Urinary Flashcards
What is the single underlying cause of renal papillary necrosis?
Ischemia.
What are 3 potential sources for emboli that could lead to renal infarction (i.e., that originated outside the kidney)?
(1) Emboli from cardiac valvular endocarditis. (2) Thromboembolism due to sepsis. (3) Emboli from neoplasms. (4) Bacterial emboli.
Explain how renal failure leads to renal fibrous osteodystrophy.
Renal disease –> Reduced glomerular filtration rate (GFR) –> Phosphorus retained in body –> Ca and P interact and precipitate –> Decreased available calcium –> Increased parathyroid hormone release in response –> Calcium resorption from bone –> Renal osteodystrophy (“rubberjaw”)
You are performing a necropsy on a dog and notice gritty, white, horizontal (ladder-like) streaks in the pleura of the intercostal spaces. What does this suggest?
These lesions occur due to soft tissue deposition of calcium secondary to uremia / renal failure. Intercostal mineralization is characterized, particularly in dogs, by calcification of the subpleural connective tissue of the cranial intercostal spaces.
Explain the difference between primary and secondary renal papillary necrosis in terms of the cause.
(1) Primary: Caused by non-steroidal anti-inflammatory drugs (NSAIDS). (2) Secondary: Caused by reduction of renal medullary blood flow for some reason other than NSAIDS, such as fibrosis, calculi in renal pelvis or lower urinary tract obstruction.
Draw a flow chart explaining the pathogenesis of soft tissue mineralization in animals in renal failure.
Renal disease –> Reduced glomerular filtration rate (GFR) –> Phosphorus retained in body –> Ca and P interact and precipitate –> Soft tissue mineralization.
Explain the pathogenesis of the oral ulceration that may be seen in a uremic animal.
(1) Endothelial damage (vasculitis) caused by azotemia leads to thrombosis and infarction of blood vessels. (2) Caustic injury to epithelium is secondary to the production of large concentrations of ammonia after splitting of salivary urea by bacteria.
Compare the appearance of an acute versus chronic renal infarct caused by blockage of an interlobar artery.
(1) Acute: Red, swollen and hemorrhagic. (2) Chronic: Pale, shrunken and fibrotic.
Describe the gross appearance of the characteristic subpleural lesions seen in a uremic dog or cat.
Gritty, white, horizontal (ladder-like) streaks of mineralization are seen in the subpleural connective tissue of the intercostal spaces.
What is the characteristic renal lesion in a puppy that has died of herpesviral infection?
Ecchymotic hemorrhages are common in the renal cortex of neonatal puppies infected with herpesvirus.
What, in general terms, causes post-renal failure/disease?
Inadequate discharge of urine from the kidney.
Explain the pathogenesis of the gastric ulceration that may be seen in a uremic animal.
(1) Endothelial damage (vasculitis) caused by azotemia leads to thrombosis and infarction of blood vessels. (2) Caustic injury to epithelium is secondary to the production of large concentrations of ammonia after splitting of gastric urea by bacteria.
Describe the characteristic shape of a renal infarct caused by blockage of glomerular capillary tuft.
Pinpoint.
What are the two major factors that determine the gross appearance of a renal infarct?
(1) The size of the blocked vessel. (2) The age of the lesion.
What is the term for enlargement of the parathyroid glands seen in animals in renal failure?
Renal secondary hyperparathyroidism.
Explain the pathogenesis of the pulmonary edema that may be seen in a uremic animal.
Endothelial damage (vasculitis) caused by azotemia leads to edema.
Describe the characteristic shape of a renal infarct caused by blockage of an interlobar artery.
Wedge-shaped, with the point at the interlobar artery and the wide base at the renal surface.
Give two reasons why the kidneys are prone to infarction.
(1) Kidneys have an end-arterial supply, with little collateral circulation. (2) Kidneys receive 25% of cardiac output and, therefore, emboli are likely to reach the renal arteries.
Explain the pathogenesis of the large intestinal hemorrhage and ulceration that may be seen in a uremic horse or cow.
Endothelial damage (vasculitis) caused by azotemia leads to (1) edema and (2) thrombosis and infarction of blood vessels.
Explain, in terms of the unique vasculature of the kidney, why the medullary tubules are so susceptible to ischemic injury.
The blood supply to medullary tubules is entirely dependent on an intact glomerular circulatory system. For example, a thrombus near a glomerulus may lead to ischemic necrosis of the tubules associated with that glomerulus.
Explain the pathogenesis of the bone softening that may be seen in a uremic animal.
Renal disease –> Reduced glomerular filtration rate (GFR) –> Phosphorus retained in body –> Ca and P interact and precipitate –> Decreased available calcium –> Increased parathyroid hormone release in response –> Calcium resorption from bone –> Renal osteodystrophy (“rubberjaw”)
Are lesions of uremia more or less severe in acute renal failure (when compared with chronic renal failure)? Why?
Less severe. The severity of lesions of uremia depends on the length of time that the animal has survived in the uremic state. Therefore, in acute renal failure, non-renal lesions are few, whereas many lesions can be present in chronic renal failure.
Explain the pathogenesis of the soft tissue mineralization that may be seen in a uremic animal.
Renal disease –> Reduced glomerular filtration rate (GFR) –> Phosphorus retained in body –> Ca and P interact and precipitate –> Soft tissue mineralization.
You are performing a necropsy on a pig and notice numerous renal cortical petechial hemorrhages. What, in general terms, does this suggest?
Petechial hemorrhages are common in the renal cortex of pigs that die of viremia or septicemia, e.g.,: hog cholera (swine fever), African swine fever, erysipelas, streptococcal infections, salmonellosis, other embolic bacterial diseases (e.g., Actinobacillus spp.)
You are performing a necropsy on a horse and notice several discrete to coalescing areas of coagulative necrosis in the inner renal medulla. What is the most likely (a) diagnosis and (b) cause?
(a) Renal papillary necrosis. (b) Non-steroidal anti-inflammatory drugs (NSAIDS), especially phenylbutazone or flunixin meglumine.
What, in general terms, causes pre-renal failure/disease?
Inadequate perfusion of the kidney.
Describe the gross appearance of an end-stage kidney.
The characteristic end-stage kidney is pale tan to white, is shrunken & pitted, is firm (fibrosis) to gritty (mineral), has adhesions between the cortex and capsule and has a thinned cortex.
Explain the pathogenesis of the enlarged parathyroid glands that may be seen in a uremic animal.
Renal disease –> Reduced glomerular filtration rate (GFR) –> Phosphorus retained in body –> Ca and P interact and precipitate –> Decreased available calcium –> Increased parathyroid hormone release in response –> Parathyroid glands enlarge to achieve this (i.e., renal secondary hyperparathyroidism)
Explain how renal failure leads to renal secondary hyperparathyroidism.
Renal disease –> Reduced glomerular filtration rate (GFR) –> Phosphorus retained in body –> Ca and P interact and precipitate –> Decreased available calcium –> Increased parathyroid hormone release in response –> Parathyroid glands enlarge to achieve this (i.e., renal secondary hyperparathyroidism).
Explain the pathogenesis of the atrial, aortic or pulmonary arterial thrombosis that may be seen in a uremic animal. (2)
Endothelial damage (vasculitis) caused by azotemia leads to thrombosis. In addition, loss of the anticoagulant antithrombin III by glomerular leakage is conducive to the formation of large mural thrombi at these sites.
What is uremia?
The clinical syndrome (toxicosis) of renal failure.
True or false: uremia refers to an increase in urea and other nitrogenous waste products in the blood.
False. This statement describes azotemia, not uremia.
Explain why the lesions of uremia are more severe in an animal with chronic renal failure than in an animal with acute renal failure.
The severity of lesions of uremia depends on the length of time that the animal has survived in the uremic state. Therefore, in acute renal failure, non-renal lesions are few, whereas many lesions can be present in chronic renal failure.
Name two drugs that commonly cause renal papillary necrosis in horses.
(1) Phenylbutazone. (2) Flunixin meglumine.
What, in general terms, are the three requirements for a functioning kidney?
(1) Adequate blood supply. (2) Adequate volume of functional renal tissue. (3) Adequate drainage of urine from the kidney.
What is an end-stage kidney?
End-stage kidneys show changes related to nephron loss that are not specific to the original disease or insult, but are common end-stage responses to many disease processes. At the time of diagnosis/necropsy the original inciting cause of disease is usually not evident and may never be known.
Approximately what percentage of renal function must be lost before renal failure results?
Approximately 75%.
What is the term for loss of bone mineral seen in animals in renal failure?
Renal fibrous osteodystrophy.
The various lesions of uremia are generally attributable to one of three mechanisms. What are these three mechanisms?
(1) Endothelial damage. (2) Caustic injury by ammonia. (3) Altered Calcium:Phosphorus ratios.
What typically causes primary renal papillary necrosis in small animals?
Non-steroidal anti-inflammatory drugs (NSAIDS), especially ibuprofen, aspirin, or acetaminophen.
True or false: an azotemic animal is, by definition, in renal failure.
False. Azotemia is simply an increase in nitrogenous wastes in the blood. An azotemic animal does not necessarily show any clinical signs.
Should you use the terms “dit-dots”, “thingies” and “ugly bits” in your exam answers?
No.
What is azotemia?
An increase in nitrogenous wastes in the blood.
What typically causes primary renal papillary necrosis in horses?
Non-steroidal anti-inflammatory drugs (NSAIDS), especially phenylbutazone or flunixin meglumine.
What are the two broad categories of disorder that cause renal hemorrhages?
(1) Endothelial damage. (2) Clotting disorders.
Explain the pathogenesis of the pericarditis and endocarditis that may be seen in a uremic animal.
Endothelial damage (vasculitis) caused by azotemia leads to (1) edema and (2) thrombosis and infarction of blood vessels.
Name 6 common lesions that may be seen in a uremic animal.
[Any six] (1) Ulcerative stomatitis & glossitis. (2) Gastric ulceration & mineralization. (3) Ulcerative and hemorrhagic colitis (cattle and horses). (4) Fibrinous pericarditis / ulcerative endocarditis. (5) Atrial and aortic thrombosis. (6) Pulmonary edema (uremic pneumonitis). (7) Various soft tissue mineralization. (8) Fibrous osteodystrophy. (9) Renal secondary hyperparathyroidism.
Aside from NSAIDs, what other factors or diseases can lead to renal papillary necrosis?
Anything that causes a reduction of renal medullary blood flow, such as fibrosis, calculi in renal pelvis or lower urinary tract obstruction.
True or false: renal papillary necrosis and renal medullary crest necrosis in dogs are the same disease.
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Explain the difference between acute renal failure and chronic renal failure.
(1) ARF: Renal function is abruptly impaired such that ~75% of function is lost. ARF is potentially reversible but can rapidly cause death if untreated. (2) CRF: Renal function is progressively and irreversibly lost until failure occurs at ~75% of loss of function.
What information does an end-stage kidney provide about the original cause of the renal injury?
Very little to none. End-stage kidneys show changes that are not specific to an original disease or insult, but are common end-stage responses to many disease processes. At the time of diagnosis/necropsy the original inciting cause of disease is usually not evident and may never be known.
Describe the gross appearance of the kidney of a horse on long-term NSAIDs for lameness who has developed renal papillary necrosis.
There are discrete to coalescing areas of coagulative necrosis in the inner renal medulla. These appear greenish, and may also be accompanied by hemorrhage.
Name two conditions that commonly cause hemoglobinuric nephrosis in dogs.
(1) IMHA (immune-mediated hemolytic anemia). (2) Leptospirosis.
In which species of domestic animal is glomerulonephritis the most common cause of renal failure?
Dogs.
Name one dog breed that has a familial/hereditary/genetic predisposition to renal amyloidosis.
Shar Pei.
You are performing a necropsy on a dog and notice that both kidneys are very darkly stained and that the renal pelvic fat is yellow. This dog has a history of passing red-brown urine. What is the most likely cause of this?
Hemoglobinuric nephrosis due to intravascular hemolysis (several causes, including IMHA in dogs, copper toxicity in sheep, leptospirosis in cattle & dogs & red maple toxicosis in horses). Myoglobinuric nephrosis is less likely because it tends not to stain fat yellow.
Explain the pathogenesis of the hypercholesterolemia that may be seen in the nephrotic syndrome.
Loss of plasma proteins into urine –> liver responds by generalized increased protein production, and cholesterol production is also upregulated.
Proteinuria, although suggestive of glomerular disease, is not exclusively caused by glomerular disease. What else can cause proteinuria?
Inflammation of the lower urinary tract.
Which type of cell in the renal corpuscle is responsible for phagocytosis of deposited immune complexes?
Mesangial cell.
How are the basement membranes of the glomerular capillary tufts different from basement membranes elsewhere in the body?
The glomerular basement membrane is thick (300-350 nm). Its negative charge and collagen network impede the passage of large protein molecules, most importantly albumin and hemoglobin.
Describe the typical gross appearance of a kidney affected by amyloidosis.
Grossly, kidneys affected by amyloid deposition are diffusely tan, waxy (firm), friable and of normal size or slightly enlarged.
What clinicopathologic finding is the hallmark of glomerular disease?
Proteinuria.
Why is it deleterious to the glomerulus having immune complexes deposited in the glomerular basement membrane? Explain the pathogenesis.
Deposition in glomeruli –> Complement fixation –> Chemotaxis of neutrophils –> Release of harmful mediators of inflammation –> Continued damage by release of inflammatory mediators from monocytes in chronic stages. All this leads to thickening of the glomerular basement membrane. Paradoxically, this thickening makes the GBM “leaky” probably due to changes in charge and pore size.
How often is the specific cause of glomerulonephritis in domestic animals identified?
Rarely.
You are performing a necropsy on a foal and notice that both kidneys contain dozens to hundreds of randomly scattered pinpoint white foci. What is the most likely bacterial cause of this?
Actinobacillus equuli.
Name a condition that commonly causes hemoglobinuric nephrosis in horses.
Red maple toxicity.
What are the two major categories of immune complex deposition in the glomerular basement membrane and which is by far the more common in domestic animals?
(1) Deposition of circulating antibody-antigen complexes that have formed in response to a variety of chronic diseases. (2) Autoantibodies directed at the glomerular basement membrane. Cause number 1 is by far the most common in domestic animals.
Name a condition that commonly causes hemoglobinuric nephrosis in cattle.
Leptospirosis.
Which parts of the lily (leaves or flowers) are nephrotoxic to cats?
Both leaves and flowers are toxic.
How are the endothelial cells lining the glomerular capillary tufts different from endothelial cells elsewhere in the body?
Glomerular capillary endothelial cells have pores (fenestrations) in their cytoplasm that make them “leaky” (i.e., freely permeable to most blood constituents except red blood cells, white blood cells and platelets).
