Small animal medicine > Nephrology/urology 2 > Flashcards

Nephrology/urology 2 Flashcards

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1
Q

Which species has no renal pelvis

A

Cattle

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2
Q

What are pale streaks seen in the inner cortex of dogs

A

Fat in the collecting ducts

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3
Q

Which species excrete excess calcium as calcium carbonate in urine

A

Horses
Rabbits

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4
Q

Why is equine urine foamy

A

Due to mucus content; has mucus glands in renal pelvis

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5
Q

In the vascular supply to the kidney which arteries are possible functional end arteries and which are always functional end arteries

A

Possible ones: interlobar arteries
Definitie = interlobular arteries
TOtal supply = renal artery –> interlobar – arcuate –> interlobular –> afferent artery of glomerulus –> efferent

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6
Q

What is the functional reserve capacity of the kidney

A

60-75%
At ~60% start seeing PU/PD
At 75% start seeing azotaemia

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7
Q

What GFR would be considered renal insufficiency vs renal failure

A

Renal insufficiency = 25-50% of GFR left; here can have azotaemia
Renal failure = just 20-25% left; get uraemia

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8
Q

What is the difference between azotaemia and uraemia

A

Azotaemia = elevated urea and creatinine concentrations vs uraemia = clinical signs and pathology assocaited with azotaemia

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9
Q

What happens in acute renal failure

A

Sudden loss of 70-100% of nephrons
related to ischaemia, nephrotoxin exposure, complete obstruction

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10
Q

What is the key difference in body pathology with chronic renal failure vsacute

A

With chronic there is time for non-renal lesions of uraemia to develop

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11
Q

Non-renal lesions of chronic renal failure (basic)

A
  • Gastric haemorrhagic ulceration; due to ammonia
  • Calcium deposits on gastric mucosa and pleura
  • Uraemic pneumonitis
  • Oral cavity ulcerative gingivitis due to conversion of urea to ammonia in saliva

+ can see retinal separation due to hypertension
+ can see osteodytrophia ue to renal secondary hyperparathyroidism
+ can get anaemia

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12
Q

Why can we see anaemia with chronic kdieny disease

A

Impairment of erythropoietin secretion from kidney
Uraemia assocaited with increased RBC fragilits

= normocytic, normochromic non-regnerative anaemia

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13
Q

What is the difference between dystrophic and metastatic mineralisation

A

Dystrophic = mineralisation in areas of necrosis because dying cells unable to regulate calcium influx

Metastatic = in normal tissues secondary to hypercalcaemia

See both in renal disease because there is vascular necrosis due to ammonia presence AND raised calcium

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14
Q

Pathology with uraemic pneumonitis

A

Lungs have firm glassy cut surface
Pulmonary oedema
Mineralisation of alveolar walls
Blood vessel degeneration

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15
Q

Why do we get ulcerative gingiivitis, stomatitis etc in chronic renal failure

A

Due to conversion of urea to ammonia in saliva causing vascular necrosis

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16
Q

Why can we get retinal separation in chronic renal failure

A

Renal iscaemia activates juxtaglomerular complex and RAAS system to secrete renin to increase blood pressure to restore perfusion
BUT in chronic renal failure, prolonged hypertension damages small arteries/arterioes, exacerbating renal hypoperfusion more so get progressive hypertension

End stage is nephrosclerosis; non-functional glomerulus exacerbates RAAS activation and hypertension even more

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17
Q

What cardiac effect can we get with chronic renal failure

A

Left ventricular hypertrophy; due to chronic RAAS activation and hypertension

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18
Q

What is osteodystrophia fibrosa in relation to renal disease

A

REnal disease reduced phosphorus excretion
- This causes reciprocal ionised Ca2+ fall which stimulates PTH release (+ PTH release stimulates directly by raised phosphorus)

PTH can’t cause increased phosphorus secretion in chronic renal failure because kidney not functional; still have hyperphosphataemia and more PTH release

PTH causes resorption of calcuim from bone and replacement with fibrous tissue
+ reduction in vit D related Ca2+ uptake because vitD is activated in kidney

–> Get osteodystrophia fibrosa = extensive bone resorption and proliferation of fibrous tissue

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19
Q

What do animals with chronic renal failure die from

A

Heart failure related to metabolic acidosis, hyperkalaemia, pulmonary oedema

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20
Q

What is more common between glomerulitis and glomerulonephritis and what is the difference

A

Glomerulitis = focal nephritis affecting just the glomerulus; tends to be part of systemic disease where bacteria from bacteraemia lodge in glomeruli

Glomerulonephritis = inglammation of glomeruli and nephrons; more common
- Tends to be related to immune complex deposition in dogs/cats

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21
Q

Where do immune complexes in glomerulonephritis come from

A
  • Low pathogenicity infection that causes persistend antigenaemia –> complexes then deposit in the glomerulus
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22
Q

What does a kidney with glomerulonephritis look like in acute vs chronic stages

A

Acute = swollen, pinpoint red dots in cortex
Chronic = shrunken cortex, fine granularity, white dots on cortex

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23
Q

What is glomerulosclerosis

A

End stage of chronic glomerulitis; glomeruli and thickened and non-functinoal

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24
Q

In amyloidosis, where is the amyloid deposited

A

Mostly in mesangium and glomerular BM

Can get medullary deposition in cats and SHar-pei dogs

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25
What are the 3 types of amyloidosis
1) Primary = monoclonal gammopathy; immunoglobulin light chain related 2) Secondary; amyloid AA from serum amyloid A i.e with chronic inflammatino 3) Familial amyloidosis
26
Gross pathology of amyloidosis kidney
Pale, waxy kidneys with pale swollen cortex Pin point white foci = glomeruli Odema
27
What other effects aside from kdieny may be seen in amyloidosis
Effects of amyloid deposition on other tissues e.g causing diarrhoea Can get liver elaboration in response to hypoproteinaemia (nephrotic syndrome) from glomerular damage --> hyper cholesterolaemia seen
28
Histopath of amyloidosis in kidney
Protein casts in renal tubules Amyloid stained with congo red expanding glomerulus Eosinophilic deposits in glomeruli expant the flomerulus
29
How does amyloidosis lead to uraemia
Amyloid deposition and glomerular damage --> leaky basement membrane --> proteinura, hypoproteinaemia (= nephrotic syndrome) --> oedema as disease workens, capillaries in glomerulus occluded and get failure of filtration, uraemia etc
30
Wht is nephrotic syndrome
Where thereare leaky glomerular BMs (from amyloidosis or glomerulonephritis) which causes loss of plasma proteins into urine --> hypoproteinaemia, oedema/ascites etc
31
Why do we get hypercholesterolaemia in nephrotic syndrome
Response to hypoproteinaemia --> liver elaboration This also gives hypercholesterolaemia
32
Difference in infarct appearance in interlobar/arcuate artery occlusion vs interlobular artery occlusion
Interlobar gives infarcted triangle of cortex AND medulla Interlobular arteries jsut affects section of cortex
33
Macroscopic appearance of kidney infarct and how does it change over time
WEdge shape and red in acute phase Then becomes bale Then get fibrosed and sunken
34
What is hydronephrosis
Where there is dilation of renal pelvis and pressure atrophy of rest of kidney due to obstruction of renal flow in face of continued filtration
35
What is renal dysplasia and when might it be seen
disorganised development of renal parenchyma - In utero or early post-natal life before nephrogenesis is complete Get a small, mishsapen, cystic and fibrsed kidney
36
Histopathology of kidney with renal dysplasia
Structures are inappropriate to development stage; e.g retained fetal glomeruli
37
Key difference between renal cysts and hydronephrosis
In cysts, the fluid expands from cyst in medulla/cortex vs from renal pelvis in hydronephrosis
38
Which breeds is polycystic kidney disease seen in
Bull terriers, Persian cats Westies, cairn terriers
39
Which breed has hereditary nephropathy related to X linked COL4A5 gene
Samoyeds
40
What is E cuniculi
Obligate intracellular microsporidian parasite Affects rabbits
41
What signs can E cuniculi cause in rabbits
Neurological disease; head tilt, paresis Renal disaese; PU/PD, weight loss, haematuria non-regnerative anaemia
42
What do the kidneys look like in rabbit with E cuniculi
Irregularly pitted Have granulomatous interstitial nephritis and fibrosis
43
What do we tend to fnd on histopathology in chronic kidney disease
diffuse tubulointerstitial nephritis and fibrosis with secondary glomerulonephritis and mineralisation
44
What must we ensure before IRIS staging CKD
That the animal is stable and hydrated to avoid contributions to azotaemia from pre-renal azotaemia
45
What are the IRIS stages of CKD
1 = normal creatinine/normal to increase SDMA but there are indicators of renal disease present 2 = mild renal azotaemia; only mild clinical signs 3 = moderate renal azotaemia with clincial signs present 4 = severe renal azotaemia; high risk of getting into crisis
46
What is the main cause of renal proteinuria in CKD
Tubular dysfunction causing inability to rebasorb protein There is also contribution from increased glomerular protein flux with flomerular hypertension secondary to nephron loss
47
Factors associated with the progression of CKD
Mineral and bone disorders Proteinuria Hypertension Hypoxia, hypoperfusion, ischaemia
48
How does CKD cause metabolic bone disease and what factor mediates this
Net increase in serum phosphate in early stages triggers FGF-23 increase which inhibits PTH and active vit D (calcitriol) FGF-23 is renaly cleared; as GFR falls it is excreted less + less phosphate removal so more FGF-23 End organ resistance to FGF-23 decreases ability to inhibit PTH Get reduction in ionised calcium which stimulated PTH secretion and causes calcium and phosphate resorption Eventually have high Ca2+ and high phsophate at high time
49
What electrolyte changes lead to mineralisation of tissues in end stage CKD
High calcium and phosphate
50
Why do we have normal phosphate in IRIS stage 1 and 2
Because there is intial compensation via FGF-23 - Increase in PTH precedes hyperphosphataemia
51
Consequences of CKD-MBD
Renal osteodystrophy; rubber jaw Soft tissue mineralisation
52
How is hypertension a risk factor for CKD progression
Exacerbates glomerular hypertension and causes glomerulosclerosis and proteinuria
53
How does hypoperfusion lead to renal medullary hypoxia
Efferent arteriole vasoconstricts to preserve GFR but this decreases blood flow to glomerulus, exacerbating hypoxia to the medulla
54
How to increase hydration in CKD
Switch to wet food water fountains IV fluids Subcut fluids Feeding tube
55
Dietary management of CKD
Most important = phosphorus restriction; if not at target via diet add in phosphate binders Highly digestible protein Add in soluble fibre to reduce colonic pH to act as a nitrogen trap and reduce urea K+ supplementation; lost in PU Metabolic acidosis common so may want alkalinising deit
56
At what IRIS stage do we introduce renal diets
2
57
What is a risk of starting a renal diet when the serum phosphate is not high i.e already in target
Can get hypercalcaemia which drives renal progression So want to switch to senior or EARLY renal diet
58
What is the goal for blood pressure in CKD treatment and what do we use for this
Want between 120-160mmHg Amlodipine, ACe inhibtiors
59
Why do we not start with amlodipine to treat hypertension in dogs and why can we in cats
In dogs it preferentially dilates the afferent arteriole which can increase capillary hydrostatic pressure and GFR and glomerular hypertension Doesn;t happen in cats
60
How much sodium do we want in renal diets
Too low associated with RAAS activation and doesn't decrease BP Want mild sodium restriction to enhance anti-hypertensive effects of drugs
61
How much do we want to reduce proteinuria by depending on original UPC
If UPC starts at <2 then go to <0.5 in dogs and 0.4 in cats If UPC >2 want minimum of 50% decrease
62
How does RAAS activation work in CKD
Decreased GFR in CKD causes activation of RAAS; get contsriction of efferent arteriole to improve the GFR BUT leads to glomerular hypertension, proteinuria, pro-inflammatory and pro-fibrotic pathways Get progression of disease
63
What is ACE escape
When ACE-independent pathways produce angiotensin II which makes them refractory to treatment part way through
64
Which angiotensin receptor do we want to block
the AT1: since this one causes vasoconstriction, symp activation etc Don't want to block AT2 since this is renoprotective and causes vasodilation etc
65
What advantage do angiotensin receptor blockers have over ACE-inhibtiros
Not affected by ACE escape
66
When should we take caution with reducing blood pressure in CKD
In stage 4 CKD, GFR is so low already that cuasing this vasodilation will make it much worse Avoid if patient is dehydrated because this angiotensin II mediated efferent arteriole constriction may be the only thing maintaining the GFR
67
What electrolyte are renal diets supplemented with
K+
68
Treating anaemia in CKD
Darbopoietin = human recombinant erythropoietin; use mostly in stage 3/4 + can add in parenteral iron monthly injections
69
Where do we want to get the PCV to in CKD
Lower end of normal
70
When could we do calcitriol treatment in CKD and what are the risk
Only if phosphate controlled and ionised calcium/phosphate monitored well There is a risk of causing hypercalcaemia and leading to renal minterlisation and progression = to suppress PTH
71
Summary of management of glomerular disaese
Treat hypertension Treat proteinuria Renal diets May do immunsuppression only if renal biopsy indicated immune based pathogenesis
72
When might we add in darbopoietin as part of CKD treatment
If PCV <20% in cats, <25-30% in dogs `
73
Hallmarks of nephrotic syndrome
Proteinuria Hypoalbuminaemia Oedema Hypercholesterolaemia
74
When should we start blood pressure treatment straight away in kidney patients
If BP >200mmHg or there is target organ damage e.g retinal retachment, left ventricular hypertrophy, brain hypertensive encephalopathy
75
How do phosphate binders work
Complex with dietary phosphate to prevent GI absorption - Must be done alongside renal diet with low phosphat
76
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