TYPES OF GLOMERULITIS

Viral Glomerulitis
• Glomerulitis, caused by a direct viral insult to the glomerulus, occurs in acute systemic viral
diseases, such as:
• acute infectious canine hepatitis
• equine arteritis virus infection
• hog cholera
• avian Newcastle disease,
• neonatal porcine cytomegalovirus infection.
Acute viral GN produces the following gross lesions:
• Kidneys are often slightly swollen.
• Renal capsular surface is smooth.
• Kidneys are normal color or pale.
• Glomeruli are visible as pinpoint red dots on the cut surface of the cortex.
Infectious Canine Hepatitis, Kidney, Cortex, Dog. Renal glomerular endothelial
cells contain intranuclear inclusion bodies (arrow). H&E stain.
 TYPES OF GLOMERULITIS

Immune-Mediated Glomerulonephritis
• Glomerulonephritis (GN) most often results from immune-mediated mechanisms.
• Antibodies to the basement membrane (anti-GBM disease) bind and damage the glomerulus
through fixation of complement and resulting leukocyte infiltration.
• This mechanism of GN has been well documented in human beings and nonhuman primates but
only rarely in other domestic animals.
 TYPES OF GLOMERULITIS

Immune-complex GN (ICGN)
• occurs most commonly in dogs and cats and is the most common glomerular disease in dogs,
accounting for 48% of glomerular diseases in a recent study.
• ICGN often occurs in association with persistent infections or other diseases that
characteristically have a prolonged antigenemia that enhances the formation of soluble immune
complexes.
Proliferative Glomerulonephritis (GN), Kidney, Dorsal Section, Dog. The small,
white, round foci in the cortex are enlarged glomeruli.
 DISEASES WITH IMMUNE-COMPLEX
GLOMERULONEPHRITIS
HORSES
CATS DOGS
• Equine infectious anemia • Infectious canine hepatitis
• Feline leukemia virus
• Streptococcus sp. • Chronic hepatitis
(FeLV) infection • Chronic bacterial diseases
CATTLE • Endometritis (pyometra)
• Feline infectious
• Bovine viral diarrhea • Pyoderma
peritonitis (FIP) • Prostatitis
• Trypanosomiasis
• Feline immunodeficiency • Dirofilariasis
SHEEP • Borreliosis (Lyme disease)
• Hereditary virus (FIV) • Systemic lupus erythematosus
hypocomplementemia in • Progressive polyarteritis • Polyarteritis
Finnish Landrace lambs • Autoimmune hemolytic
• Neoplasia anemia
PIGS • Immune-mediated polyarthritis
• Progressive membranous
• Hog cholera • Neoplasia—mastocytoma
glomerulonephritis (GN • Hereditary C3 deficiency
• African swine fever
TUBULOINTERSTITIAL DISEASE
 INTERSTITIAL NEPHRITIS
• Inflammation of kidney characterized by
degeneration and necrosis of tubular epithelium,
edema and infiltration of inflammatory cells in
Etiology
• Ochratoxins and atrinin.
interstitium.
• Leptospira
• Used to characterize a group of inflammatory • Toxins/ poisons e.g. Pesticides.
diseases that involve the interstitium and tubules. • Herpes virus
• Tubulointerstitial nephritis can result from
• Endogenous toxaemia e.g. Ketosis
• Immune complexes
bacterial or viral septicemias, in which these
infectious microbes first infect the kidney tubules
and damage them, which then incites an
inflammatory response in the interstitium.
 INTERSTITIAL NEPHRITIS
Macroscopic and microscopic features
• Enlargement of kidneys
• Necrosis, congestion and hemorrhage
• Edema, congestion, hemorrhage
• Necrosis and degeneration of tubular epithelium
• Infiltration of inflammatory cells like neutrophils, macrophages and lymphocytes in interstitium.
• Loss of tubules, foci of mononuclear celis, fibrosis in chronic cases
• Immune complexes are deposited in granular form causing degeneration of epithelial cells of tubules
and mononuclear cell infiltration.
 CAUSES OF INTERSTITIAL NEPHRITIS

PIGS
HORSES
• Leptospira interrogans serovar pomona
• Equine viral arteritis
• Porcine reproductive and respiratory syndrome
CATTLE
DOGS
• Escherichia coli septicemia, “white-spotted
• Leptospira interrogans serovars canicola,
kidney”
icterohaemorrhagiae, and others
• Leptospira interrogans serovar canicola
• Infectious canine hepatitis virus, recovery phase
• Malignant catarrhal fever
• Theileria parva
SHEEP
• Sheeppox
ACUTE LEPTOSPIROSIS, KIDNEY.

A, Interstitial nephritis, acute leptospira infection, dorsal section, dog. Radiating pale streaks
are caused by cortical tubular necrosis and acute interstitial inflammatory infiltrates. The hilar
fat and medulla are yellow from jaundice.
 ACUTE LEPTOSPIROSIS, KIDNEY.

B, Acute tubular necrosis, early regeneration, dog. Note the segments of tubular epithelium devoid of nuclei (coagulation
necrosis) (top left) and the hemorrhage. At this early stage, there is an almost complete lack of inflammatory cells in the
interstitium, but later in the subacute stage of leptospirosis there are interstitial infiltrates of lymphocytes and plasma cells,
which tend to be near the corticomedullary junction. H&E stain.
 ACUTE LEPTOSPIROSIS, KIDNEY.

C, Leptospira, cow. Numerous leptospira (arrows) are present in the lumens of tubules. Leptospira
colonization of tubule epithelial cells is typical of this bacterium. Warthin Starry silver stain.
 GRANULOMATOUS NEPHRITIS

• Granulomatous nephritis is an interstitial disease that often accompanies chronic

systemic diseases that are characterized by multiple granulomas in various
organs.
• In domestic animals, granulomatous nephritis can be caused by a variety of
granuloma-inducing infectious microbes. These can include:
• fungi such as Aspergillus sp., Phycomycetes, or Histoplasma capsulatum;
• algae such as Prototheca sp.;
• parasites;
• protozoa such as Encephalitozoon cuniculi;
• bacteria such as Mycobacterium bovis; and
• viruses such as feline coronavirus and porcine circovirus
Granulomatous Nephritis, Feline Infectious Peritonitis, Kidney, Cat. A, Lesions are typical of the noneffusive (dry) form
of feline infectious peritonitis. There are multifocal, coalescing white to gray granulomas (arrow), which can be
confused with the nodular form of lymphoma (lymphosarcoma), thus warranting histologic examination.
Granulomatous Nephritis, Feline Infectious Peritonitis, Kidney B, Dorsal section. Multifocal,
coalescing white to gray granulomas extend into the cortical parenchyma (arrow).
Granulomatous Nephritis, Hairy Vetch Toxicosis, Kidney, Cow. A, Cortical striations are
obliterated by coalescing granulomatous foci associated with hairy vetch toxicosis
Granulomatous Nephritis, Hairy Vetch Toxicosis, Kidney, Cow. B, Cortex. Lesions associated with hairy vetch
toxicosis are characterized by a mixed cell interstitial inflammatory infiltrate (macrophages, lymphocytes, and
occasional multinucleated giant cell [arrow]) with renal tubular atrophy. It is specifically known as an unusual type
of poisoning because of its ability to induce granulomatous inflammation in addition to the necrosis. The kidney is
not the primary organ affected. H&E stain.
 NEPHROSCLEROSIS
• Nephrosclerosis is chronic fibrosis of kidney characterized by loss of glomeruli and tubules and
extensive fibrosis.
Macroscopic and microscopic features
• Hard, atrophied kidneys.
• Fibrous nodules on kidneys.
• Thickening of capsule. Etiology
• Small white firm kidneys. • Glomerulonephritis
• Ischemia, tubular atrophy
• Loss of glomeruli and tubules • Interstitial nephritis
• Extensive fibrosis • Arterioloscleresis
• Deposition of hyaline mass
• Infiltration of mononuclear cells
DISEASES OF THE TUBULES AND
INTERSTITIUM
 AZOTEMIA AND UREMIA

• Assays for plasma or serum concentrations of urea, creatinine, and

the nitrogenous waste products of protein catabolism are routinely
used as indices of diminished renal function. The intravascular
increase of these nitrogenous waste products is referred to as
azotemia.
• Renal failure can result in the following:
• Intravascular accumulation of other metabolic wastes such as guanidines,
phenolic acids, and large-molecular-weight alcohols (e.g., myoinositol)
• Reduced blood pH (metabolic acidosis)
• Alterations in plasma ion concentrations, particularly potassium, calcium, and
phosphate
• Hypertension
 NONRENAL LESIONS OF UREMIA

Lesion Mechanism
Pulmonary edema Increased vascular permeability
Fibrinous pericarditis Increased vascular permeability
Ulcerative and hemorrhagic gastritis Ammonia secretion and vascular necrosis
Ulcerative and necrotic stomatitis Ammonia secretion in saliva and vascular necrosis
Atrial and aortic thrombosis Endothelial and subendothelial
damage
Hypoplastic anemia Increased erythrocyte fragility
and lack of erythropoietin
production in the kidney
Soft-tissue mineralization Altered calcium-phosphorus
metabolism (stomach, lungs,
pleura, kidneys)
Fibrous osteodystrophy Altered calcium-phosphorus
metabolism
Parathyroid hyperplasia Parathyroid hyperplasia
• Alterations in calciumphosphorus metabolism in the uremic animal are a
hallmark of chronic renal failure and result from a complex set of events as
outlined in the following:

• When the glomerular filtration rate is chronically reduced to less than 25% of
normal, phosphorus is no longer adequately secreted by the kidneys and
hyperphosphatemia results.
• Because of the mass law interactions between serum calcium and
phosphorus, ionized calcium concentration in serum is reduced as a result of
precipitation of calcium and phosphorus.
• Reduced ionized serum calcium concentration stimulates parathyroid hormone
(PTH) secretion, causing calcium release from the readily mobilizable calcium
stores in the bone and from osteoclastic bone resorption.
• These changes in calcium-phosphorus metabolism are made more severe by the
reduced ability of the diseased kidneys to hydroxylate 25-hydroxycholecalciferol
to the more active 1,25- dihydroxycholecalciferol (calcitriol), resulting in
decreased intestinal absorption of calcium.
• Calcitriol production is further inhibited by hyperphosphatemia.
• In addition, calcitriol normally suppresses PTH secretion; therefore reduced
calcitriol production further increases PTH secretion.
• With time, these events lead to parathyroid chief cell hyperplasia (renal secondary
hyperparathyroidism), fibrous osteodystrophy (renal osteodystrophy), and soft tissue
calcification.
• Renal secondary hyperparathyroidism is further thought to perpetuate and
enhance renal disease by stimulating nephrocalcinosis, the process by which
renal tubular epithelium is damaged by an increase in intracellular calcium.
Calcium is precipitated in mitochondria and in tubular basement membranes.
• Soft tissue calcification associated with uremia occurs in numerous sites and
represents both dystrophic and metastatic calcification.
Ulcerative Glossitis, Uremia, Tongue, Ventral Surface, Cat. Bilaterally symmetrical ulcers (arrows)
are present on the rostrolateral borders of the ventral surface of the tongue.
Uremic Gastritis, Stomach, Dog. Because of uremia, the stomach wall is hemorrhagic
(right) and the stomach contents may contain blood and mucus (not shown here). Note
the edematous mucosal thickening (arrow).
Uremic gastritis, stomach, dog. A, There is accentuation of the gastric rugae and
calcification in the deep mucosa.
Uremic gastritis, stomach, dog. The mucosa has laminar
mineralization of
gastric glands (arrow). von Kossa stain.
 Thoracic Cavity, Parietal Pleura, Cat. Horizontally oriented
streaks (arrows) of mineral (intercostal mineralization) are present in
the subpleural intercostal connective tissue as a result of chronic uremia.
(Courtesy Dr. J. King, College of Veterinary Medicine, Cornell
University.)
 Nephrocalcinosis, Kidney, Dorsal Section, Dog. Note the
white streaks (arrows) in the cortex and medulla attributable to mineralization
of the interstitium, basement membranes, and tubules. This lesion
results from diseases that increase plasma calcium concentrations (e.g.,
hyperparathyroidism). Renal tubular epithelium is damaged by an increase
in intracellular calcium, which is initially precipitated in mitochondria and
tubular basement membranes. (Courtesy Dr. M.D. McGavin, College of
Veterinary Medicine, University of Tennessee.)
 RENAL FAILURE (LOSS OF FUNCTION).

• Renal failure occurs when one or more of the functions previously listed are altered. When renal
functional capacity is abruptly impaired approximately 75% or more, such that the kidneys fail to
carry out their normal metabolicand endocrine functions, acute renal failure can ensue.
 ACUTE RENAL FAILURE

• Acute renal failure can be caused by:

(1) tubular necrosis from infectious microbes, such as bacteria(Leptospira spp., Escherichia coli,
Streptococcus spp., Staphylococcus spp., and Proteus spp.) or viruses (infectious canine hepatitis
virus and canine herpesvirus).
(2) obstructive nephropathy from urolithiasis transitional cell neoplasms of the lower urinary
system,or trauma.
 (3) renal ischemia with tubular necrosis from occlusivevasculitis/vasculopathy caused by
bacteria, bacterial toxins, or tumor emboli.
(4) tubular necrosis from nephrotoxic drugs, such as aminoglycoside-based antimicrobial
drugs or antineoplastic drugs.
(5) tubular necrosis from chemicals, such as ethylene glycoland heavy metals.
(6) prerenal (compromised renal perfusion) intrarenal (compromised kidney
function),postrenal (obstruction of the urinary tract) factors
• Prerenal and intrarenal factors are most responsible for episodes of acute renal failure, with
prerenal azotemia and ischemic tubular damage actually being a continuum. Intrarenal disease
can target tubules by
THREE MECHANISM:
• • Ascending disease, such as pyelonephritis
• • Intraluminal toxic metabolites derived from glomerular filtrate
• • Ischemia
Acute renal failure occurs when the kidney fails to excrete waste products and to maintain fluid and
electrolyte homeostasis.The four main pathologic alterations in acute renal failure are as follows:
• • Decreased ultrafiltration
• • Intratubular obstruction
• • Fluid back leak
• • Intrarenal vasoconstriction
These alterations can occur after many insults, including the following:
• • Decreased renal perfusion
• • Decreased glomerular filtration
• • Ischemic tubular damage
• • Toxic tubular damage
• • Obstructive renal tubular damage
• • Tubulointerstitial inflammation, edema, or fibrosis
• Chronic Renal Failure. Chronic renal failure usually results from
• progressive renal disease with loss of nephrons and severe scarring
 ACUTE TUBULAR NECROSIS

• Acute tubular necrosis is the singlemost important cause of acute renal failure.
• Often referred to as nephrosis, lower nephron nephrosis,tubular nephrosis, tubular dysfunction,
or acute cortical necrosis, is principally the result of nephrotoxic injury to the renal tubular
epithelial cells or ischemia.
 CAUSES OF ISCHEMIC ACUTE RENAL FAILURE IN
SMALL ANIMALS
INTRAVASCULAR VOLUME DEPLETION
• Dehydration • Blood loss

• Vomiting • Trauma

• Diarrhea • Surgery

• Sequestration or shock • Hypoalbuminemia

• Thermal burns • Hypoadrenocorticism

• Hyponatremia (nondilutional)
 DECREASED CARDIAC OUTPUT

• Congestive heart failure

• Low output
• Restrictive pericardial disease
• Tamponade
• Arrhythmia
• Positive-pressure ventilation
• Prolonged resuscitation after cardiac arrest
 ALTERED RENAL AND SYSTEMIC VASCULAR
RESISTANCES

• Renal vasoconstriction • Myoglobinuria

• Circulating catecholamines • Hemoglobinuria
• Renal sympathetic nervous stimulation • Systemic vasodilation
• Vasopressin • Arteriolar or mixed vasodilator therapy
• Angiotensin II • Anaphylaxis
• Hypercalcemia • Gaseous anesthesia
• Amphotericin B • Sepsis
• Hypothermia • Heatstroke
• Myoglobinuria
• INCREASED BLOOD VISCOSITY
• Multiple myeloma
• Polycythemia (absolute or relative)

• INTERFERENCE WITH RENAL AUTOREGULATION

• DURING HYPOTENSION
• Nonsteroidal antiinflammatory drugs

• WARM OR COLD ISCHEMIA

Acute tubular necrosis induces clinical oliguria (decrease in urine production) or anuria (absence of
urine production) by one or several mechanisms.

These mechanisms include the following:

• • Leakage of tubular ultrafiltrate from damaged tubules across disrupted
• basement membranes into the renal interstitium
• • Intratubular obstruction resulting from sloughed necrotic
• epithelium
The apoptotic pathway can be triggered by the following:

• • Binding of ligands to the tumor necrosis factor (TNF) superfamily

• • Deficiency of cellular growth factors
• • Imbalance between proapoptotic and antiapoptotic oncogenes
• • Alteration of other mediators of apoptotic signaling pathways such as reactive oxygen
metabolites, caspases, and ceramide.
 GROSS LESIONS OF ACUTE TUBULAR NECROSIS

• The recognition of acute tubular necrosis is often difficult.

• The cortex is swollen, pale mahogany to beige, and with a slightly translucent smooth, thinned,
capsular surface.
• The cut surface of the renal cortex bulges and is excessively moist; striations are muted or
accentuated by radially oriented opaque and white streaks.
• The medulla is either pale or diffusely congested.
 MICROSCOPIC LESIONS OF ACUTE TUBULAR
NECROSIS
The microscopic appearance of kidneys with acute tubular necrosis varies,depending on the
following:
• • The extent of the tubular necrosis
• • The duration of exposure to the damaging agent
• • The length of time between the injury and death.
 TUBULAR NECROSIS

• Tubular necrosis is randomly distributed in nephrons,but the proximal convoluted tubules are most
severely affected because of their high metabolic demands and first line of exposure

• Prolonged ischemia can produce necrosis of epithelium of the proximal and distal convoluted
tubules, the loops of Henle, and the collecting ducts throughout the cortex and, to a lesser extent,
the medulla.
• Tubules that remain in an affected site are less functional in resorption, can be dilated and lined by
flattened epithelium,or are notably atrophic, appearing shrunken with a collapsed lumen lined by
flattened epithelium and fail to heal completely by regeneration, resulting in tubular atrophy
•
• Glomeruli are resistant to ischemia and often remain morphologically normal, even when ischemia is
prolonged.

• Proximal tubular epithelium is swollen, and the cytoplasm is vacuolated or granular and intensely
eosinophilic.
•
• In such cells, the nuclear changes are pyknosis, karyorrhexis, or karyolysis. Necrotic tubular
epithelium is subsequently sloughed into tubular lumens resulting indilated, notably hypocellular
tubules that contain necrotic cellular debris and hyalinized or granular casts.

• A characteristic histologic lesion of ischemic tubular necrosis is possible disruption of the tubular
basement membranes, referred to as tubulorrhexis
Acute Tubular Necrosis, Kidney, Proximal
Tubules,
Cat. A, This lesion is characterized primarily by
coagulation necrosis of
tubular epithelial cells (arrows) and nuclear
pyknosis and intratubular
nuclear and proteinaceous debris (arrowheads).
H&E stain
This lesion is characterized primarily by nuclear pyknosis
(arrows), karyorrhexis (arrowheads),and karyolysis
(arrowheads 1) with intratubular nuclear and
proteinaceous debris and coagulation necrosis with
detachment of the epithelium from the tubular basement
membrane (arrowheads 2). H&E stain. (Courtesy Dr. J.F.
Zachary, College of Veterinary Medicine, University of
Illinois.)
ACUTE TUBULAR NECROSIS IS DUE TO THE
FOLLOWING:

1. Damage to membranes of proximal convoluted tubular epithelial cells.

2. Mitochondrial damage produced by these toxins; damage is often related to the

interaction of these metals with protein sulfhydryl groups
 COMMON NEPHROTOXINS OF DOMESTIC
ANIMALS
HEAVY METALS NONSTEROIDAL ANTIINFLAMMATORY DRUGS
Mercury Aspirin
Lead Phenylbutazone
Arsenic Carprofen
Cadmium Flunixin meglumine
Thallium Ibuprofen
PLANTS Naproxen
Pigweed (Amaranthus retroflexus)
Oaks (Quercus sp.)
Isotropis sp.
Yellow wood tree (Terminalia oblongata)
Lilies (Zantedeschia spp., Lilium spp., and Hemerocallis
spp.)
 Common Nephrotoxins of Domestic
Animals
OXALATES ANTIBACTERIAL AND VITAMIN D
Ethylene glycol (antifreeze) ANTIFUNGAL AGENTS Vitamin D supplements
Halogeton (Halogeton glomeratus) Aminoglycosides Calciferol-containing rodenticides
Greasewood (Sarcobatus vermiculatus) Gentamicin Cestrum diurnum
Rhubarb (Rheum rhaponticum) Neomycin Solanum sp.
Sorrel, dock (Rumex sp.) Kanamycin Trisetum sp.
Streptomycin
Tobramycin
Tetracyclines
Amphotericin B
 COMMON NEPHROTOXINS OF DOMESTIC
ANIMALS

GROWTH-PROMOTING AGENTS ANTINEOPLASTIC COMPOUNDS

Monensin Cisplatin

BACTERIAL AND FUNGAL TOXINS FOOD AND FOOD CONTAMINANTS

Clostridium perfringens epsilon toxin Grapes or raisins
Ochratoxin A Melamine
Citrinin Cyanuric acid
 Nephrosis, Lead Toxicosis, Kidney, Cortex, Rat. Acid-fast
intranuclear inclusion bodies (arrow) present in the proximal convoluted
tubular epithelium are diagnostic of lead poisoning. Acid-fast stain with
H&E counterstain. (Courtesy Dr. J. King, College of Veterinary Medicine,
Cornell University.)
 Acute Tubular Necrosis, Oak Toxicity, Kidney, Cow.
Ingestion of leaves, buds, or acorns from oak trees produces cortical petechiation,
acute tubular necrosis, and perirenal edema. The toxic principle is a
metabolite of oak tannins and causes acute tubular necrosis, which heals by
scarring.
 HEMOGLOBINURIC NEPHROSIS

A set of events leading to ischemic tubular necrosis frequently occurs in hypoperfused kidneys
complicated by hemoglobinuria or myoglobinuria. Hemoglobinuria accompanies episodes of
hemoglobinemia seen secondary to severe intravascular hemolysis as observed in the following:

1. Chronic copper toxicity in sheep

2. Leptospirosis or babesiosis in cattle
3. Red maple toxicity in horses
4. Babesiosis or autoimmune hemolytic anemia in dogs
 Hemoglobinuric Nephrosis, Kidney. A, Dog. Severe diffuse
hemoglobin staining of the cortex and medulla is secondary to hemoglobinemia
from an acute intravascular hemolytic crisis. Note the yellow staining
(jaundice) of the pelvic fat and the intima of cross sections of the arcuate
artery at the corticomedullary junction.
 Sheep. Several distal tubules
contain hyaline and coarsely granular hemoglobin casts that occurred
following
intravascular hemolysis (hemoglobinemia) from chronic copper toxicosis.
H&E stain.
 MYOGLOBINURIC NEPHROSIS

Myoglobinuria results from acute and extensive muscle necrosis and occurs in the
following:

• Exertional rhabdomyolysis in horses, greyhounds, and wild or exotic animals (see the
section on Kidney and Lower Urinary Tract, Disorders of Horses) Cassia spp. And
Karwinskia spp. Toxicity

• Severe direct trauma to muscle (e.g., traffic accident)

 Myoglobinuric Nephrosis, Kidney, Horse. A, Diffuse
myoglobin staining of the cortex and medulla (reddish-brown) is secondary
to myoglobinemia from severe rhabdomyolysis.
 Myoglobin casts are
present in dilated distal tubules, which are lined by flattened epithelial cells.
H&E stain.
 INCIDENTAL LESIONS OF RENAL TUBULES

 Pigment can be present in the renal tubules. The origin of hemosiderin pigment is
most likely from degradation of hemoglobin resorbed from the glomerular filtrate by
proximal tubular epithelium.

 In dogs, microscopic granules of hemosiderin are frequent incidental findings in the

cytoplasm of proximal convoluted tubular epithelial cells in kidneys that are
otherwise normal.

 Fine golden granules of lipofuscin (“wear and tear pigment”) can accumulate in renal
proximal and distal convoluted tubules of old cattle and in striated muscle, resulting
in lipofuscinosis. Grossly the renal cortex can have streaks of brown discoloration,
but renal function is not affected.
Cloisonné kidneys, which occur in goats, are the result of tubular membrane
thickening as a result of deposits of ferritin and hemosiderin.

GROSS
• - kidneys have diffuse, intense, black or brown discoloration of the cortex
• - medulla is spared. Although this lesion is striking, renal function is normal.
Cloisonné Kidney, Dorsal Section, Goat. The cortex is
diffusely black; the medulla is unaffected. (Courtesy Dr.
J. King, College of
Veterinary Medicine, Cornell University.)
 KLOSSIELLA EQUI INFECTION

 Klossiella equi is a sporozoan parasite of the horse, which has various stages of development in
the kidney after oral infection.
 No gross lesions are noted.
 Various stages of schizogony can be found microscopically in proximal convoluted tubular
epithelium and to a lesser extent in glomerular endothelium.
 Stages of sporogony are present in the epithelial cells of the loop of Henle, but different coccidial
stages occur multifocally in affected tubules.
 Occasionally,however, Klossiella equi has been associated with multifocal lesions of mild tubular
necrosis and, in the case of tubular rupture, with interstitial infiltrates of lymphocytes and plasma
cells.
 Renal function is typically normal.
 Klossiella equi Infection, Kidney, Horse. Tubular epithelium
containing various developmental stages of Klossiella equi (arrows).
H&E stain. (Courtesy Dr. J. Simon, College of Veterinary Medicine,
University
of Illinois.)
 Oxalate Nephrosis, Kidney. A, Pig. Oxalate nephrosis
following ingestion of oxalate-containing plants. The kidney is
diffusely pale beige and
swollen
 Dorsal section, dog. The cortex is beige and finely
mottled due to the deposition of multiple small foci of
oxalate crystals in the renal tubules
Dog. Tubular dilation, necrosis, and early regeneration (increased numbers of
epithelial cells lining several tubules). Numerous tubules contain oxalate
crystals (arrows), which have dilated the tubules and compressed their
epithelium. H&E stain.
Cat. Birefringent radiating sheaves of calcium oxalate
crystals in renal tubules. Polarized light. H&E stain.
 Pulpy Kidney Disease

Pulpy kidney disease is a unique manifestation of Clostridium perfringens type D enterotoxemia in

small ruminants, especially sheep.

The disease is precipitated by access to excessive starch in the small intestine, which allows for
anaerobic bacterial proliferation therein. Hyperglycemia and glucosuria can occasionally be
detected.

Histologic lesions include mild degeneration and necrosis of epithelium of the proximal
convoluted tubules with edema, congestion, and interstitial hemorrhage in the renal cortex and
congestion of the medulla.

Lesions are medullary congestion and hemorrhage and also soft to almost liquified (pulpy)
cortex
Pulpy Kidney Disease, Clostridium perfringens Type
D
Toxin, Kidney, Lamb. The epsilon exotoxin from an
enteric overgrowth
of Clostridium perfringens type D causes soft, swollen,
and pale kidneys,
often with hemorrhage, and are termed pulpy kidneys.
 The soft pulpy
nature of the kidney is the result of acute tubular
epithelial cell degeneration
and/or necrosis, interstitial edema, and hemorrhage. H&E
stain
DISEASES OF THE RENAL PELVIS
 HYDRONEPHROSIS

Hydronephrosis refers to dilation of the renal pelvis and accompanying renal atrophy.
The cause is partial or complete obstruction of urine outflow causing a progressive increase in
pelvic pressure.
Obstruction leading to hydronephrosis can be caused by congenital malformations of the ureter,
vesicoureteral junction, or urethra or from congenitally malpositioned kidneys with secondary
kinking of the ureter.

The more common causes of hydronephrosis are as follows:

• Accidental ligation of the ureter
• Ureteral or urethral blockage due to urinary tract calculi (see the section on Lower Urinary
Tract)
• Chronic inflammation
• Neoplasia of the ureter, bladder, and urethra
• Neurogenic functional disorders
Hydronephrosis, Kidney, Dorsal Section. Sheep. The
pelvis of each kidney is markedly dilated.
 Cow. Bovine kidneys are lobulated, and each
lobule has its own renal papilla surrounded by
a calyx, an extension of the pelvis. Thus in
early hydronephrosis, each of these calyces is
distended, and these distended calyces should
not be confused with the cysts of a cystic or
polycystic kidney.
 Chronic Hydronephrosis, Kidney, Dorsal Section, Cat.
Advanced hydronephrosis is characterized by loss of medullary tissue
and atrophy or even loss of the entire cortex in response to elevated
pelvic fluid pressure. Note that this case was so severe that only the renal
capsule, which contains clear yellow fluid, remains.