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Semester II Pathology > Patterns of Disease: Kidney 1 > Flashcards

Patterns of Disease: Kidney 1 Flashcards

-Review basic renal anatomy and physiology- species differences, structure and function -Renal failure -Portals of entry for disease -Defence mechanisms -Renal diseases/lesions- locations, species differences, pathogenesis, entry, matching gross and histological lesions to find likely aetiology. -Lower urinary tract.

1
Q

RENAL ANATOMY

A

Inner medulla, outer cortex.
DOG/CARNIVORES/HORSES- Unilobar, urine collects in renal pelvis (drains to ureters).
COW- Multilobar, urine collects in calyces to drain to ureter
PIG- Appears smooth on outside, but is multilobar internally. Urine collects in renal pelvis.

RENAL CORPUSCLES can be seen histologically. These consist of glomerulus plus Bowman’s capsule and are present in the cortex.
The medulla contains the tubules, and is separated from the cortex by the cortico-medullary junction.

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2
Q

RENAL FUNCTION

A

-Filter blood to make urine.
20-25% of cardiac output goes to the kidney to allow this.
The functional unit of the kidney is the NEPHRON.
-Urine formation
-Acid base regulation (bicarbonate reclamation from glomerular filtrate at PCT)
-Water conservation- reabsorption, countercurrent mechanism, ADH, urea gradient.
-Maintenance of extracellular potassium
-Endocrine fucntions- renin-angiotensin, erythropoetin, vitamin D activation.

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3
Q

RENAL VASCULATURE

A

RENAL ARTERY enters at kidney hilus
-> INTERLOBAR ARTERY
-> ARCUATE ARTERY (at corticomedullary junction)
-> INTERLOBULAR ARTERIES.
The interlobular arteries are terminal- they have no anastomoses. This makes them susceptible to infarction and ischaemic necrosis.

INTERLOBULAR ARTERIES

  • > AFFERENT ARTERIOLES
  • > GLOMERULAR CAPILLARIES
  • > EFFERENT ARTERIOLES
  • > PERITUBULAR CAPILLARY NETWORK
  • > VASA RECTA (medulla) and INTERLOBULAR VEIN
  • > ARCUATE VEIN
  • > INTERLOBAR VEIN
  • > RENAL VEIN.

The glomeruli are supplied first, then the tubules.

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4
Q

GLOMERULUS

A

Tuft of fenestrated, endothelial cell lined capillaries, held together by a supporting structure of cells in a glycoprotein matrix (mesangium).
FILTER blood to remove nitrogenous waste (BUN and creatinine)
Keep in protein- repel negative charges eg. albumin.
Filtration is by particle size and charge.
FILTRATION BARRIER SEPARATES BLOOD AND URINE.

Microscopically, we can see capillaries, urinary space, visceral epithelial cells (podocytes), parietal epithelial cells, Bowman’s space between these cells, mesangial cells and endothelial cells.

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5
Q

FILTRATION BARRIER

A 
In the glomerulus. 
Separates blood and urine. 
Three parts:
1. FENESTRATED ENDOTHELIUM
2. GLOMERULAR BASEMENT MEMBRANE
3. PODOCYTES- formed from folded over tubule epithelium (visceral epithelium)

The space between the parietal and visceral tubule epithelium is the Bowman’s capsule.

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6
Q

GLOMERULAR FUNCTION

A

Filtration- local
Blood pressure regulation- systemic. Involves the juxtaglomerular apparatus and the RAAS (Renin-Angiotensin-Aldosterone System).

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7
Q

TUBULES

A

PROXIMAL TUBULES- secretory and absorptive function. Reabsorb Na, Cl, K, albumin, water, glucose, bicarbonate.
Produce a hypotonic filtrate.

DISTAL TUBULES- reabsorb water.
-> collecting ducts- water, K and Na reabsorption, acid-base balance.

THE TUBULES FUNCTION TO CONCENTRATE URINE.

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8
Q

RENAL FAILURE

A

Best addressed by clinicopathologic parameters- complete blood count, biochemistry, urinalysis.
Characterised by DECREASED GLOMERULAR FILTRATION RATE.
Can be pre-renal, renal or post-renal.
Acute or chronic.
A SIGNIFICANT PORTION OF KIDNEY FUNCTION MUST BE LOST BEFORE CLINICAL SIGNS ARE SEEN (75% -> azotaemia/uraemia)

Failure of glomerulus leads to proteinuria (albumin)- protein in urine.
Failure of tubules leads to isosthenuria, azotaemia, uraemia, acid-base imbalance.
Injury to one segment of the nephron will impair the remainder, eventually leading to end stage kidneys.

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9
Q

PORTALS OF ENTRY

A
  1. HAEMATOGENOUS- pathogens localise in large renal vessel, interstitial vessel and glomerulus.
    eg. infection, immune mediated. Septic or non-septic.
  2. ASCENDING FROM LOWER URINARY TRACT- secondary to GI, genital or dermal contamination, targets tubules and interstitium primarily. More common in females due to shorter, wider urethra.
  3. DIRECT PENETRATION- within tubules eg. toxic.
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10
Q

DEFENCE MECHANISMS

A
  • VASCULATURE- Basement membrane
  • GLOMERULUS- Glomerular basement membrane (filtration barriers, glomerular mesangial cells have some phagocytic abilities)
  • TUBULES- Basement membrane (physical barrier and scaffolding)
  • INTERSTITIUM- Innate humoral and cell-mediated immune responses.

Structure is key in defence machanisms

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11
Q

RENAL RESPONSES TO INJURY

A

Responses vary between glomeruli, tubules, interstitium and vasculature, but there is NO regeneration of the ENTIRE nephron.
Podocytes are INCAPABLE of regeneration if damaged.
Tubular regeneration can occur- indicated by clusters of basophilic cells on histology.

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12
Q

LESIONS

A 
Caused by diseases of the kidney. 
Classified by route and location of injury. 
1. DEVELOPMENTAL
2. VASCULAR
3. GLOMERULAR
4. TUBULOINTERSTITIAL
5. PELVIS/ASCENDING
6. END STAGE KIDNEY- lesions everywhere
7. ANY LOCATION
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13
Q

DEVELOPMENTAL LESIONS

A

APLASIA- no kidney development
HYPOPLASIA- small kidney- often still functional, often at a lower level than the normal kidney.
DYSPLASIA- eg. Progressive Juvenile Nephropathy. Inappropriate maturation leads to a non-functionin kidney. Often the WHOLE kidney will be dysplastic if any of it is.

Are these clinically important? (often no- the animal can function with one working kidney)
How much of the kidney is affected?

ECTOPIC/FUSED (HORSESHOE) KIDNEYS- histologically normal; found incidentally post mortem.
RENAL CYSTS/POLYCYSTIC KIDNEYS (see tubule lesions)

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14
Q

VASCULAR LESIONS

A

HAEMORRHAGE- can occur with any systemic vascular injury eg. septicaemia, vasculitis, DIC. Additional renal lesions may be seen.

INFARCT- Most important. Location and size of infarct suggests which artery is affected.

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15
Q

INFARCTION

A

Acute- raised, red
Chronic- depressed and pale- fibrosis/scar tissue.

Cortex only- INTERLOBULAR ARTERY affected.
Cortex and medulla- ARCUATE or INTERLOBAR ARTERY affected.
Larger infarcts are less clearly defined than those that affect the cortex only.

The most common overall cause of infarct is THROMBOEMBOLISM.

Whether the infarct is clinically significant or not depends on the location, size and vessel affected.

Anything that makes an animal prothrombotic means infarct is more likely to be seen eg. Cushing’s disease, amyloidosis.

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16
Q

GLOMERULAR LESIONS

A
  • Glomerulonephritis
  • Glomerulosclerosis
  • Glomerular amyloidosis
  • Acute suppurative glomerulitis (embolic bacterial nephritis)
  • Viral glomerulitis.

END POINT OF GLOMERULAR DISEASE- PROTEIN LOSING NEPHROPATHY.

17
Q

LONG TERM SEQUELAE OF GLOMERULAR DISEASE

A 
Hypoproteinaemia
Decreased oncotic pressure
Loss of antithrombin III
-> clotting disorders. 
Nephrotic syndrome
18
Q

NEPHROTIC SYNDROME

A

Seen as a long term sequelae to glomerular disease. 4 components:

  1. HYPOPROTEINAEMIA
  2. PROTEINURIA
  3. ASCITES
  4. HYPERCHOLESTEROLAEMIA.

Protein losing glomerular injury has tubular effects- protein casts and resorption droplets can be seen histologically in the tubule. This should not be seen in the healthy kidney.

19
Q

GLOMERULONEPHRITIS

A

-IMMUNE MEDIATED- most common is immune complex deposition (Type III Hypersensitivity) associated with bacterial or viral infections eg. FeLV, FIP, pyometra, chronic parasitism, autoimmune (lupus), neoplasia.

3 main patterns of glomerulonephritis:

  1. MEMBRANOUS- thickened capillary basement membrane with subepithelial deposits. Most common in cats.
  2. PROLIFERATIVE- hypercellularity of glomerulus eg. equine infectious anaemia, equine streptococcal infections (not usually clinical renal failure)
  3. MEMBRANOPROLIFERATIVE- combination of both, with hypercellularity and subepithelial deposits. Seen most commonly in dogs.
20
Q

GLOMERULONEPHRITIS- MECHANISM

A

Glomerular basement membrane is continually damaged via podocyte effacement and detachment, resulting in protein loss.

Grossly, the kidney usually appears normal. May see uniform tan/red dots can be seen- these are glomeruli.
DIAGNOSIS- Renal biopsy then histology with H&E, special stains, electron microscopy and immunofluorescence.
Immune deposits can be seen with special stains (trichrome)- these should not be seen in the healthy kidney.

21
Q

GLOMERULOSCLEROSIS

A

Seen in the end stage glomerulus.
OBSOLESCENT GLOMERULUS.
Obliteration of capillary loops with increased matrix and fibrous connective tissue.
NONSPECIFIC RESPONSE TO CHRONIC GLOMERULAR INJURY.
Has an effect on tubules via decreased flow in efferent arterioles.
Mild, multifocal (only some glomeruli affected) glomerulosclerosis is common in aged animals.

22
Q

GLOMERULAR AMYLOIDOSIS

A

Amyloid is an insoluble fibrillar protein, associated with chronic inflammation (may also be idiopathic).
Reactive amyloidosis (AA amyloid)- fragments of serum amyloid-associated protein.
-GLOMERULAR deposition is common in most specues.
-CATS show MEDULLARY deposition.
-Grossly see possibly enlarged, pale, waxy kidneys.
-Iodine and sulphuric acid show the glomeruli grossly (black dots)
-Histologically, amyloid deposits can be seen expanding the mesangium. Congo red stain shows red amyloid.
Amyloid also shows apple green birefringence.

23
Q

EMBOLIC NEPHRITIS

A

aka. ACUTE SUPPURATIVE GLOMERULITIS
Glomerular/vascular lesion, may progress to tubulointerstitial.
Seen with haematogenous spread of bacteria leading to lodging in glomerular capillaries.
eg. Foal with actinobacillus equii, pigs with erysipelothrix endocarditis.
-Gross- Multifocal tan pinpoint foci in cortex.
-Bacterial colonies (microabscesses) can be seen histologically.

24
Q

VIRAL GLOMERULITIS

A 
eg. Dog- acute infectious canine hepatitis
Horse- equine viral arteritis
Pig- swine cholera
Bird- Newcastle disease
Pig- neonatal porcine cytomegalovirus

Usually see a transient proteinuria.

Semester II Pathology (24 decks)

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