Renal Pathology Flashcards

1
Q

How does the structure of the kidney compare is different species?

A

UNIPYRAMIDAL = unilobar = cats, dogs, horses, sheep, goats

MULTIPYRAMIDAL = multilobar = pigs and cattle
- no renal crests, multiple renal papillae
- each lobe acts as its own kidney

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2
Q

What is the normal cortex to medulla ratio of the kidney?

A

1:2-3

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3
Q

What multipyramidal kidney is the only one with external lobation?

A

cattle kidneys

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4
Q

This kidney is seen in a feline patient. Is this normal?

A

YES - cat tubular epithelium has a lot of lipids, which makes it pallor and prominent veins are normal

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5
Q

This kidney is seen in a bovine patient. Is this normal?

A

NO - this kidney is pale, probably caused by anemia (Haemonchus in abomasum) or diffuse necrosis
- external lobation is normal!

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6
Q

What are the 4 structural units of the kidney? What makes up the functional unit of the kidney?

A
  1. renal corpuscle (glomerulus + Bowman’s capsule)
  2. tubules
  3. interstitium
  4. vasculature

nephron = renal corpuscle + renal tubules

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7
Q

What is the function of the renal interstitium?

A

contains renal vasculature, which supplies blood to the kidney

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8
Q

What part of the kidney receives blood first?

A

glomerulus —> renal tubules

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9
Q

What parts of the renal architecture make it prone to infarction?

A
  • arteries do not anastomose
  • arteries are at a 90-degree angle
  • 1 artery with multiple angles supply the organ
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10
Q

How does blood flow in the kidney?

A
  • renal artery
  • interlobar artery
  • interlobular artery
  • intralobular atery
  • afferent arteriole
  • glomerular capillary
  • efferent arteriole
  • intralobular vein
  • interlobular vein
  • renal vein
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11
Q

How can the tubules in the kidney be differentiated?

A

PROXIMAL = microvilli/brush border increases absorptive surface for water, urinary molecule, and protein absorption

DISTAL = no brush border

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12
Q

Renal corpuscle:

A
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13
Q

What 3 structures make up the glomerular filtration barrier? What is this barrier’s function?

A
  1. endothelial cells of glomerular capillary
  2. basment membrane of glomerular capillary
  3. visceral epithelial cells (podocytes)

filter plasma to maintain ionic and osmotic homeostasis in the blood

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14
Q

How does chronic renal disease commonly affect the kidney? What does this tend to result in?

A

has a tendency to affect multiple components of the kidney, resulting in chronic renal failure (CRF) and shrunken, scarred end-stage kidneys

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15
Q

What are 5 specific functions of the kidney? What is its overall function?

A
  1. excrete metabolic waste
  2. maintain normal concentrations of salt, water, ad electrolytes
  3. regulate acid-base balance
  4. produce hormones
  5. convert vitamin D into its active form (1,25-dihydroxy cholecalciferol)

maintains constant extracellular environment in the body

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16
Q

What 3 hormones are produced in the kidney?

A
  1. erythropoietin
  2. renin
  3. prostaglandins
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17
Q

What is required for normal kidney function?

A

adequate renal perfusion (>60 mmHg), sufficient renal tissue, and normal elimination of urine

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18
Q

What are the 3 common outcomes of renal disease? What is the most commonly used index of renal failure?

A
  1. imbalance of salt and water - EDEMA
  2. imbalance of acids and bases - METABOLIC ACIDOSIS
  3. retention of wastes

urea and/or creatinine retained in the blood

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19
Q

What does the disturbance of the 5 functions of the kidney result in?

A
  1. excretion of metabolic waste = UREMIA
  2. maintenance of salt and water concentrations = EDEMA
  3. regulation of acid-base balance = ACIDOSIS (low bicarbonate)
  4. production of hormones = ANEMIA, HYPERTENSION, ISCHEMIC NECROSIS
  5. synthesis of activated vitamin D = initial HYPOCALCEMIA that overly stimulates the parathyroid gland leading to HYPERCALCEMIA
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20
Q

When is renal failure observed? How can acute and chronic kidney failure be differentiated?

A

when renal function capacity is impaired by ~75% or more

ACUTE: swollen kidney with pale cortex; cut surface tends to bulge —> interstitium and necrotic cells block urine filtration
CHRONIC: shrunken, necrotic chalky

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21
Q

What are 3 causes of acute renal failure?

A
  1. PRERENAL - transient hypoperfusion due to hypotension, decreased cardiac output, or decreased arterial blood volume (hypovolemia)
  2. POSTRENAL - obstruction or urinary tract
  3. RENAL - acute glomerulonephritis (septicemia by bacteria/virus), acute interstitial nephritis (septicemia), acutre tubular necrosis (nephrotoxins/ischemia)**
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22
Q

What are the 2 results of acute renal failure due to tubular necrosis?

A
  1. OLIGURIA: decreased urine production due to impairment of epithelial cells (BM), allowing urine to move into the interstitium
  2. ANURIA: no urine production due to tubular obstruction
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23
Q

Perirenal edema, acute renal failure by tubular necrosis:

A

necrotic epithelium = leakage into interstitium

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24
Q

Diffuse pallor, acute renal failure by tubular necrosis:

A

(cysts are incidental findings, especially in bovine kideys)

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25
Q

Acute renal failure tubular necrosis, histology:

A
  • tubules lost nuclei (karyolysis)
  • eosinophilic cellular debris within lumen
  • nuclear pyknosis and karyorrhexis
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26
Q

What 3 outcomes lead to death by acute renal failure?

A
  1. increased serum potassium (hyperkalemia) = cardotoxicity
  2. metabolic acidosis (decreased bicarbonate)
  3. pulmonary edema, retention of fluid (swollen, wet)
27
Q

What is characteristic of chronic renal failure? What is thought to be its cause?

A

progressive renal disease with loss of nephrons and severe scarring

may be a progression from ARF, but most of the time its idiopathic

28
Q

What are 3 common results of chronic renal failure? What is the hallmark?

A
  • lacking the ability to concentrate urine —> polyuria, polydipsia
  • nonregenerative anemia

alteration in calcium-phosphate metabolism —> hyperphosphatemia, hypo/hypercalcemia

29
Q

How do fibrous osteodystrophy and soft tissue calcification result from chronic renal failure?

A

increased PTH secretion from secondary hyperparathyroidism due to initial hypocalcemia causes calcium to be released from bone, making it much softer

30
Q

What are 6 common observations on histology of the kidneys during chronic kidney disease?

A
  1. mononuclear interstitial inflammation
  2. interstitial fibrosis
  3. tubular atrophy and loss
  4. glomerulosclerosis
  5. thickened Bowman’s capsules
  6. tubular and glomerular ectasia
31
Q

Acute vs. chronic kidney disease:

A
32
Q

What is azotemia?

A

biochemical abnormality characterized by elevation of blood urea and/or creatinine, but WITHOUT obligatory clinical manifestation of renal disease

33
Q

What is uremia?

A

urine in the blood; CLINICAL SYNDROME of renal failure, caused by biochemical disturbances and is often accompanied by extrarenal lesions

34
Q

What are the extrarenal lesions of uremia?

A
  1. uremic gastropathy (dogs and cats)
  2. uremic colitis (horses and cattle)
  3. soft tissue mineralization
  4. pulmonary edema
  5. ulcerative/necrotizing glossitis and stomatitis
  6. uremic endocarditis and perocarditis
  7. parathyroid hyperplasia
  8. fibrous osteodystrophy
35
Q

What is uremic gastropathy? What is a less common result?

A

development of ulcers and hemorrhage secondary to vasculitis, where the urea and creatinine in the blood is toxic to the endothelium and bacteria in the GI tract are able to turn the urea into ammonia, causing mucosal damage

mucosal calcfication due to alteration of Ca/P metabolism

36
Q

Uremic gastropathy, mucosal calcification:

A
37
Q

Uremic gastropathy, necrotizing vasculitis:

A
38
Q

What aspect of chronic renal failure causes uremic colitis?

A

ulcers and hemorrhage secondary to vasculitis and the bacterial synthesis of ammonia from urea in the colon

39
Q

What aspect of chronic renal failure causes soft tissue mineralization?

A

altered calcium-phosphorus metabolism

(increased calcium deposits on pleura - DOGS)

40
Q

Soft tissue mineralization, larynx:

A
41
Q

Soft tissue mineralization, nephrocalcinosis:

A

mineralization further increases kidney damage

42
Q

What aspect of chronic kidney failure causes pulmonary edema?

A

presence of uremia and creatinine in the blood causes vasculitis, increasing vascular permeability

43
Q

Uremic pneumonitis:

A

mineralization of alveolar septa

44
Q

What aspects of chronic kidney failure cause ulcerative glossitis and stomatitis? How can this be observed in a physical exam?

A
  • vasculitis
  • ammonia production by bacteria from the urea present in the saliva
  • urine-like breath
45
Q

Ulcerative glossitis and stomatitis:

A

+ icterus because dog has leptospirosis, which affects the kidneys, spleen, and liver

46
Q

What aspect of chronic kidney failure causes necrotizing glossitis (infarct)?

A

fibrinoid necrosis of the arterioles

47
Q

What aspects of chronic kidney disease cause uremic endocarditis and pericarditis?

A

endothelial damage > increased vascular permeability

48
Q

Uremic endocarditis, left atrium histology:

A

neutrophils, fibrin, and granular basophilic material (mineralization)

49
Q

What aspect of chronic kidney disease causes parathyroid hyperplasia?

A

altered calcium-phosphate metabolism
(can rarely be due to a high-phosphate diet)

kidney damage —> increased P —> decreased Ca —> chief cells become hyperplastic to compensate and produce more PTH and raise calcium levels

50
Q

What aspect of chronic kidney disease causes fibrous osteodystrophy?

A

altered calcium-phosphate metabolism

  • increased P and decreased Ca cause osteoclasts multiply and resorb Ca from the bone into the blood to compensate for kidney damage
  • bone becomes replaced with fibrous connective tissue causing the production of a swollen-looking maxilla +/- mandible
51
Q

Fibrous osteodystrophy:

A

altered Ca/P metabolism
(AKA rubber jaw)

52
Q

Fibrous osteodystrophy, alpaca:

A

bone so soft it can be cut by a knife

53
Q

Extrarenal lesions of uremia, summary:

A
54
Q

What is renal agenesis? What species have an increased predilection?

A

complete lack of development of renal tissue, usually unilateral, but can be bilateral

  • Beagles
  • Shetland Sheepdogs
  • Dobermans
55
Q

What is renal hypoplasia? What are the 2 criteria for diagnosis?

A

incomplete development of kidneys leading to reduced size without scarring

  1. reduction in size of the kidneys by more than 50%
  2. no pre-existing renal disease
56
Q

Unilateral renal hypoplasia:

A
57
Q

What is renal dysplasia? What are the 2 types?

A

disorganized development of renal parenchyma caused by anomalous differentiation - malformation with messed up architecture

  1. JUVENILE NEPHROPATHY: non-inflammatory, degenerative chronic renal disease of obscure pathogenesis in young animals, presenting clinical signs early in life
  2. FAMILIAL/BREED NEPHROPATHY: inheritence of nephropathy is determined with an age of onset from a few weeks to several years (usually 4-18 months)
58
Q

What is the gross appearance of renal dysplasia?

A

shrunken, misshapen, fibrotic, pale due to degenerative lesions, often cystic

59
Q

What is characteristic on histology of renal dysplasia?

A

asynchronous maturation

  • primitive ducts and mesenchyme
  • fetal glomerulus
  • paucity of tubules with non-inflamed connective tissue
    seen in nephrogenesis, not fully mature kidneys
60
Q

What is an ectopic kidney?

A

presence of a kidney in an unusual place, leaving an increased chance of also having displaced ureters
- usually unilateral and an incidental finding

61
Q

What are fused kidneys?

A

an incidental finding with no functional defects where the cranial or caudal poles become fused during nephrogenesis
- AKA horseshoe kidneys

62
Q

What are the 2 types of renal cysts?

A
  1. CONGENITAL - few in number, same size, incidental finding on a necropsy (polycystic kidney disease in cats)
  2. ACQUIRED - tubules or glomeruli are obstructed by scar tissue, leaving kidneys with extensive interstitial fibrosis (renal insult, chronic renal disease)
63
Q

What causes feline polycystic kidney disease? In which cats is it commonly found in?

A

autosomal dominant mutation in PKD1 and PKD2 genes that encode for polycystin, which is a part of the primary cilia of the tubular epithelial cells that usually sense fluid movement through the lumen

Persians and Persian-crosses

64
Q

What do polycystic kidneys look like? What other organs can be affected?

A

cysts may arise anywhere along the nephron, be located in the cortex or medulla, and vary from barely visible to several centimeters in diameter —> highly variable!

pancreas and liver