Lecture 1: Urinary 1

Question 1

What is the single underlying cause of renal papillary necrosis?

Answer 1

Ischemia.

Question 2

What are 3 potential sources for emboli that could lead to renal infarction (i.e., that originated outside the kidney)?

Answer 2

(1) Emboli from cardiac valvular endocarditis. (2) Thromboembolism due to sepsis. (3) Emboli from neoplasms. (4) Bacterial emboli.

Question 3

Explain how renal failure leads to renal fibrous osteodystrophy.

Answer 3

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”)

Question 4

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?

Answer 4

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.

Question 5

Explain the difference between primary and secondary renal papillary necrosis in terms of the cause.

Answer 5

(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.

Question 6

Draw a flow chart explaining the pathogenesis of soft tissue mineralization in animals in renal failure.

Answer 6

Renal disease –> Reduced glomerular filtration rate (GFR) –> Phosphorus retained in body –> Ca and P interact and precipitate –> Soft tissue mineralization.

Question 7

Explain the pathogenesis of the oral ulceration that may be seen in a uremic animal.

Answer 7

“(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.
“

Question 8

Compare the appearance of an acute versus chronic renal infarct caused by blockage of an interlobar artery.

Answer 8

(1) Acute: Red, swollen and hemorrhagic. (2) Chronic: Pale, shrunken and fibrotic.

Question 9

Describe the gross appearance of the characteristic subpleural lesions seen in a uremic dog or cat.

Answer 9

Gritty, white, horizontal (ladder-like) streaks of mineralization are seen in the subpleural connective tissue of the intercostal spaces.

Question 10

What is the characteristic renal lesion in a puppy that has died of herpesviral infection?

Answer 10

Ecchymotic hemorrhages are common in the renal cortex of neonatal puppies infected with herpesvirus.

Question 11

What, in general terms, causes post-renal failure/disease?

Answer 11

Inadequate discharge of urine from the kidney.

Question 12

Explain the pathogenesis of the gastric ulceration that may be seen in a uremic animal.

Answer 12

“(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.
“

Question 13

Describe the characteristic shape of a renal infarct caused by blockage of glomerular capillary tuft.

Answer 13

Pinpoint.

Question 14

What are the two major factors that determine the gross appearance of a renal infarct?

Answer 14

(1) The size of the blocked vessel. (2) The age of the lesion.

Question 15

What is the term for enlargement of the parathyroid glands seen in animals in renal failure?

Answer 15

Renal secondary hyperparathyroidism.

Question 16

Explain the pathogenesis of the pulmonary edema that may be seen in a uremic animal.

Answer 16

Endothelial damage (vasculitis) caused by azotemia leads to edema.

Question 17

Describe the characteristic shape of a renal infarct caused by blockage of an interlobar artery.

Answer 17

Wedge-shaped, with the point at the interlobar artery and the wide base at the renal surface.

Question 18

Give two reasons why the kidneys are prone to infarction.

Answer 18

(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.

Question 19

Explain the pathogenesis of the large intestinal hemorrhage and ulceration that may be seen in a uremic horse or cow.

Answer 19

Endothelial damage (vasculitis) caused by azotemia leads to (1) edema and (2) thrombosis and infarction of blood vessels.

Question 20

Explain, in terms of the unique vasculature of the kidney, why the medullary tubules are so susceptible to ischemic injury.

Answer 20

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.

Question 21

Explain the pathogenesis of the bone softening that may be seen in a uremic animal.

Answer 21

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”)

Question 22

Are lesions of uremia more or less severe in acute renal failure (when compared with chronic renal failure)? Why?

Answer 22

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.

Question 23

Explain the pathogenesis of the soft tissue mineralization that may be seen in a uremic animal.

Answer 23

Renal disease –> Reduced glomerular filtration rate (GFR) –> Phosphorus retained in body –> Ca and P interact and precipitate –> Soft tissue mineralization.

Question 24

You are performing a necropsy on a pig and notice numerous renal cortical petechial hemorrhages. What, in general terms, does this suggest?

Answer 24

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.)

Question 25

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?

Answer 25

(a) Renal papillary necrosis. (b) Non-steroidal anti-inflammatory drugs (NSAIDS), especially phenylbutazone or flunixin meglumine.

Question 26

What, in general terms, causes pre-renal failure/disease?

Answer 26

Inadequate perfusion of the kidney.

Question 27

Describe the gross appearance of an end-stage kidney.

Answer 27

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.

Question 28

Explain the pathogenesis of the enlarged parathyroid glands that may be seen in a uremic animal.

Answer 28

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)

Question 29

Explain how renal failure leads to renal secondary hyperparathyroidism.

Answer 29

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).

Question 30

Explain the pathogenesis of the atrial, aortic or pulmonary arterial thrombosis that may be seen in a uremic animal.

Answer 30

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.

Question 31

What is uremia?

Answer 31

The clinical syndrome (toxicosis) of renal failure.

Question 32

True or false: uremia refers to an increase in urea and other nitrogenous waste products in the blood.

Answer 32

False. This statement describes azotemia, not uremia.

Question 33

Explain why the lesions of uremia are more severe in an animal with chronic renal failure than in an animal with acute renal failure.

Answer 33

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.

Question 34

Name two drugs that commonly cause renal papillary necrosis in horses.

Answer 34

(1) Phenylbutazone. (2) Flunixin meglumine.

Question 35

What, in general terms, are the three requirements for a functioning kidney?

Answer 35

(1) Adequate blood supply. (2) Adequate volume of functional renal tissue. (3) Adequate drainage of urine from the kidney.

Question 36

What is an end-stage kidney?

Answer 36

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.

Question 37

Approximately what percentage of renal function must be lost before renal failure results?

Answer 37

Approximately 75%.

Question 38

What is the term for loss of bone mineral seen in animals in renal failure?

Answer 38

Renal fibrous osteodystrophy.

Question 39

The various lesions of uremia are generally attributable to one of three mechanisms. What are these three mechanisms?

Answer 39

(1) Endothelial damage. (2) Caustic injury by ammonia. (3) Altered Calcium:Phosphorus ratios.

Question 40

What typically causes primary renal papillary necrosis in small animals?

Answer 40

Non-steroidal anti-inflammatory drugs (NSAIDS), especially ibuprofen, aspirin, or acetaminophen.

Question 41

True or false: an azotemic animal is, by definition, in renal failure.

Answer 41

False. Azotemia is simply an increase in nitrogenous wastes in the blood. An azotemic animal does not necessarily show any clinical signs.

Question 42

Should you use the terms “dit-dots”, “thingies” and “ugly bits” in your exam answers?

Answer 42

no

Question 43

What is azotemia?

Answer 43

An increase in nitrogenous wastes in the blood.

Question 44

What typically causes primary renal papillary necrosis in horses?

Answer 44

Non-steroidal anti-inflammatory drugs (NSAIDS), especially phenylbutazone or flunixin meglumine.

Question 45

What are the two broad categories of disorder that cause renal hemorrhages?

Answer 45

(1) Endothelial damage. (2) Clotting disorders.

Question 46

Explain the pathogenesis of the pericarditis and endocarditis that may be seen in a uremic animal.

Answer 46

Endothelial damage (vasculitis) caused by azotemia leads to (1) edema and (2) thrombosis and infarction of blood vessels.

Question 47

Name 6 common lesions that may be seen in a uremic animal.

Answer 47

[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.

Question 48

Aside from NSAIDs, what other factors or diseases can lead to renal papillary necrosis?

Answer 48

Anything that causes a reduction of renal medullary blood flow, such as fibrosis, calculi in renal pelvis or lower urinary tract obstruction.

Question 49

True or false: renal papillary necrosis and renal medullary crest necrosis in dogs are the same disease.

Answer 49

true

Question 50

Explain the difference between acute renal failure and chronic renal failure.

Answer 50

(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.

Question 51

What information does an end-stage kidney provide about the original cause of the renal injury?

Answer 51

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.

Question 52

Describe the gross appearance of the kidney of a horse on long-term NSAIDs for lameness who has developed renal papillary necrosis.

Answer 52

There are discrete to coalescing areas of coagulative necrosis in the inner renal medulla. These appear greenish, and may also be accompanied by hemorrhage.