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Flashcards in Urinary Deck (91)
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1

A horseshoe kidney is caused by what?

Can they be functional?

Fusion of the cranial or caudal poles of the kidneys

Yesm if no urethral obstruction is present

2

Ectopic kidney

Abnormal kidney migration - may be found in the inguinal ring or pelvic cavity (urethral obstruction may occur)

3

Name seven congenital abnormalities of the kidneys.

  1. Ectopic kidney (fused
  2. Aplasia
  3. Hypoplasia
  4. Dysplasia
  5. Familial renal disease
  6. Cystic renal disease
  7. Tubular function abnormalities (genetic)

4

What features of the kidney should be examined at necropsy?

  • Examine shape, position + size of kidneys.
  • Contours / adherence of capsule. 
  • Cortex is finely radially striated + dark red / brown (except cats). Medulla pale brown.
  • Cortex ratio of approx 1:2 to 1:3 with medulla of domestic spp  (smaller in desert species which have larger medulla).

5

Familial renal disease

Which breeds are predisposed?

Renal disease often presenting under the age of 2, proteinuria is common, kidneys appear small, pale with loss of nephrons and fibrosis

Breeds: Cocker, Doberman, Samoyed, Shih Tzu

6

Describe this histo slide of a 2yo cocker with familial renal disease.

  • Clumps of inflammatory cells
  • Dilated tubules
  • Dense proteinaceous fluid within the tubules - protein
  • Marked fibrosis 
  • Nephron loss

7

What pathological finding is often found alongside renal dysplasia?

What can be the cause of this phenomenon?

Hydroureter

  • Familial
  • Viral
    • CHV
    • FPV
    • BVDV

8

Describe this lesion.

What can these lesions result in?

Which breeds are prone?

The cortex of the kidney contains multifocal raised round fluid filled nodules of varying sizes (from 2mm to 10mm in diameter). Some of the nodules extend into the medulla.

May lead to pressure atrophy of adjacent renal tissue

Persian and WHW terriers.

9

Describe three types of tubular functional abnormalities and their breed specific signs.

  1. Cystinuria - cysteine stones in the bladder - X-linked
  2. Primary renal glycosuria - reduced ability to reabsorb glucose - Elkhounds
  3. Fanconi syndrome - multiple defects = aa/glycos/protein/phosphuria - Basenjis
  4. Urate metabolism - urate crystal preone - Dalmatians
  5. DI 

10

Describe the response to injury of the glomerulus.

Fibrosis and loss

11

Describe the response to injury of the tubular epithelium

Repair if the basement membrane remains intact

Compensatory hypertrophy and atrophy if basement membrane is damaged

12

Describe this lesion

Multifocal to coelescing, round, dark red-black 1x1mm lesions. Coelescing to two large areas (affecting 70% of the tissue). 

Acute multifocal to coelescing severe haemorrhage of the kidney

Disseminated intravascular coagulation

13

Describe this lesion

Multifocal to coelescing round 2x2mm red lesions found on the kidney surface and penetrating the cut surface (cortex). The kidney appears firm (no-oozing of fluid).

Acute multifocal to coelescing moderate haemorrhagic nephritis

CHV, salmonella, CSF, erysipelas

14

Describe this lesion.

Focal area of dark red to black fluid found on the surface of this kidney. 5x5cm. Irregular demarcation. 

Acute focally extensive severe traumatic haemorrhage of the kidney

15

Describe these lesions

Interlobular and interlobar acute infarcts.

Pale tan wedged shaped lesions.

Peripheral haemorrhage

Indented cortical surface

Caused by microthrombi in renal blood supply

16

Outline the difference between interlobular and interlobar infarcts.

Differences in blood supply

17

Chronic infarct leading to wedge shaped necrosis and consolidation of tissue

Leaves a deep cortical depression visible on the renal surface

18

Describe

Papillary necrosis (where collecting ducts empty into the pelvis)

Reduced renal blood flow secondary to NSAIDs (bute!)

19

Renal cortical necrosis - kidney is diffusely damaged due to microthromi.

Hypereosinophilic cells

Tubular structures are filled with degenerate necrotic debris

Inflammatory cells have infiltrated interstitium

Gram-ve microthrombi

20

Fibrin and cell debris within tubular lumen. Hypereosinophilic cells w/out nuclei.

Causes:

  • Toxic/ ischemic insult
  • Myoglobinuria
  • Increase in serum Hb
  • AIHA

 

21

With amyloidosis of the kidney which areas are most commonly affected?

Glomerulus 

In cats the medulla

22

What effect does amyloid have on the glomerulus?

Pressure atrophy - protein uria - hypoproteinaemia

23

Describe

Cortex is diffusely affected, appears pale tan and waxy, firm. 

Amyloidosis - protein depositation (stained red with congo red)

24

Urine blockage can lead to hydronephrosis. What characteristic lesions would be found in this case?

Pressure atrophy

Dilation of the pelvis 

Medulla ischemia (vascular occlusion)

Cortical atrophy

Causes: ureteral anomalies/ obstruction, LUT inflammation, neoplasia, bladder paralysis

Leads to secondary infection

25

Hypercalcaemic nephropathy

A secondary lesion (hpth etc)

Mineralisation of tubular basement membrane

26

What can cause glomerulitis?

Viral - EVA, CSF, newcastle disease virs

Bacterial emboli - Actinobacillosis

Septicaemic endothelial damage

27

Glomerulonephritis

Damage to the glomerulus leading to inflammation downstream

28

Outline the mechanism of glomerulonephritis.

Name three causes.

Type three hypersensitivity (immune complexes) causing inflammation.

Causes: FIP, FeLV, AIHA, neoplasia, CSF, PRRS, BVDV

 

29

Glomerulonephritis - chronic leading to fibrosis

30

Pale tan cortex and petechial haemorrhage

Acute glomerulonephritis with PDNS