Urinary Pathology Study Questions Flashcards
What are the features of acute vs. chronic renal failure?
Acute: norm/high PCV, norm/high K, norm/enlarged kidneys, norm BCS, mildly elevated BUN compared to chronic, anuria, more severe metabolic acidosis
Chronic: anemia, norm/low K, small kidneys, muscle wasting, high BUN compared to acute, PU/PD, less severe metabolic acidosis
What are non-renal lesions that can be associated with renal failure?
Gastric ulcers, uremic gastritis
Ulcerative glossitis/stomatitis
Mineralization of intercostal pleura
Uremic pneumonitis
Parathyroid hyperplasia
Anemia
Define renal aplasia/agenesis
Absence of one or both of the kidneys
Can be incidental finding at necropsy
Define renal hypoplasia
Kidney(s) are smaller than normal
Define horseshoe kidney
Kidneys are fused at one pole, roughly at the midline
They are functionally normal
Can be incidental finding
What is PKD?
What breed does it mainly affect & how is it inherited in this breed?
When do animals typically exhibit evidence of renal dysfunction and renal failure?
What are the lesions of PKD?
From what part of the nephron do cysts develop?
PKD = polycystic kidney disease
Mainly affects Persian cats but can also affect Himalayans and British shorthairs
Autosomal dominant inheritance - defect in the PKD1 gene
Evidence of renal dysfunction at 3-10 y/o & renal failure at >7 y/o
Lesions: cysts that can arise from any segment of the nephron & can also have hepatic cysts
What shape are renal infarcts and why are they this shape?
Wedge shaped because of the end arterial circulation of a kidney
Administration of which drugs is associated with papillary necrosis?
What is the pathogenesis of papillary necrosis?
Horses treated with Bute and NSAIDs
NSAIDs inhibit COX which decrease PGE2 production → PGE2 maintains vasodilation in arterioles in the region of juxtamedullary nephrons → loss of this vasodilatory effect results in ischemia & necrosis
What do hydronephrosis & hydroureter occur secondary to?
Secondary to obstruction - usually partial or intermittent
What structures can be altered in GN?
What is the pathogenesis of immune complex GN?
What are conditions commonly associated with immune complex GN?
Are underlying conditions often identified at the time the animal is symptomatic for renal disease?
Structures than can be altered: basement membranes, mesangial matrix, mesangial cells, immune complex deposition
Pathogenesis: circulating immune complexes deposited in or adjacent to glomerular BM or Ab formed against the glomerular BM. Immune complexes may be deposited subendothelially, in the BM, or subepithelially. Complement fixation, leukocytic infiltration, and production of inflammatory mediators by mesangial cells may contribute to glomerular injury. Filtration barrier becomes compromised → protein loss
Conditions: chronic inflammatory stimuli - viral, chronic bacterial infections, parasitic and protozoal, autoimmune diseases, and neoplasms
The initial inciting cause is often not determined once the animal is symptomatic for renal disease.
What is the urinalysis finding that is most suggestive of glomerular disease?
What is the most sensitive way to measure it?
Proteinuria in the absence of inflammation or hemorrhage
Measure via UPC ratio (takes the USG into account)
What type of amyloid is most commonly present in glomerular amyloidosis?
Which animals have systemic reactive amyloidosis?
What histochemical stain would you use to confirm material in the glomeruli is amyloid?
What effect does amyloid deposition have on glomeruli and what does this lead to?
Most common type: serum amyloid A (acute phase protein)
Dogs and cats have systemic reactive amyloidosis - most commonly Shar Peis & Abyssinian cats
Lugol’s iodine applied to fresh tissue stains it dark brown
Congo red applied to histologic sections stains it red
Extensive glomerular amyloid deposition → compromise of the filtration barrier → proteinuria→ progressive renal insufficiency
What happens to tubules with significant glomerular disease?
Tubular degeneration - vacuolation of epithelial cells
Where in the kidney do bacteria most commonly lodge in septicemic processes?
Which bacteria most commonly cause embolic glomerulitis in horses?
In pigs?
In cattle?
Bacteria lodge mainly in glomerular and peritubular capillaries
Horses: Actinobacillus equuli
Pigs: Erysipelothrix rhusiopathiae
Cattle: Trueperella pyogenes from vegetative valvular endocarditis
What causes ischemic tubular necrosis?
Which part of the nephron is most significantly affected?
Can basement membranes be preserved in this condition, and why is this important?
Cause: hypotension/shock from hemorrhage, cardiogenic shock, etc
Proximal tubules mostly affected d/t high energy requirements
Depending on severity, disruption of the basement membranes can occur which means there is no scaffold for tubular epithelial regeneration
