Path urin Flashcards
What is this lesion and why are the kidneys susceptable ?
Kidney Infarction
The kidneys are susceptable
- Arterial blood supply to the cortex is terminal
- few anastomoses of the renal blood vessels - Receives a large portion of overall blood volume 25%
Define azotaemia and uraemia ?
Azotaemia = Excess urea and creatine in the blood.
Uraemia = Urinary constituents in the blood plus the condition (lesions and clinical signs) caused by their pressence.
What are the portals of entry for injurous agents to the kidney ?
Describe the defense mechanisms of the kidney ?
Defense mechanisms of the kidney
- Glomerular basement membrane - fenestrated endothelium and podocytes protect from circulating inflammatory cells
- Tubular basement membrane - prevents intraluminal organisms accessing interstitium
- Interstitium - lymphocytes
- Vasculature
Identify this lesion within the kidneys ?
Renal aplasia
(developmental abnormality)
Failure of development of one or both kidneys
- no recognisable renal tissue present + / - ureters
- familial tendancy
- Unilateral aplasia is compatible with life
Identify this lesion and describe its pathology ?
Renal hypoplasia
Incomplete development of the kidneys
- fewer than normal nephrons present at birth
- inherited condition large white
- clinically silent unless significant renal mass compromised
Definerenal dysplasia ?
Renel dysplasia
(developmental disorganised development of renal parenchyma)
Abnormal differentiation leads to altered structure
- inherited comdition suffolk sheep
- teratogenic effects BVDV cattle, canine herpes
Microscopic features
- immature glomerular tufts
- interstitial persistences of mesenchyme
- persistant metanephric ducts
- osseous and cartiliginaous metaplasia
Identify this lesion and describe its pathology ?
Renal cyst (developmental)
Spherical thin walled variable sized dilation of the renal tubules.
- weakened tubular basement membrane
- increased intratubular pressure
- clear water fluid
- common incidental findings in pigs
Identify this lesion and describe its pathology ?
Polycystic kidney disease
(developmental)
Pathology
- congenital (occurs sporadically in many species)
- may be acquired (usually secondary to nephron obstruction)
- inherited
- persian cats, terriers
Clinical signs
Many cyst that involve numerous nephrons
- renal function impaired with extensive involvement
Discuss the response of the glomerulus to injury ?
The reponse of the glomerulus to injury
Primary glomerular change is often caused by;
- deposition of immune complexes
- entrapment of thrombo-emboli (DIC) or bacterial emboli
- direct infection by bacteria viruses
Morphological changes
- necrosis,
- thickening of membranes
- infiltration of leukocytes
- atrophy and fibrosis (sclerosis) of glomerular tuft.
- reduced vascular perfusion
- filtration membrane damage (vascular permeability)
Major clinical finding of Glomerular disease
- proteinuria
- urine protein : creatine >2
Identify this lesion and describe its pathology ?
Glomerulonephritis
This encompases several diseases which are all characterised by inflammation of the glomerular.
GN most often results from immune mediated mechanisms
- deposition of immune complexes within glomeruli
- or formation of antibodies directed against the glomerular basement membrane.
Deposition of immune complexes usually occurs with persistent infections
- Porcine dermatitis nephropathy syndrome
- Feline leukaemia virus
- pyometra
- dirofilariasis heart worm in dogs
Describe the goss lesions of immune-mediated glomerulonephritis ?
Immune mediated glomerulonephritis
Gross lesions
Acute GN; gross lesions are usually subtle
- kidneys often slightly swollen, normal - pale
- with a smooth capsular surface
- cut surface of glomeruli, glomeruli are visible as pinpoint red dots.
Chronic GN;
Shrinking and pitting of capsule with cortical thining and fibrosis.
Three main forms = proliferative, membranous and membranoproliferative.
- highlight with periodic acid shift stain
Identify this lesion and describe its pathology ?
Glomerular amyloidosis
Pathology
Amyloid: insoluble fibrillar protein deposited in tissue
- glomerular most common site
- amyloid proteins composed of fragments of a serum acute phase reactive protein (SAA).
- chronic inflammatory response
Clinical signs
- Kidney enlarged
- diffusely pale
- waxy, firm
- smooth to finely granular capsular surface
- Glomeruli can become enlarged hypocellular eosinophilic spheres.
proetin losing nephropathy - proteinuria and diminished blood flow - renal papillary necrosis
How can renal amyloidosis be tested for ?
Congo red
Lugol’s iodine
- glomeruli become visible as multiple blue/ black dots
Identify this lesion and describe its pathology ?
Acute suppurative glomerulitis
(bacterial embolic nephritis)
Inflammation of the glomerulus
Suppurative glomeryulitis is the result of bacteraemia
- Erysipelothrix rhusiopathiae pigs
- Corynebacterium pseudotuberculosis (sheep and goats.
Clinical signs
Bacteria lodge in random glomeruli and to a lesser extent in interstitial cappillaries.
- multiple foci of inflammation
- microabscesses throughout the renal cortex
- neutrophils and haemorrhages
Identify the below lesion and describe its pathology ?
Glomerulosclerosis
Develops with any chronic disease where there is severe damage to the glomerulus.
Mild multifocal glomerulosclerosis
- glomeruli shrink
- become hyalinized because of an incease fibrous connective tissue
- exacerbates intial damage
- reducing the blood flow to tubules further
Glomeruli are hypocellular and essentially non functional.
Describe how the renal tubular epithelium responds to injury ?
Tubular epithelial cell responses include;
- degeneration, necrosis, apoptosis and atrophy
- compensatory hypertrophy in remaining tubules
- occurs when nephrons are lost, in an attempt to maintain renal function.
- the tubular epithelium can regenerate as long as the basement membrane remains intact + there are sufficient epithelial cells
Severe or chronic injury can result in necrosis and loss of function of the entire nephron
New nephrons cannot be generated
What are the clinical findings of tubular disease ?
Clinical findings of tubular disease
Highly variable dependant upon severeity
- mild acute injury unrecognised
- repeated bouts = chronic kidney disease CKD
- sudden major insult can cause acute tubular necrosis (ATN)
Describe the pathology underlying primary renal glucosuria ?
Primary renal glucosuria ?
Capacity of the tubular epithelial cells to absorb glucose is reduced.
- glucosuria (glucose in urine)
- incidental
- Norwegian elkhounds, scottish terriers
Describe the pathology underlying Fanconi’s syndrome ?
Fanconi syndrome
Generalised defect in tubular reabsorption
- Basenji dogs
- glucosuria, proteinuria, electrolytes
- can lead to renal insufficiency
- also acquired defects in tubular reabsorption
- antibiotics, toxins
Describe the pathology of acute tubular necrosis (injury)
Acute tubular necrosis
The single most important cause of acute renal failure ARF.
abrupt loss of 75% or more of renal capacity
Acute tubular necrosis injury is not caused by inflammation but may be followed with inflammation.
Cause
1. nephrotoxic damage - usually do not damage tubular basement memebranes
2. Ischaemic (hypoxic damage) to renal tubular cells - rupture shrunken collapsed lumens more severe
Toxins
pigments
heavy metals
NSAID
Fungal
Plant
Ethylene glycol
Substance is filtered by the glomeruli and high renal blood flow.
A. Proximal convoluted tubules
- both toxic and ischaemic damage usually involevs the proximal tubules.
- high metabolic rates
- first line of exposure
Identify this lesion ?
How would ischaemia cause oliguria or anuria ?
Three are three different mechanisms
Identify this nephrotoxic pigment ?
Haemoglobinuric nephrosis
- severe intravscular haemolysis
- haemoglobin secreted in urine
Haemoglobnuria casts have an additive deleterious effect on the tubular epithelium already undergoing ischaemic necrosis.
copper poisoning sheep
leptospirosis
autoimmune haemolytic anaemia
Identify this cast ?
Haemoglobin cast
- severe proximal tubule epithelial degeneration and necrosis
- tubular lumens filled with orange - red refractile material
Identify this type of nephrosis ?
Myoglobinuric nephrosis
(reddish brown staining corttex and medulla due to myoglobin)
Identify this tubular cast ?
Myoglobinuric nephrosis (horse)
Myoglobin casts present in dilated distal tubules.
Identify this lesion, and describe its pathology ?
Nephrotoxin = heavy metal Lead toxicity
Cause damage to membranes of the proximal tubular epithelial cells.
- renal lesions are non specific (except lead toxicity pictured).
- acid fast intranuclear inclusion bodies present in the proximal tubules
Identify this lesion of the keidney and describe its pathogenesis ?
Ethylene glycol intoxication.
Pathology
readily absorbed in the GI tract
metabolised in the liver generating toxic metabolites
glycolic acid
Oxalic acid combine with calcium - calcium oxylate crystals
- pale yellow foci of crystals in lumen - cause direct damage
- melamine cyanuric acid crystal
Identify this lesion ?
Identify the aetiology of this lesion and its pathology ?
Pulpy kidney Clostridium perfringens type D
Entertoxaemia
Change to carbohydrate rich diet
- tubular epithelium degeneration, necrosis, interstitial oedema and haemorrhage in both kidneys
- soft swollen
- pale ‘mushy’
- kidneys often haemorrhagic in fresh carcase
Pulpy kidneys
Identify this pathogen and describe its pathology ?
Leptospirosis
(warthin starry silver stain)
Bacterium Leptospira interrogans
- worlds most common zoonoses
- tubulointerstitial nephritis
- haemolysis, liver disease
- degeneration and necrosis of epithelial cells
Haematogenous route to localise in renal interstitium
Clinical signs
- nodular thin cortex
- infiltrate of mononuclear cells and fibroblasts
Identify this lesion and its pathology ?
White spotted kidney
(bacterial emboli - interstial nephritis)
- E.coli, salmonella, Brucella
- microabscess formation when bacteria seed the kidney
- multiple small white nodules of varying sizes through the cortex.
