Primary or Acquired
- Aquired: tubules dilated due to total or partial occlusion of functioning tubules, common in renal disease involving fibrosis.
- Commonly at corticomedullary junction
- End-artery supply
- Usually interlobular artery blocked and cortex involved
- Infarcts often wedge-shaped with base against cortex and apex towards medulla = zone of cortical parenchyma supplied by the obstructed interlobular artery
- Necrosis of the renal medulla due to ischaemia
- Papillotoxic drugs: Phenylbutazone/Flunixin Meglumine administration to dehydrated horses, high dose paracetamol, ibuprofen, aspirin in small animals
- Target medullary interstitial cells, which have key role in synthesis of prostaglandins, antihypertensive factors and GAG matrix. Causes reduced PG synthesis, which reduces normal renal blood flow and causes ischaemia
- Degenerative change in tubular epithelium and inner medulla
- Anything reducing blood supply to medulla -> very susceptible to anoxia due to poor blood supply from vasa recta and high metabolic demand of tubules
- Ischaemic necrosis of papillae
- Chronic haemolytic disease
- Golden brown/yellow pigment in cytoplasm of macrophages, stains with prussian blue 'heart failure cells'
- Erythrocytes engulfed by macrophages -> haemoglobin split into porphyrin & globulin
- Brown discolouration of renal cortex
- Ayrshire cattle, old dairy cows
- Lipofuscin 'wear & tear' pigment
- Masseter muscles, heart, adrenal cortex
- Vitamin E/Selenium deficiency -> lipid peroxidation by free radicals
Amyloid = insoluble protein with beta-pleated sheet conformation formed after incomplete proteolysis of several soluble amyloidogenic proteins
AL= fragments from monoclonal immunolgobulin light chains (plasma cell tumour, multiple myeloma)
AA= reactive amyloidosis, chronic inflammatory disease -> macrophage activation -> IL-1 -> liver cells -> serum acute phase protein called serum amyloid-associated protein (SAA) -> amyloid deposits composed of fragments of SAA
- Deposition of amyloid in glomeruli
- Enlarged, pale, firm kidneys, affected glomeruli seen as yellowish spots in cortex
- Iodine stains glomeruli brown, subsequent dilute sulphuric acid turns them blue-purple
- Histopath: pink homogenous material in glomerulus
- Amyloid stains pink with Congo Red and appears 'apple-green' in polarised light
Pulpy Kidney (Clostridium)
Lead, mercury, cadmium, bismuth
2. Deposition of minerals
Urates (birds & reptiles), also joints
Oxalates (ethylene glycol toxicity, plants)
3. Storage degeneration
Glycogen & lipid in diabetes mellitus
Lipid in Cushings or acetonemia in ruminants
- Deposition of immune complexes in basement membrane
- Seen grossly as diffuse pitting on surface
Membranous: Diffuse, even thickening of the basement membrane, seen predominantly in cats due to subepithelial immunoglobulin complex deposition. Following removal of deposited material, cavities in basement membrane filled with basement membrane-like material -> sceloritic change. Periodic acid schiff positive material on basement membrane.
Membranoproliferative: Thickening of basement membrane & proliferation of mesangial cells and parietal epithelium with adhesions between vascular tuft and capsule. Most common form in dogs.
- Embolic nephritis
- Pyogranulomatous nodules on cortex of cats with FIP
- Neutrophils, macrophages, fibrin
- Swollen, red cortex & medulla
- Leptospirosis in pigs, cattle
- Initially enlarged kidneys, then shrinkage with extensive fibrosis and capsular adhesions
- Histopath: Initially hyperaemia, lymphoplasmacytic inflammation, tubular necrosis, fibrous tissue laid down which destroys 'normal' tubules and becomes self-perpetuating
- Cats causes polar scarring of the kidney
Usually ascending, frequently accompanied by inflammation of ureters & bladder, predisposing factor urinary stasis
- Urinary stasis: Common during pregnancy in cows & sows, disease very common post-partum, can also occur following service in the sow.
- Vesiculoureteral reflux during micturition, occurs more readily when pressure increased in bladder e.g. urethral obstruction. Bacterial lower UTI can enhance vesiculoureteral reflux. When the bladder is inflamed (cystitis), the normal competancy of the vesiculoureteral valve can be compromised. Endotoxin can inhibit normal urinary peristalsis, increasing reflux.
- Acute pyelonephritis: Swollen kidney, patchy congestion, on cut surface necrotising, exudative, haemorrhagic inflammation in renal pelvis with ascending inflamed tracts into medulla and cortex. Ureters are dilated, inflamed and contain pus.
- Chronic pyelonephritis: Medulla appears excavated with fibrous tracts running to the capsule. Kidney is shrunken, distorted and has grey patches among diffuse tan discolouration
- Histopath: zones of necrosis, colonies of bacteria, neutrophils in cortex which have tracked up from medulla. In chronic stage fibrous scar tissue in the medulla with ascending fibrous tracts into cortex, mononuclear inflammatory infiltrate
- Cows: Corynebacterium renale, obligate urinary tract pathogen, requires urinary stasis to colonise. Urease splitter, ammonium smell on sectioning fresh kidney. Common in pregnancy due to gravid uterus causing damage to parasympathetic ganglion & urinary stasis.
- Sow: Corynebacterium suis, Coliforms, Staph, Strep, usually mixed infection
Mainly seen in pigs at slaughter, rare in dogs & cats
Arise from metanephric blastema, malignant transformation during normal nephrogenesis or from neoplastic transformation on nests of embryonic tissue that persist in postnatal kidneys
Primitive glomeruli, attempts at tubule formation, loose mesenchyme
Rare, malignant, dogs & horses
- Originate in cortex, usually at one pole, some well-differentiated, others metastasise
- Secondary spread common at time of diagnosis
Common in foals and calves
- In the foetus, urachus connects bladder to alantois
- Failure to close at birth results in discharge of urine from umbilicus, partial failure to close can cause cysts along the pathway
- Occasionally, the mucosa closes, but the bladder musculature closure is incomplete -> diverticulum of bladder
Bovine Enzootic Haematuria
Bracken fern poisoning
Persistent haematuria & anaemia
Chronic inflammatory changes in the bladder procede to neoplasia (epithelial/mesenchymal), metastasis in 10%
May also cause carcinomas of alimentary tract
Smaller than normal kidneys of an adult dog
What conditions might you consider?
Hypoplasia, dysplasia, 'end-stage' kidney from chronic interstitial nephritis/glomerulonephritis
For each condition, what might you find on histopathology?
- Hypoplasia: reduced number of nephrons
- Dysplasia: variable areas of improperly formed nephrons, improperly formed glomeruli and fibrosis
- Chronic interstitial nephritis: diffuse fibrosis, mineralisation, cattered foci of lymphocytes & plasma cells
- Glomerulonephritis: increased density of glomerular tissue with adhesion to Bowman's capsule
What is the usual outcome for an animal with such kidneys?
- Chronic renal failure and uraemic syndrome
Capsule and cut surfaces of cow kidney, irregular pale areas on the capsule bordered by a red rim. The cut surface shows the pallour to extend downwards into the kidney
Describe the pathogenesis of these lesions
- Embolus blocks interlobar/interlobular arteries, usually at the corticomedullary junction and blood supply is cut off. As the kidney has an end-arter supply, the area supplied by this blocked artery undergoes necrosis. The red rim is haemorrhage seeping in from adjacent, non-infected tissue.
What is the name commonly given to these lesions?
What is the term given to the histopathological appearance of these lesions?
- Coagulative necrosis
Where else in the body might you look for the cause of these lesions and what might it look like?
- Mitral and aortic valves on left side of the heart, may be thrombus formation - adherent whitish mass covered by a film of blood
How does it arise?
- Partial blockage of the urinary tract, pressure of retained urine compresses the renal pelvis, tubules undergo atrophy and supportive connective tissue condenses & becomes more prominent
What is the implications of unilateral vs bilateral hydronephrosis?
- Bilateral: usually at level of urinary bladder or lower
- Unilateral: blockage usually at ureter
Which is the more serious condition?
- Bilateral, if only one kidney is affected, the other will compensate for the loss of renal function
What factors may lead to this condition?
- Compression from within: urolitiasis, neoplasia
- Compression from outside: surgical ligatures, nearby tumour
Diffuse degeneration and necrosis of convolutes tubules, sparing collecting ducts and glomeruli in a foal that died suddenly
What is the condition?
Acute or chronic?
What types of substances might cause this?
Enterotoxaemia ('pulpy kidney' in lambs), mycotoxins, heavy metals, plant poisons (oak leaves & acorns)
What might the gross appearance of the kidney have been?
- Enlarged, pale, greasy, outwardly bulging on cutting through the capsule
Dog died after a short illness including staggering and stupor. The animal was a guard dog in a breaker's yard and had been seen drinking from a puddle. Histopathology of the kidney shows substance within tubules and intratubular crystal formation is evident under polarised light
What common substance produces this type of lesion?
Ethylene glycol (antifreeze)
What is the sequence of events?
Initial inebriation, then becomes brighter before dying from renal failure
How do you treat it?
4-methylpyrazole, competes with ethylene glycol for metabolism in the liver (in cats use ethanol)
Metastatic melanoma (dog)
Black masses with brown discolouration of fluid due to pigment leakage
Not primary renal neoplasia, but common site for secondary tumours due to receiving 25% of CO
Lesions on digita & oral cavity carry poor prognosis (malignant)
Lesions on head and trunk usually benign
Diffuse pitting on capsule due to fibrosis secondary to inflammation, cut surface shows retention cysts at corticomedullary junction caused by fibrosis squeezing the remaining tubules and partial blockage causes tubules above to dilate
Lesions can be found in other tissues, what might these be?
- Necrotic stomatitis
- Haemorrhagic necrosis of gastric mucosa
- Necrotic endocarditis
- LV hypertrophy (hypertension)
- Necrosis of parietal pleura over intercostals
- Pulmonary oedema 'uraemic pulmonary oedema'
- Calcification in soft tissues including kidney and lung
- Osteodystrophia fibrosa
- Parathyroid hyperplasia
- Anaemia (bone marrow)
What is this syndrome called?
- Uraemic syndrome
Which endocrine gland becomes very active in this syndrome?