a contralateral dysplasia or hypoplasia accompanies a unilateral renal aplasia, in which case the affected animal will eventually succumb to renal failure. Renal aplasia is rare in all species except in some beagles and Doberman pinschers where there is an increased familial incidence.
The failure of a kidney to develop its normal parenchymatous volume is referred to as renal hypoplasia. This lack of development results is the formation of a kidney that is abnormally small. Hypoplasia of the kidneys may also be unilateral or bilateral. In cases of unilateral hypoplasia, there is usually a compensatory hypertrophy of the contralateral kidney and the individuals often live normal lifespans. In cases of bilateral hypoplasia, the affected animals usually develop renal failure at some point and die. True renal hypoplasia is rare and many of the reported cases actually represent cases of renal dysplasia or renal atrophy or of some other acquired renal damage with scarring.
Grossly, the hypoplastic kidney is smaller than normal, and the reduction in size tends to be fairly uniform. In externally lobulated kidneys, such as in cattle, it may be more severe in certain lobules and therefore affected kidneys may be irregular in shape. The capsule is usually thickened and it is often adhered to the cortex. The parenchyma is usually grayish in color and tends to be firm. On cut surface, a reduction in parenchymal volume is evident in the cortex and the medulla; however, the cortex often seems to be more severely affected than the medulla but this is usually a visual artifact.Microscopically, there is a reduction in the number of nephrons. This is evident in that there are fewer glomeruli than normal. The remaining nephrons are usually hypertrophic. The tubules in the medulla are often dilated and their epithelial cells are flattened. Also, there is usually considerable interstitial fibrosis which causes separation of the tubules.
Malposition of the kidney is rare in animals but is most frequently reported in swine. It may be unilateral or bilateral. Malpositioned kidneys are most commonly displaced caudally, with the kidneys assuming a pelvic or inguinal disposition. In these cases the renal arteries usually arise from the terminal aorta near its bifurcation and the ureters are correspondingly shortened. They often have kinks which predispose affected kidneys to develop hydronephrosis. Malpositioned kidneys are usually otherwise normal. Malposition of the kidneys in swine may be associated with vitamin A deficiency in sows.
Persistence of fetal lobulation occurs due to a failure of fusion of individual renal segments. As noted previously, it is a normal finding in cattle, polar bears, and otters. This also occurs abnormally with greater frequency in swine and again has been associated with vitamin A deficiency.
This anomaly has been reported in each of the domestic species. 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. These kidneys tend to function normally.
Renal dysplasia is disorganized development of the renal parenchyma due to anomalous differentiation. It is usually a congenital alteration; however, in some species (e.g. cats, dogs, and pigs) it may develop in the early neonatal period. It may occur unilaterally or bilaterally and its existence may be evident grossly and/or histologically.
Grossly, affected kidneys are usually smaller than normal. This accounts for the frequent misdiagnosis of this condition as hypoplasia. They are usually misshapen and fibrosed and they often contain thick-walled cysts. Their ureters are usually tortuous and dilated.Histologically, any number of developmental anomalies may be evident. These often include: immature glomeruli in adolescent or adult kidneys, collecting tubules ending blindly, or primitive ducts surrounded by concentric layers of mesenchym
Renal cysts are thin-walled fluid filled structures which develop in the renal parenchyma. They vary in size from barely visible to very large, often exceeding the size of the affected kidney. They may be solitary or multiple. Most often, they are a congenital anomaly; however, some develop postnatally. They have been reported in all species but they seem to occur most commonly in swine. Renal cysts can arise in any part of the nephron or in collecting tubules and most congenital cysts are not caused by an obstructive lesion. There may be some association between renal dysplasia and the formation of renal cysts because most dysplastic kidneys also have cysts. 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.
Various familiar renal diseases have been reported in animals. These include familial glomerulonephritis (reported in numerous breeds of dogs), progressive renal fibrosis (reported in mutant Southdown sheep), and 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 of some other etiology. Other than the juvenile nature of these diseases, they are similar clinically to other diseases causing renal failure and the gross and histologic features do not provide distinguishing characteristics. Care must be exercised not to diagnose an acquired condition as a familial problem or vice versa.
Renal failure refers to the condition resulting from suboptimal renal function. Azotemia/uremia are characteristic features of renal failure and the symptoms include tiredness, nausea, vomiting, pruritis and twitching. Renal failure may develop acutely (develops in minutes, hours, or a few days), in which case it may be reversible. Chronic renal failure develops over a longer period of time and usually progresses to terminal stages. Certain conditions involve kidney failure, such as diabetes insipidus due to tubular insensitivity to ADH, but these conditions lack the characteristic azotemia/uremia and are not true renal failure. Renal failure may result from decreased perfusion of the kidneys, as often occurs in shock, but usually it is due to decreased functional parenchyma of the kidneys.
Renal failure is characteristically accompanied by uremia which is associated with various changes. In addition, renal failure is usually accompanied by loss of sodium homeostasis resulting in either dehydration or over hydration depending on sodium intake. Renal failure will also lead to metabolic acidosis and to hyperparathyroidism. As renal mass shrinks, phosphorus retention
occurs causing a drop in the concentration of ionized calcium. This stimulates the parathyroid gland to release parathormone which attempts to correct the deficit involving ionized calcium. This renal secondary hyperparathyroidism will eventually result in a renal secondary osteodystrophy and metastatic mineralization. The metastatic mineralization is often referred to as "uremic frosting".
Hyperemia of the kidney may be active or passive in nature. Active hyperemia is seen in acute nephritis and in acute septicemias and bacterial intoxications. In either case, the kidney will be swollen and uniformly dark grossly. Microscopically, all vessels, especially capillaries, are dilated and engorged with blood.
Hemorrhage refers to the escape of blood from its normal vascular channels. In the kidney, it is not uncommon and occurs frequently with a variety of bacteremias and viremias. Petechia in the kidneys are a common finding in piglets dead of any cause and they probably represent an agonal change. Pinpoint hemorrhages occur beneath the capsule in hog cholera and in porcine salmonellosis. This is responsible for the appearance that is described as a "turkey egg kidney".
An infarct is an area of necrosis in an organ or tissue resulting from obstruction of the local circulation. This most often is due to thrombosis or embolism of the afferent vessel for the organ. Kidneys require a continuous flow of large volumes of blood and thus they are easily infarcted. The sequelae to infarction of the kidney depend on the nature of the infarcting material. If the obstructing material is nonseptic, typical infarcts are formed. If the obstructing material is septic, abscesses may develop. Occlusion of a renal artery will cause infarction of the entire kidney; but, infarction of a branch of the renal artery will cause infarction of the corresponding region of the kidney. Most renal infarcts involve the interlobular arteries and result in a pyramid-shaped area of necrosis in the cortex of the kidney.
Renal cortical necrosis and acute tubular necrosis are discussed together. The two conditions are quite similar, differing primarily in the size of the affected areas. In acute tubular necrosis, the individual lesions tend to be small and patchy, affecting only a few tubules. In renal cortical necrosis, the necrotic foci tend to involve larger cortical areas and result in necrosis of tubules and glomeruli. These lesions occur infrequently in animals but either may be severe enough to cause renal failure and death. Various mechanisms are incriminated in the different species; however, it is probable that these lesions result from ischemia. The ischemia may be due to decreased perfusion of the cortex (as in hypotension) or a generalized Shwartzmann reaction with disseminated intravascular coagulation (DIC). Any mechanism that might initiate a generalized Shwartzmann reaction (e.g. endotoxemic mastitis or metritis or endotoxic gastrointestinal diseases) could be responsible.
Grossly, the lesions tend to be variable, probably depending on the severity, the distribution, the duration, and the quality of the reflow to the area. In acute tubular necrosis, the cortices are finely mottled by either reddish or yellowish foci. These constitute hemorrhagic or necrotic foci respectively and represent varying stages in the development of the lesion. In renal cortical necrosis, the entire cortex may be affected or the lesion may be patchy. When the lesions are patchy, they tend to resemble infarcts. Affected areas are pale, slightly swollen, and sharply demarcated from the medulla.Histologically, there is irregular necrosis of the cortex of the kidney. In acute tubular necrosis, the necrosis is limited to small foci involving only a few tubules. The necrosis results in disruption of the basement membranes of the tubules and usually tubular casts develop in collecting tubules. In renal cortical necrosis, various patterns of infarction may be seen, causing necrosis of tubules and glomeruli in affected areas in the cortex.
Under certain circumstances, renal medullary necrosis occurs as the primary manifestation of renal disease. The mechanism for this is poorly understood, but it seems to involve a vascular change. In cases where venous return from the kidneys is obstructed, the medulla tends to be more devastated. This is because the elevated intrarenal pressure maintains the patency of the cortical vessels but not the medullary vessels causing medullary infarction. Also, prostaglandin synthetase is found, in the kidney, primarily in the medulla, and inhibition of this enzyme results in decreased production of PGE2 and loss of its vasodilatory effects on juxtamedullary arterioles. This sequence has been incriminated in the development of renal papillary necrosis associated with analgesic therapy "analgesic nephropathy". Papillary or medullary crest necrosis is also associated with urinary obstruction and pyelonephritis. Sequelae to medullary necrosis are due primarily to loss of ability to concentrate urine and include renal failure and uremia.
Grossly, there is considerable variation depending on the extent and the stage of development of the lesion. Acute infarction may be an agonal change in cases of severe dehydration and electrolyte imbalances due to neonatal diarrhea. Massive medullary necrosis would undoubtedly lead to renal failure and possibly death. If the medullary necrosis is not severe enough to cause death, scarring of the medulla occurs. The necrotic portion of the medulla may slough and lodge in the renal pelvis eventually becoming mineralized.Microscopically, the lesions range from areas of coagulative necrosis with hemorrhage in early lesions to areas of connective tissue scarring in healed lesions.
Renal involvement is almost always a feature of systemic amyloidosis.
Grossly, affected kidneys are slightly enlarged and the cortical parenchyma tends to be pale and slightly firm in consistency. In cattle, affected kidneys are markedly enlarged and finely stippled due to the presence of pale spots (affected glomeruli) and grayish translucent spots (dilated tubules).Histologically, most of the glomeruli in affected kidneys are enlarged and their architecture is almost completely destroyed by accumulations of a finely granular or homogeneous, eosinophilic material (amyloid) in glomerular capillaries. In cats, amyloidosis primarily involves the medulla, with amyloid deposits occurring in the interstitium of the medulla.
Inflammation primarily of the glomerular tuft is called glomerulonephritis. Involvement may be limited to a few glomeruli, in which case it would be considered multifocal, or nearly all of the glomeruli may be involved, in which case it would be considered generalized. The term diffuse is reserved for use indicating involvement of the entire glomerulus in contrast to segmental involvement. In addition, acute and chronic stages of glomerulonephritis are described. In most cases, there are secondary changes involving tubules and the interstitium and sometimes blood vessels. In the absence of secondary lesions, the term glomerulitis is preferred.
Clinically, there is minimal variety in the manifestations of renal disease. Simple glomerulitis would be manifested primarily by proteinuria but glomerulitis is virtually always accompanied by secondary changes which in turn cause renal failure. Hematuria, proteinuria, oliguria, hyposthenuria, and azotemia occur in glomerulonephritis and proteinuria, occurring in the absence of urinary tract inflammation, is particularly indicative of glomerular disease. The proteinuria is caused by increased permeability of glomerular membranes and is seen in glomerulonephritis as well as glomerular amyloidosis. Most of the filtered protein will be albumin and this results in hypoalbuminemia. Eventually, this will lead to the "nephrotic syndrome" which is characterized by hypoalbuminemia, generalized edema, and hypercholesterolemia. Several distinct inflammatory conditions involving the glomerulus are recognized in animals.
6.7.2.1 ACUTE PROLIFERATIVE GLOMERULONEPHRITIS
Acute proliferative glomerulonephritis is a clinical syndrome with characteristic inflammatory lesions involving glomeruli that has been reported in children and animals. In humans, particularly children, the disease is frequently associated with an acute upper respiratory infection which it tends to follow at about a 2 week interval. It is characterized by sudden onset, fever, nausea, weakness, subcutaneous edema, and excretion of brownish or bloody urine.
Poststreptococcal glomerulonephritis, in humans, is an immunologically mediated disease and it is associated with certain specific strains of streptococci. This explains the 2 week incubation period, which is the time needed for sufficient antibody production.
Grossly, the kidneys are enlarged and pale and petechial hemorrhages tend to outline glomeruli.Histologically, there is enlargement of the glomerular tufts with increased numbers of endothelial cells filling the Bowman's spaces. In early stages, neutrophils appear in glomeruli but as the disease progresses, there is proliferation of epithelial cells in the visceral layer of the Bowman's capsule and adhesions often develop between the parietal and visceral layers. These eventually form the epithelial "crescents" seen in the subacute and chronic forms. Thrombosis and necrosis of glomerular capillaries may occur with subsequent hemorrhage into the renal corpuscle.
6.7.2.2 MEMBRANOUS GLOMERULONEPHRITIS
The pathogenesis for the development of membranous glomerulonephritis involves an immunologic process in which immunoglobulins or antigen-antibody complexes are deposited in the glomerular basement membrane. The inciting antigens may be exogenous, as in serum sickness, or endogenous, as in systemic lupus erythematosis. The symptomatology will include the typical findings of a glomerulonephritis as well as the clinical features of the inciting disease problem. Hypergammaglobulinemia is frequently reported in these cases.
Grossly, affected kidneys are enlarged and pale due primarily to fatty change in renal tubular epithelial cells and edema of the interstitium. In the latter stages of the disease, the kidney may become shrunken and fibrotic.Histologically, there is thickening, splitting, and reduplication of the glomerular basement membrane, loss of the foot processes of the podocytes (epithelial cells of the visceral layer of the Bowman's capsule), and swelling and fatty change of glomerular epithelial cells.
6.7.2.3 MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
Membranoproliferative glomerulonephritis (MPGN) is characterized by alterations in the basement membranes as well as proliferation of mesangial and parietal epithelial cells of the Bowman's capsule. Because the proliferation primarily involves the mesangium, this lesion is also referred to as mesangiocapillary glomerulonephritis. Several forms of membranoproliferative glomerulonephritis have been reported in the human literature including types I, II, and III. The pathogenesis of the three types seems variable. Type I MPGN is usually characterized by immune complex deposition in glomeruli. Type II is usually associated with a deficiency of the third component of complement (C3). This may be an inherited or an acquired problem and in the case of the acquired form, it may be autoimmune in nature. Type III is rare and has not been reported in animals.
An autosomal recessive inherited version of MPGN has been reported in Finnish Landrace sheep. This genetic defect is characterized by a deficiency of C3 and affected lambs begin to develop glomerular lesions in utero.
Clinically, affected lambs seem normal at birth but die at about 3 months of age due to renal failure.Grossly, the kidneys tend to be enlarged and their cortices are pale. Small red spots, representing enlarged glomeruli, are visible throughout the cortices of affected kidneys.
Histologically, the glomeruli are enlarged and hypercellular with most of the increase in cellularity due to proliferation of mesangial cells. In addition, there is uneven thickening of the glomerular capillary basement membranes with peripheral portions of the glomerulus more severely affected.
Membranoproliferative glomerulonephritis tends to be unremitting and it usually progress to chronic renal failure.
6.7.2.4 CHRONIC GLOMERULONEPHRITIS
Chronic glomerulonephritis is best considered a common end-stage finding for the various forms of glomerulonephritis previously described in this section. Occasionally, it is reported with no documented anteceding renal problem, but in most cases chronic glomerulonephritis is preceded by an acute or subacute, proliferative or membranous glomerular problem.
Grossly, affected kidneys are smaller than normal and have a rough or pitted contour. They are usually firm and they tend to be difficult to incise. The cut surface tends to be coarse, granular, and/or cystic.Histologically, the glomeruli are enlarged and hypercellular with most of the increased cellularity due to proliferation of mesangial and endothelial cells. Many of the glomerular capillary lumens are occluded and the visceral layer of the Bowman's capsule is adhered to the parietal layer in many renal corpuscles. In advanced stages, glomeruli are often obliterated and replaced by hyaline connective tissue. Decreased blood flow through glomeruli results in decreased perfusion of the tubules and leads to tubular nephrosis and interstitial fibrosis. Crescent formation may be evident in many renal corpuscles causing collapse of the glomeruli. (Crescent formation is a hallmark of severe glomerular damage and probably arises due to proliferation of parietal cells of the Bowman's capsule.)
6.7.2.5 OTHER FORMS OF GLOMERULONEPHRITIS
Several other forms of glomerulonephritis have been identified in humans but counterparts for these diseases have not received much notoriety in the veterinary literature. These include: rapidly progressive glomerulonephritis, lipoid nephrosis, and focal proliferative glomerulonephritis.
Glomerulosclerosis refers to a condition in which glomeruli become firm or hardened. Glomerulosclerosis is most frequently found in association with diabetes mellitus and the mechanism for its development is uncertain. There are two basic forms of glomerulosclerosis which are diffuse glomerulosclerosis and nodular glomerulosclerosis. Nodular glomerulosclerosis is also known as intercapillary glomerulosclerosis or Kimmelstiel-Wilson disease. Glomerulosclerosis is usually accompanied by secondary tubular and interstitial changes and therefore renal failure often develops. The clinical features are similar to those of glomerulonephritis and are accompanied by the features of diabetes mellitus.
There is considerable variation in the gross appearance of affected kidneys depending largely on the duration of the problem and the extent of the secondary changes. Severely affected kidneys are smaller than normal and usually have an irregular or nodular contour. They tend to be pale and firm and the cut surface tends to be mottled.
Histologically, there is diffuse (diffuse glomerulosclerosis) thickening of the glomerular capillary membranes or segmental (nodular glomerulosclerosis) thickening of glomerular capillary basement membranes. These changes tend to be obscure histologically and special stains and ultrastructural studies are often need to demonstrate the lesions.
The nephrotic syndrome results from excessive glomerular permeability tp plasma proteins, mainly albumin. It occurs most glomerular diseases including glomerulonephritis, glomerulo-sclerosis, and amyloidosis. Clinically, there is proteinuria (principally albuminuria), hypoproteinemia (principally hypoalbuminemia), generalized edema, hyperlipemia, and lipiduria.
Diseases affecting renal tubules are primarily reflected in morphologic changes in the tubular epithelial cells; however, some defects caused by enzymatic deletions may not have morphologic representation. In should be noted that renal tubules and the interstitium are closely related, and defects involving one tend to cause problems in the other. Regeneration of tubular epithelium can occur, if the basement membranes are preserved, but because postnatal development of new nephrons is either nonexistent or limited to early neonatal periods in a few species, the response of the kidney to injury is limited to hypertrophy of existing nephrons.
Renal tubular epithelial cells suffer from degenerative changes similarly to many other cell types. These changes may be manifested as cellular swelling, hydropic degeneration, and/or fatty change. Various types of inclusion bodies are reported in renal tubular epithelial cells. These include viral inclusions, inclusions of unknown origin, and inclusions from accumulation of material from the ultrafiltrate.
Some conditions are characterized by thickening of the tubular basement membranes. In renal amyloidosis, amyloid is deposited in tubular basement membranes as well as in glomeruli. This is especially true of renal amyloidosis in cats, in which case, amyloid deposits are more severe in tubular basement membranes and in the interstitium.
Acute tubular necrosis was discussed with renal cortical 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, which are usually found in the ultrafiltrate. 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. Ischemic necrosis may accompany nephrotoxic tubular necrosis in severe cases due to tubular swelling resulting in impaired circulation. In severe cases, nephrotoxic tubular necrosis will lead to glomerulonephritis or intersititial nephritis and subsequently renal failure or kidney failure. The pathogenesis of renal failure in acute tubular necrosis is uncertain. It probably involves leakage of tubular contents into the interstitium and subsequent interference with blood flow to the nephron, because as regeneration of the tubular epithelium takes place, in less severe cases, azotemia subsides. Examples of substances which cause nephrotoxic tubular necrosis include:
6.8.2.1 ORGANOMERCURIALS
Organomercurials were commonly used as a fungicide for various grains and were inadvertently fed to animals and humans. These compounds caused severe necrosis in proximal tubules. They have been banned in many countries, including the U.S.
6.8.2.2 CHLORINATED NAPHTHALENES
Chlorinated naphthalenes, which also cause specific hyperkeratosis in cattle, cause necrosis of renal tubular epithelial cells. These compounds have also been excluded from use in the farm environment.
6.8.2.3 AMINOGLYCOSIDES
This group of compounds includes several drugs which are excreted primarily by glomerular filtration and they tend to accumulate in proximal tubular epithelial cells. Neomycin, kanamycin, gentamycin, streptomycin, and tobramycin are all nephrotoxic. The damage is dose related and may be exacerbated by preexisting renal disease. Clinical signs are typical of renal failure and they include inability to concentrate urine, polyuria, proteinuria, hematuria and azotemia. Regenerated tubular epithelial cells appear to be less susceptible to injury by aminoglycosides.
6.8.2.4 TETRACYCLINES
Tetracyclines have been associated with several nephrotoxic syndromes in humans and animals. In dogs, acute renal tubular necrosis has been reported due to overdoses of tetracycline. Degradation products in outdated tetracycline have been incriminated in the pathogenesis of acute nephrosis in calves. Tetracycline use is contraindicated in any animal experiencing renal dysfunction.
6.8.2.5 SULFONAMIDES
Excessive intake of sulfonamide medication may cause nephrotoxic tubular necrosis. This is especially likely in dehydrated animals. Earlier sulfonamide compounds were more likely to cause this nephrotoxicosis because newer formulations tend to be less toxic. Animal on sulfonamide therapy should have unlimited access to drinking water.
6.8.2.6 AMPHOTERACIN B
Amphoteracin B is an antifungal agent whose most important toxic side effect is nephrotoxicity. It causes decreased renal blood flow and glomerular filtration due to renal vasoconstriction. In addition, it causes necrosis of proximal and distal tubular epithelial cells.
6.8.2.7 ETHYLENE GLYCOL
Ethylene glycol is used as antifreeze for automotive cooling systems. It has a sweet taste and is voluntarily ingested by animals. The primary toxic metabolite of ethylene glycol is glycolic acid which is formed by oxidation of glycoaldehyde, another metabolite of ethylene glycol. Clinically, animals suffering from antifreeze poisoning have central nervous system signs initially and after a few day they develop acute renal failure. The renal lesions are most severe in the tubules where various metabolites of ethylene glycol cause severe tubular necrosis. Tubular lesions range from hydropic degeneration to necrosis to regeneration and the most striking histologic finding is the presence of calcium oxalate crystals in tubules and in the interstitium. These crystals tend to be yellowish in color and are usually arranged in sheaves or prisms. They are birefringent in polarized light.
6.8.2.8 OXALATES
Plants are the usual source of oxalate poisoning in animals which is more frequently reported in sheep and cattle. Plants which contain high concentrations of oxalate include: Halogeton glomeratus (halogeton), Sarcobatus vermiculatus (greasewood), Rheum rhaponticum (rhubarb), Oxalis cernua (soursob), Rumex spp. (sorrel) and a few others of less importance. Following absorption, the oxalates combine with calcium and form calcium oxalate which crystalizes in vessel walls and in renal tubules. The calcium oxalate crystals, when they form in renal tubules, cause acute renal failure.
6.8.2.9 MYCOTOXIN
Aspergillus and Penicillium produce a variety of nephrotoxic mycotoxins, including ochratoxins, citrinin, oxalate, and viridicatum toxin. These toxins may be found contaminating feed grains. Of these ochratoxin is the only one associated with clinical disease and it is characterized by tubular degeneration and atrophy, with cortical interstitial fibrosis and glomerular hyalinosis. Acute renal changes are rare but they resemble the lesions of pigweed toxicosis, e.g. perirenal edema and hemorrhage.
6.8.2.10 AMARANTHUS RETROFLEXUS
Amarathus retroflexus is commonly known as redroot pigweed. Ingestion of this plant causes perirenal edema and hemorrhage and acute renal failure due to toxic nephrosis. Pigweed toxicosis occurs more frequently in cattle and swine and is reported occasionally in horses. Gross lesions include perirenal edema and hemorrhage which may be accompanied by ascites as well as edema of other abdominal organs. Histologically, there is degeneration and coagulative necrosis of renal tubular epithelial cells. Sometimes this is accompanied by mild glomerular injury with hypercellularity.
6.8.2.11 OAK POISONING
Oak poisoning has been reported in ruminants and horses and develops following ingestion of acorns, leaves, or buds of oak shrubs. The toxic substances in oak related materials are tannins. Most animals ingesting oak materials merely develop simple indigestion but a few develop gastroenteritis and acute tubular necrosis. Gross findings include perirenal edema and hemorrhage, swollen pale kidneys, and petechial hemorrhages throughout the renal cortex. In less severe cases, the animal may recover but in severe cases, the renal damage progresses to a terminal chronic renal disease.
6.8.2.12 HEAVY METAL TOXICITY
Heavy metal toxicity causes glucosuria and aminoaciduria due to tubular degeneration.
Nephrogenic diabetes insipidus has been reported in several breeds of dogs. It is characterized by polyuria, polydipsia, and hyposthenuria and an unresponsiveness to water deprivation, exogenous ADH, or infusion of hypertonic saline. The basic defect involves a lack of responsiveness of cells of the distal tubules and the collecting tubules to ADH. The condition may be congenital or acquired. Acquired cases usually develop from tubulointerstitial diseases such as pyelonephritis.
Several hereditary renal tubular defects have been reported. These include hyperuricosuria in Dalmations, essential cystinuria in Basenjis, renal glucosuria in various breeds, hereditary Fanconi-like syndrome in Basenjis, and renal glycosuria in Norwegian Elkhounds.
In most cases, conditions which cause tubular damage also cause alterations in the interstitium as well, therefore there is considerable overlap conditions in this category and those in the "Diseases of Renal Tubules". Also, conditions 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.
Nonsuppurative interstitial nephritis refers to an inflammatory condition involving primarily the interstitium of the kidney. The causes are not usually identified, especially in chronic cases, and they probably vary considerably. It may be acute or chronic and multifocal or generalized. Acute cases are characterized by sudden onset and histologically there is edema and accumulations of leukocytes in the interstitium and focal tubular necrosis. In chronic cases, mononuclear cell infiltration and connective tissue proliferation in the interstitium are the dominant histopathologic features. Likely pathogens for nonsuppurative interstitial nephritis include Leptospira canicola, Leptospira ictero-hemorrhagiae, canine adenovirus-I and Encephalitozoon cuniculi in dogs and Leptospira pomona in cattle and swine. It has also been reported in "white-spotted kidney" of calves, malignant catarrhal fever in cattle, theileriosis in cattle, "lumpy-skin disease" in cattle, sheeppox in sheep and in equine infectious anemia in horses.
Suppurative interstitial nephritis refers to a pyogenic inflammatory condition involving primarily the interstitium of the kidney. It is usually caused by pyogenic bacteria which may reach the kidney via hematogenous routes (usually resulting in embolic suppurative nephritis) or urogenous routes (usually resulting in pyelonephritis).
Embolic suppurative nephritis usually develops when bacteria are seeded into the kidney parenchyma, either during a bacteremia or in septic emboli. The most common cause of embolic suppurative nephritis in horses is Actinobacillus Equuli. Typically, infection by this agent occurs primarily in neonates. It probably represents an umbilical infection and it is acquired either in utero, during parturition, or shortly after birth. Abscesses, which sometimes are as much as 3mm in diameter, are found throughout the renal parenchyma. These are usually evident grossly and microscopically. The most common cause of embolic suppurative nephritis in swine is probably Erysipelothrix rhusiopathiae. The most common cause in adult cattle is probably Corynebacterium pyogenes.
Pyelonephritis refers to inflammation of the renal pelvis and renal parenchyma characterized by the formation of a purulent exudate in those areas. It usually develops from an ascending infection and is usually accompanied by ureteritis and cystitis. The most common pathogens are E. coli., staphylococci, streptococci, Enterobacter, Proteus, Pseudomonas, Corynebacterium renale, and Corynebacterium suis. These bacteria are carried up the urinary tract, retrograde to the flow of urine. They may be carried as far up as the renal corpuscle. Retrograde flow of urine from the urinary bladder to the ureter is called vesicoureteral reflux. It only causes problems when the urine is septic. Reverse peristalsis may occur in the ureter when there is a cystitis. These factors probably contribute to the ascending spread of infection in cases of pyelonephritis.
In the kidney, the medulla is more susceptible to ascending infections. This is probably due to its location as it relates to ascending infections, and to other factors including it relatively hypoxic state, hypertonicity, and its increased concentrations of ammonia.
Pyelonephritis is usually bilateral but not necessarily symmetrical. Acute pyelonephritis is seen more commonly in sows and chronic pyelonephritis is most often reported in cows and dogs.
Hydronephrosis should probably be discussed with lower urinary tract conditions, but it does result in considerable damage to the renal parenchyma. It refers to dilatation of the renal pelvis and calyces with progressive atrophy of the renal parenchyma and cystic enlargement of the kidneys. It is caused by some form of urinary tract obstruction. Obstructing lesions may be complete or partial and they may be congenital or acquired. There are many possible acquired causes including urinary calculi, cystitis, prostatic enlargement, compression of the ureters by surrounding inflammatory or neoplastic tissue, displacement of the bladder, and acquired urethral strictures. If the obstruction involves only one ureter, the hydronephrosis will be unilateral; however, if both ureters are involved, or if the bladder or the urethra is involved, the hydronephrosis will be bilateral. It may not be symmetrical. Complete or severe bilateral obstruction usually causes death, due to uremia, before much dilatation of the renal pelvis occurs. Urinary stasis predisposes to infections and therefore, pyelonephritis may be superimposed on hydronephrosis or vice versa.
The pathogenesis involves persistence of glomerular filtration in spite of urinary tract obstruction. If the obstruction persists, the kidney parenchyma will eventually undergo complete degeneration and necrosis and will be replaced by fibrous connective tissue, forming a cystic structure with a fibrous connective tissue wall.
Grossly, there is progressive dilatation of the renal calyces and pelvis and blunting of the papillae or medullary crests. In severe cases, this may progress to form a large unilocular or multilocular cyst from the affected kidney.Histologically, tubular dilatation is the most striking feature with damage occurring in the proximal regions of the nephron first. In severe cases, there is liquefactive necrosis in the medulla causing progressive reduction in the medullary parenchyma.
Enterotoxemia is a condition caused by a toxin which is produced by a clostridial organism (Clostridium perfringens type D). It occurs most frequently in sheep and goats and it has been reported in calves. It usually occurs in younger animals and most often it is characterized by peracute death. Those that live longer may have enteric signs, such as diarrhea, and usually there is excessive salivation, hyperesthesia, rapid breathing, and terminal convulsions or coma. One of the more striking gross postmortem lesions is advanced autolysis of the kidneys resulting in a distinctive pulpy consistency to the renal parenchyma (Pulpy Kidney Disease). This may also be accompanied by hemorrhages in the kidney, which in adult goats or sheep is often more pronounced.
Hemoglobinuria accompanies intravascular hemolysis and the hemoglobin will impart a dark reddish discoloration on the renal parenchyma. Initially the discoloration is uniform but after a short period of time the hemoglobin is lost from most nephrons and remains in a few causing a brownish speckled appearance. Microscopically, the hemoglobin is found in small eosinophilic granules in tubular epithelial cells and in casts in more distal portions of the nephron.
Myoglobin may leak from damaged or necrotic muscle cells into the vascular system. Once in the blood, the myoglobin is filtered in the glomerular ultrafiltrate into the nephron where it imparts a brownish discoloration on the kidney. The discoloration associated with myoglobin is very similar to that seen with hemoglobin. Histologically, the myoglobin is found in small eosinophilic granules in tubular epithelial cells and in casts in more distal portions of the nephron.
Hemosiderosis develops subsequent to chronic hemolytic anemia and as residues of acute hemolytic anemia. The pigment is produced by degradation of resorbed hemoglobin and is usually found in renal tubular epithelial cells. It usually imparts a brownish discoloration on the kidney.
Lipofuscinosis is a condition in which a brownish iron-free pigment is deposited in tissues. This pigment is called lipofuscin and the condition is also known as hemochromatosis and xanthomatosis. Grossly there are brownish streaks in the cortex radiating from the medulla. Microscopically, the pigment is found in convoluted tubules.
The porphyrins of congenital porphyria impart a brownish discoloration on the kidneys, with accumulations of the pigment in tubular epithelium and in the interstitium.
A greenish-yellow discoloration of the kidneys is common in icterus.
Hyperbilirubinemia of any cause may result in a dark brownish to black discoloration of the kidneys as well.
Stephanurus dentatus is the kidney worm of swine. Adult worms are found encysted in the perirenal fat and their cysts communicate with the renal pelvis. Their eggs pass out in the urine and the larvae hatch in a few days. The natural life cycle seems to be direct. Once infective larvae enter susceptible hosts, somatic migration occurs and often extensive liver damage is the result. These parasites are found throughout the world mainly in tropical and subtropical climates.
Dioctophyma renale is the giant kidney worm. It is mainly reported in dogs, mink, cats, and other fish eating mammals but it has been reported in pigs, cattle and horses. It is the largest parasitic nematode ranging in size from 20 - 100 cm in length and 4 - 12 mm in diameter. It has an indirect life cycle involving two intermediate hosts. Adult worms are usually found in the renal pelvis and they usually cause extensive damage to the renal parenchyma.
There are several species of capillaria that infect the urinary tract of animals. Capillaria plica (in dogs), Capillaria micronata (in mink) and Capillaria feliscati (in cats) have been found infecting the renal pelvis, ureteres and urinary bladder.
Klossiella equi is a sporozoan parasite of the kidneys of equidae. The infection seems to be quite harmless and for the most part is an incidental finding.
Primary neoplasms of the kidney are rare. They include renal adenomas, renal carcinomas, nephroblastoma, transitional cell papilloma, transitional cell carcinoma, fibroma, fibrosarcoma, hemangioma, and hemangiosarcoma.
Renal adenomas are rare in domestic animals. They are most often reported in cattle and horses. In dogs, approximately 15 % of the primary renal neoplasms are renal adenomas. Renal adenomas tend to be of minimal clinical significance and they are usually incidental necropsy findings.
Grossly they tend to be solitary spherical nodules usually less than 2 cm in diameter. They grow by expansion and in doing so they compress the surrounding renal parenchyma.
Histologically, the tumor cells are cuboidal cells with abundant eosinophilic cytoplasm.
Renal carcinoma is a primary renal neoplasm and it is the most common primary renal neoplasm in dogs, cattle and sheep. It occurs most frequently in older animals. (This might account for its relatively low incidence in swine.) It is seen almost twice as often in males as it is in females. Common clinical signs include hematuria and weight loss and often an abdominal mass is palpable. Grossly the neoplasms tend to be spherical to egg shaped and are usually sharply delineated from the surrounding renal parenchyma. Often they are at one pole and many become larger than the host kidney. The tumor is usually grayish or yellowish in color and there may be dark necrotic foci in the tumor. Histologically, there are several cell types but renal carcinomas are usually characterized by the presence of clusters of vacuolated cells called clear cells.
In dogs it is extremely difficulty to distinguish renal carcinoma with pulmonary metastasis from primary pulmonary carcinoma with renal metastasis.
Transitional cell tumors (papillomas and carcinomas) occasionally arise from the epithelium that lines the renal calyces and/or pelvis. When no primary site is found in the urinary bladder, these probably represent primary renal neoplasms.
Some mesenchymal neoplasms arise as primary neoplasms in the kidney as well.
The most common metastatic neoplasm to the kidney is lymphosarcoma.
Many congenital anomalies involving the lower urinary tract have been reported in animals. These include: agenesis of the ureter, ectopic ureter, duplication of the urinary bladder, patent urachus, diverticula of the bladder, and urethrorectal fistula.
Some acquired anatomic variations have also been reported. These include: displacement of one or both ureters, the bladder, and/or the urethra. Displacement of the bladder can occur intraabdominally as in dorsal retroflexion or torsion or the bladder can be displaced by prolapse or herniation. The bladder is sometimes involved in vaginal prolapses in cattle and swine. It also is sometimes involved in perineal hernias in dogs. In females, it sometimes becomes inverted and prolapses through the urethra.
Dilatation of one or both ureters and/or the bladder has been reported. It is usually due to obstruction but sometimes is caused by a neurologic deficit.
Long standing partial obstruction in the urethra may lead to hypertrophy of the musculature in the bladder wall while complete obstruction of the urethra or loss of neurologic functions often lead to rupture of the bladder.
Hemorrhage can occur at any location in the lower urinary tract and most often it develops due to local irritation or trauma. Urinary calculi are commonly associated with lower urinary tract hemorrhage. Improper insertion of catheters is another common cause of lower urinary tract bleeding.
Urolithiasis is one of the most important urinary tract problems in domestic animals. It refers to the presence of calculi in the urinary passages. These calculi form by precipitation of urinary solutes and they may be found in any part of the urinary collecting system including the renal pelvis, the ureters, the urinary bladder, and the urethra. Numerous predisposing and precipitating factors have been reported and these vary for the different types of calculi that are found. The calculi basically cause disease by obstructing flow in the urinary tract; however, they can be locally irritating and cause problems without causing obstruction.
Cystitis refers to inflammation of the bladder. Because inflammation of other parts of the urinary tract usually stem from inflammation of the bladder, most of the emphasis in this section will focus on bladder infections. Infection of the bladder is rare and it usually develops subsequent to interference with urine flow or damage to urinary tract epithelium. In bacterial infections, usually the pathogens can be traced to the rectal fora. The more commonly isolated pathogens include E. Coli, Proteus vulgaris, streptococci, staphylococci, Corynebacterium renale (in cattle), and Corynebacterium suis (in swine). Cystitis often leads to ureteritis and urethritis which are inflammation of the ureters and urethra respectively.
Neoplasms of the lower urinary tract are most frequently reported in cattle and dogs. In cattle, most of these neoplasms have been associated with enzootic hematuria. In reference to dogs, urinary tract neoplasia is seen more commonly in females and except for rhabdomyosarcoma it is seen primarily in older dogs.
Except in cats, tumors of the renal pelvis and the urethra are far less common than tumors of the bladder and most of them are malignant. Cats seem to develop more transitional cell carcinomas in the renal pelvis than other species.
Primary neoplasms include leiomyomas, leiomyosarcomas, fibromas, fibrosarcomas, rhabdomyosarcomas, adenomas, papillomas, carcinomas, transitional-cell carcinoma, squamous-cell carcinoma, adenocarcinoma, and undifferentiated carcinomas.
More commonly encountered secondary neoplasms in the lower urinary tract usually spread from local primary neoplasms of the prostate, rectum, and other surrounding organs or structures. Occasionally, in cattle, lymphosarcoma will metastasize to the bladder.
SLIDE 1: CANINE ABDOMINAL CAVITY (gross): UNILATERAL APLASIA OF THE KIDNEY - Note that the right kidney is missing. This could either be due to aplasia or the kidney may have been previously removed, in which case this would represent a unilateral nephrectomy. Note that the remaining kidney is enlarged. (What is the likely reason for the enlargement of the remaining kidney?)
SLIDE 2: CANINE KIDNEYS (gross): UNILATERAL HYPOPLASIA OF ONE KIDNEY WITH COMPENSATORY HYPERTROPHY OF THE OTHER - Note the marked difference in the size of these two kidneys. The one on the right in this picture is hypoplastic and a compensatory hypertrophy has caused enlargement of the other.
SLIDE 3: CANINE KIDNEYS (gross): BILATERAL HYPOPLASIA OF THE KIDNEYS - Both of the kidneys from this dog were abnormally small. Note the pale discoloration of these kidneys and the relatively smooth and uniform architecture. It is very difficult to distinguish true hypoplasia of the kidneys from acquired atrophic and/or degenerative changes. What features are evident in these kidneys which indicate that this actually represents hypoplasia and not some acquired lesion?
SLIDE 4: CANINE KIDNEY (photomicrograph): HYPOPLASIA OF THE KIDNEY This section was taken from a kidney that was abnormally small. Note the relative lack of glomeruli in this section. Also note the connective tissue proliferation in the lower portion of the view. In cases of bilateral hypoplasia of the kidneys, renal failure usually develops and tends to alter the histologic findings.
SLIDE 5: CANINE KIDNEY (photomicrograph): HYPOPLASIA OF THE KIDNEY This is a higher magnification of the same section as in slide #4. Note the virtual absence of tubules and the marked connective tissue proliferation in the interstitium. There is also a marked accumulation of inflammatory cells in the interstitium. Are these changes consistent with those observed in kidneys that are merely hypoplastic? Could these lesions represent an acquiredatrophic or degenerative change in this organ?
SLIDE 6: PORCINE KIDNEYS (gross): HORSESHOE KIDNEY - These kidneys are fused at their caudal poles. Note the horseshoe shape of the fused kidneys. Also note the irregular contour of the kidneys and the obvious connective tissue scarring in cortical parenchyma.
SLIDE 7: PORCINE KIDNEYS (gross): POLYCYSTIC KIDNEY - Note the enlarged kidney with the 2 - 4 mm sized cysts throughout the cortical parenchyma.
SLIDE 8: EQUINE KIDNEY (gross): CYSTIC KIDNEY - Note the ruptured cyst in the cortical parenchyma of this kidney. Is this cyst likely to have been clinically significant?
SLIDE 9: BOVINE KIDNEY (gross): CYSTIC KIDNEY - Note the cyst in one lobe of this kidney. Note the opaque capsule surrounding the cyst and the trabecular pattern evident through the capsule. This is most likely a multilocular cyst. What is a multilocular cyst?
SLIDE 10: CANINE KIDNEYS (gross): TRAUMATIC RUPTURE OF THE KIDNEY WITH HEMORRHAGE - Note the large blood clot associated with the ruptured kidney. This animal died due to exanguination.
SLIDE 11: CANINE KIDNEY (gross): HEMORRHAGE IN THE KIDNEY - Note the area of dark reddish discoloration of the medulla in this kidney. This is a hemorrhagic area. This animal had infectious canine hepatitis. Does this lesion resemble a typical red infarct?
SLIDE 12: CANINE KIDNEY (photomicrograph): INFECTIOUS CANINE HEPATITIS - This is a high magnification of a glomerulus in a section from the kidney in slide #11. Note the intranuclear inclusion bodies in endothelial cells in this glomerulus. What virus causes ICH?
SLIDE 13: PORCINE KIDNEY (gross): HOG CHOLERA - Note the petechial hemorrhages in the cortex of this kidney.
SLIDE 14: PORCINE KIDNEY (gross): AFRICAN SWINE FEVER - Note the intense dark reddish almost black discoloration of the renal cortex and the calyces. In addition, the medullary pyramids are pale and have a uniform reddish bronze color. This is indicative of severe hemorrhage.
SLIDE 15: CANINE KIDNEY (gross): NEONATAL CANINE HERPESVIRUS INFECTION - Note the subcapsular hemorrhages in this kidney. What histopathologic lesions would you expect to observe in this kidney? What histopathologic lesions would you expect to observe in the liver from this puppy?
SLIDE 16: PORCINE ABDOMINAL CAVITY (gross): PIG WEED TOXICOSIS - Note the perirenal edema and hemorrhage. Pig weed (Amaranthus retroflexus) causes perirenal edema and hemorrhage and renal failure due to toxic nephrosis. Pig weed toxicosis has been reported in swine, cattle, and horses. The nephrotoxic principle has not been identified.
SLIDE 17: CANINE KIDNEY (gross): INFARCTION OF THE KIDNEY - Note the fairly sharply delineated pale areas and the outlined dark reddish area in the cortex of this kidney. Note the depressed contour of the kidney over the larger pale area. These are infarcts in the cortex of this kidney. On cut surface, these areas were wedge-shaped with the base of the wedge corresponding to the capsular surface. Why are two of these infarcts pale while the other is dark red?
SLIDE 18: CANINE KIDNEY (photomicrograph): INFARCTION OF THE KIDNEY The coagulative necrosis due to infarction has seriously distorted the architecture of the kidney in the section. Note the increased cellularity, evident in the stippled basophilic appearance of the section. Is the lesion in this slide typical of a red infarct?
SLIDE 19: RABBIT KIDNEYS (gross): CORTICAL NECROSIS WITH HEMORRHAGE - Note the reduction in thickness and the pale discoloration of the cortex of the kidney on the left. This was the result of a generalized Shwartzmann reaction. How does a generalized Shwartzmann develop?
SLIDE 20: CANINE KIDNEY (gross): RENAL MEDULLARY CREST NECROSIS - Note the dark discoloration of the medullary crest if this kidney. This was caused by a reaction to nonsteroidal antiinflammatory agents.
SLIDE 21: BOVINE KIDNEYS (gross): AMYLOIDOSIS OF THE KIDNEYS - Note the enlarged yellowish kidneys in this picture. The kidney at the right is has more normal size and color. What procedure could you use on a gross specimen to determine the presence of amyloid?
SLIDE 22: BOVINE KIDNEY (photomicrograph): GLOMERULAR AMYLOIDOSIS Note the enlarged glomeruli with the homogeneous eosinophilic deposits in their capillary tufts. Note the dilated tubules containing the homogeneous, lightly eosinophilic material in their lumens. Is this material the same as the material in the glomerular tufts? If not, what is the likely nature of this material? Is it possible to distinguish between immunoglobulin-derived systemic amyloidosis and reactive systemic amyloidosis histologically?
SLIDE 23: CANINE KIDNEY (gross): ACUTE PROLIFERATIVE GLOMERULONEPHRITIS - Note the mottling of the cortex of this kidney due to the dark miliary foci scattered throughout the cortical parenchyma. This is most obvious in the subcapsular view in this case.
SLIDE 24: CANINE KIDNEY (gross): ACUTE PROLIFERATIVE GLOMERULONEPHRITIS - Note the mottling of the cortical parenchyma due to dark miliary foci scattered over the subcapsular surface.
SLIDE 25: CANINE KIDNEY (photomicrograph): ACUTE PROLIFERATIVE GLOMERULONEPHRITIS - Note the swollen hypercellular glomerulus in this view. Also note the amphophilic globules in the Bowman's space and in the tubules. These probably represent globules of proteinaceous ultrafiltrate. Is there evidence of either tubular or interstitial damage in this view? If so, describe it.
SLIDE 26: CANINE KIDNEY (photomicrograph): GLOMERULONEPHRITIS - Note the increased cellularity in this glomerulus. Pay close attention to the increased cellularity of the parietal layer of the epthelium of the Bowman's capsule and the increased thickness in the vicinity of the basement membrane of that epithelium. This proliferation of the epithelium of the Bowman's capsule, especially of the parietal layer, is typical of crescent formation. This probably represents membranoproliferative glomerulonephritis.
SLIDE 27: CANINE KIDNEY (photomicrograph): MEMBRANOUS GLOMERULONEPHRITIS - This is a special stain known as a PAS stain. Note the increased thickness and irregular structure of the glomerular basement membranes as well as the basement membranes of the Bowman's capsule and some of the tubules. Is there any other evidence of tubular damage in this view? If so, describe it.
SLIDE 28: CANINE KIDNEY (photomicrograph): GLOMERULONEPHRITIS - Note the marked enlargement of the glomerular capillary tufts in this section. The Bowman's space is not discernable. This could be due to the enlargement of the glomeruli but there are probably adhesions between the parietal and visceral layers of the Bowman's capsule. Note the thick glomerular tufts and the extensive accumulation of an eosinophilic homogeneous material in the glomeruli. This is more pronounced in one of the glomeruli in this view. These are examples of obsolescent glomeruli and they are typical of glomeruli seen in chronic glomerulonephritis.
SLIDE 29: MINK KIDNEY (gross): NEPHROSIS - Note the enlarged pale kidneys in this slide.
SLIDE30: CANINE KIDNEY (photomicrograph): CLOUDY SWELLING OF TUBULAR EPITHELIAL CELLS - Note the swollen epithelial cells in the tubule in the center of this slide.
SLIDE 31: CANINE KIDNEY (photomicrograph): VACUOLAR DEGENERATION OF THE TUBULAR EPITHELIAL CELLS - Note the swollen and vacoulated epithelial cells in this slide.
SLIDE 32: CANINE KIDNEY (photomicrograph): MINERALIZATION AND NECROSIS OF TUBULAR EPITHELIAL CELLS - Note the complete mineralization of the epithelial cells in this tubule. These cells are obviously necrotic.
SLIDE 33: PORCINE: KIDNEY (gross): SULFONAMIDE NEPHROSIS - Note the edematous and congested cortical parenchyma. This kideny was enlarged. In many of these cases, crystals are obvious grossly in the medulla and in the renal pelvis.
SLIDE 34: PORCINE KIDNEY (photomicrograph): SULFONAMIDE NEPHROSIS - Note the crystaline material within tubules in this section. Also, note the proliferation of the epithelium in these collecting tubules.
SLIDE 35: CANINE KIDNEY (photomicrograph): ETHYLENE GLYCOL POISONING - Note the greenish crystals in the tubules in this slide. These are calcium oxalate crystals and they are fairly diagnostic of ethylene glycol toxicity.
SLIDE 36: CANINE KIDNEY (photomicrograph): LEAD TOXICOSIS - Note the intranuclear inclusion bodies within tubular epithelial cells. These inclusions stained positively with an acid fast stain. They are characteristic of lead toxicosis.
SLIDE 37: CANINE KIDENY (photomicrograph): MERCURY TOXICOSIS - Note the areas of coagulative necrosis involving tubular epithelium.
SLIDE 38: BOVINE KIDNEY (photomicrograph): OAK BUD POISONING - Observe the necrosis of the tubular epithelial cells in this slide. There are also areas of hemorrhage.
SLIDE 39: BOVINE KIDNEY (gross): WHITE-SPOTTED KIDNEY - Observe the foci of whitish discoloration of the renal cortex. This disease is usually of minimal clinical significance. The cause is uncertain, but E. coli is a frequent isolate from such kidneys.
SLIDE 40: FELINE KIDNEY (gross): CHRONIC NEPHRITIS - Note the irregular contour of the kidneys in this slide. Histologically, there was extensive interstitial fibrosis in these kidneys. This is chronic interstitial nephritis.
SLIDE 41: CANINE KIDNEY (gross): CHRONIC NEPHRITIS - The contour of this kidney is remarkably smooth but there are obvious pale foci throughout the cortical parenchyma. Histologically, there was interstitial fibrosis in this kidney.
SLIDE 42: CANINE KIDNEY (photomicrograph): CHRONIC INTERSTITIAL NEPHRITIS - Note the exaggerated interstitial areas in this slide. There is thickening of the interstitium with accumulations of fibrous connective tissue and inflammatory cells. Most of the tubules in this view are dilated.
SLIDE 43: CANINE KIDNEY (photomicrograph): CHRONIC INTERSTITIAL NEPHRITIS - There is considerable thickening of the interstitium in this tissue as well. There is also a marked accumulation of what appear to be mononuclear inflammatory cells in the interstitium as well as fibrous connective tissue proliferation.
SLIDE 44: EQUINE KIDNEY (gross): ACTINOBACILLUS EQUULI INFECTION - This condition is usually encountered in neonatal foals and probably develops from a naval infection. Note the pinpoint whitish foci scattered throughout the subcapsular parenchyma of this kidney.
SLIDE 45: CANINE KIDNEY (gross): GRANULOMATOUS NEPHRITIS - Note the whitish foci in the cortex of this kidney. This was caused by a fungal organism and the inflammatory reaction was dominated by macrophages.
SLIDE 46: BOVINE KIDNEY (gross): PYELONEPHRITIS - Note the distorted kidneys and the markedly distended ureters. What is the likely pathogen in this case?
SLIDE47: BOVINE KIDNEY (gross): PYELONEPHRITIS - This is a section through one lobe of a bovine kidney. Note the dilated calyx. This was due to pyelonephritis.
SLIDE 48: PORCINE KIDNEY (gross): PYELONEPHRITIS - The kidney is abnormally small and the ureter is markedly dilated.
SLIDE 49: CANINE KIDNEY (gross): PYELONEPHRITIS - There is very little renal parenchyma left in the kidney on the right. It has been reduce to a wall of fibrous connective tissue. The renal pelvis is dilated and was filled with pus.
SLIDE 50: BOVINE KIDNEY (gross): UNILATERAL HYDRONEPHROSIS - Note the thin walled structure that remains of one kidney.
SLIDE 51: CANINE KIDNEY (gross): UNILATERAL HYDRONEPHROSIS - Note the mutiloocular arrangement of this severely damaged kidney. The contralateral kidney has become hypertrophic to compensate for the loss of functional capacity in the affected kidney.
SLIDE 52: OVINE URINARY TRACT (gross): BILATERAL HYDRONEPHROSIS - Note the dilated renal pelvis and calyces in both these kidneys. The ureters are also dilated. Is it likely that the urinary tract obstruction in this case was complete and permanent?
SLIDE 53: EQUINE KIDNEYS (gross): HEMOGLOBIN DISCOLORATION OF THE KIDNEY - These kidneys were taken from a foal that had isoimmune-hemolytic anemia. Note the dark discoloration of the cortex in both these kidneys.
SLIDE 54: BOVINE KIDNEY, LIVER, LYMPH NODE, AND COLON (gross): HEMOSIDEROSIS - Note the brownish discoloration of these organs. This was due to hemosiderin deposition.
SLIDE 55: EQUINE SPLEEN (photomicrograph): This slide was included to illustrate the accumulation of hemosoderin in macrophages.
SLIDE 56: EQUINE VERTEBRAE, TRACHEA, AND HUMERUS (gross): CONGENITAL PORPHYRIA - This picture was taken under ultraviolet light. A reddish fluorescence should be evident under ultraviolet light but it is not striking in this picture.
SLIDE 57: FELINE KIDNEYS (gross): ICTERUS - Note the yellowish discoloration of the kidney. This was due to icterus.
SLIDE 58: CANINE KIDNEYS (gross): CHOLEMIC NEPHROSIS - This dog had hyperbilirubinemia subsequent to a prehepatic condition. What is the likely nature of the condition?
SLIDE 59: PORCINE KIDNEY (gross): STEPHANURIASIS - In this slide, at least one nematode is evident in the area of the calyces. Note the distortion of the renal medulla. Very little medullary tissue is recognizable.
SLIDE 60: PORCINE KIDNEY AND URETER (gross): STEPHANURIASIS - Here a nematode is found in the ureter. Again there is destruction of the medullary parenchyma but also the ureter is severely distorted. This is probably due to chronic inflammation and represents massive fibrous connective tissue proliferation.
SLIDE 61: CANINE KIDNEY (photomicrograph): PARASITIC GRANULOMA - This slide depicts a chronic granulomatous reaction in this kidney. It was caused by migration of parasitic larvae (Toxocara canis).
SLIDE 62: BOVINE KIDNEY (gross): RENAL CARCINOMA - Note the spherical solid mass in this kidney. The mass has replaced one lobe of this kidney.
SLIDE 63: EQUINE KIDNEY (gross): RENAL CARCINOMA - Note the spherical solitary mass found in this kidney. The slide shows a cut veiw of the mass in the kidney and a cut section of the remainder of the mass.
SLIDE 64: (SPECIES UNCERTAIN) KIDNEY (photomicrograph): RENAL ADENOCARCINOMA - Note the rounded cells with rounded nuclei and the tubular or acinar arrangements.
SLIDE 65: PORCINE ABDOMINAL CAVITY (gross): EMBRYONAL NEPHROMA - Note the large mass in the abdominal cavity in this slide. This is an embryonal nephroma. What other names are also used for this neoplasm?
SLIDE 66: PORCINE KIDNEY (gross): EMBRYONAL NEPHROMA - This mass was removed from the abdominal cavity. A small portion of the kidney is evident protruding from under the mass at the left of the mass.
SLIDE 67: PORCINE KIDNEY (photomicrograph): EMBRYONAL NEPHROMA - Note the primitive glomeruli and the thick connective tissue stroma. In some embryonal nephromas there is differentiation in the connective tissue stroma forming a variety of mesenchymal tissues including muscle, fibrous tissue, cartilage, bone, and adipose tissue.
SLIDE 68: PORCINE KIDNEY (photomicrograph): EMBRYONAL NEPHROMA - Note the elongated cells, some of which contain multiple nuclei. This represents differentiation of the neoplastic cells forming what resemble skeletal muscle cells.
SLIDE 69: BOVINE KIDNEY (gross): LYMPHOSARCOMA - Note the multiple discrete dark spherical nodular masses scattered throughout the parenchyma of this kidney. Most are raised above the normal contour of the kidney and they probably extend into the parenchyma.
SLIDE 70: BOVINE KIDNEY (gross): LYMPHOSARCOMA - Note the pale nodules in the parenchyma of this kidney. They have a somewhat patchy or mottled appearance and they seem to blend into the surrounding parenchyma. This is also lymphosarcoma.
SLIDE 71: BOVINE KIDNEY (photomicroghraph): LYMPHOSARCOMA - Here rounded lymphoid cells have infiltrated this organ. This is lymphosarcoma and it represents a metastatic neoplasm when it occurs in the kidney.
SLIDE 72: CANINE KIDNEY (gross): TRANSITIONAL CELL TUMOR - Note the mass in the vicinity of the renal pelvis in this kidney. Occasionally, transitional cell tumors arise from the epithelium of the renal pelvis.
SLIDE 73: BOVINE URINARY BLADDER (gross): PATENT URACHUS - The urachus can be found extending from the bladder at the top of the view.
SLIDE 74: FELINE ABDOMINAL CAVITY (gross): HEMORRHAGIC CYSTITIS - Note the dark discoloration of this bladder due to the presence of blood in the urine. This cat had calculi in its bladder.
SLIDE 75: CANINE URINARY BLADDER (gross): HEMORRHAGIC CYSTITIS - Calculi were also found in this bladder. Note the dark discoloration and the roughened dull appearance of the mucosa of this bladder.
SLIDE 76: EQUINE KIDNEY (gross): UROLITHIASIS - Note the irregular shaped concretion in this kidney. This is a calculus.
SLIDE 77: CANINE KIDNEY (gross): UROLITHIASIS - Note the whitish calculus that was found in the pelvis of this kidney. Many uroliths will assume the shape of the region in which they form.
SLIDE 78: CANINE URINARY BLADDER (gross): UROLITHIASIS - Note the variable shaped calculi in this bladder. Do you think this animal would have been urinating frequently?
SLIDE 79: PORCINE: URINARY TRACT (gross): NECROTIC CYSTITIS - Note the accumulation of exudate in the bladder. Do you suppose this animal had clear urine?
SLIDE 80: CANINE URINARY BLADDER (photomicrograph): CANINE DISTEMPER - Note the intracytoplasmic inclusion bodies in the epithelial cells in this slide.
SLIDE 81: CANINE URINARY BLADDER (gross): TRANSITIONAL CELL CARCINOMA - Note the roughened irregular mass in the wall of the urinary bladder. This is a transitional cell carcinoma.
