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Equine II > Kidney disease > Flashcards

Kidney disease Flashcards

1
Q

Urine collection

A

terile
○ Via urinary catheter
○ Under sedation (male)
○ Possibly just stocks (mare)?

Non-sterile - via free catch
○ Stand in a box with concrete for a few hours then put in a nice fresh bed and they will want to wee

The difference is the chance of contamination with bacteria

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2
Q

pH of equine urine

A

Usually alkaline due to the forage they eat

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3
Q

Isosthenuria

A

1.008-1.014

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4
Q

Hyposthenuria

A

More dilute
<1.008

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5
Q

Hypersthenuric

A

More concentrated
>1.014

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6
Q

Microscopy of equine urine

A

Calcium crystals are common (Ca in forage high and renal excretion usually excessive)

Not a cause of concern

Casts can be seen, but not predictable even in fresh samples

Can sample single ureteral samples if suspect single kidney affected

Can check fractional excretion of electrolytes (compare serum to urine)

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7
Q

Polydipsia in horses

A

Polydipsia: >100ml/kg/day intake
○ >70ml/kg/day poss more relevant
○ Maintenance: 4-60ml/kg/day

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8
Q

Polyuria

A

> 50ml/kg/day
Hard to measure

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9
Q

Most common cause of polydipsia in horses

A

Psychogenic PD

Or less likely PPID

Or CKD

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10
Q

Creatinine in kidney disease

A

byproduct of muscle activity continually produced

Concentration proportional to glomerular filtration rate

Becomes increased once approx. 75% function of kidney gone

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11
Q

Urea in kidney disease

A

nitrogenous waste product from liver

Not very sensitive

Affected by diet, prolonged exercise etc.

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12
Q

SMDA in kidney disease

A

symmetric dimethylarginine

Endogenous arginine released into bloodstream during usual protein catabolism - excreted unchanged form in urine unless in kidney failure

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13
Q

Blood biochemistry in AKI

A

Hyponatraemia, hypochloraemia, hypocalcaemia, hypokalaemia, hyperkalaemia, and hyperphosphataemia all reported

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14
Q

Blood biochemistry in CKD

A

Hypercalcaemia (67%), hyponatraemia (65%), hyperkalaemia (56%), hypophosphataemia (47%), and hypochloraemia (46%)

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15
Q

Hypercalcaemia in CKD

A

Intestinal absorption high from forage

Lack of excretion with CKD

Also have hypoalbuminaemia from renal losses so this can mask total calcium top as protein-bound will drop

Also increased as part of a paraneoplastic syndrome - could be lymphoma

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16
Q

Acute kidney injury

A

Reduction in glomerular filtration rate

Failure to excrete nitrogenous waste

Cannot maintain acid-base

Failure to maintain fluid homeostasis

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17
Q

AKI classification

A

Pre-renal
○ Poor perfusion of the kidney so cannot do its job

Renal - intrinsic
○ Which area affected - tubular etc.

Post-renal
○ Obstruction
○ Rupture of urinary tract distal to the kidneys (ureter/bladder/urethra)

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18
Q

Oligouria

A

Reduction in production of urine

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19
Q

Anuria

A

Lack of production of urine

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20
Q

Signs of AKI

A

Many have no overt signs

Vague - dull, inappetant

Oliguric more likely than anuria

Think about AKI if severe profound conjunctival oedema with little inflammation

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21
Q

Pre-renal AKI

A

Hypoperfusion of the kidneys

Often reversible

Secondary to severe water loss or blood loss
○ Colic
○ Colitis
○ Substantial haemorrhage

Slight azotaemia may be present - if borderline creatinine monitor it or check SDMA

22
Q

Hypovolaemia vs dehydration

A

Hypovolaemia - loss of water from the circulation

Dehydration - loss of body water

Can occur together if losses have been going on long enough

23
Q

Haemorrhagic shock

A

Loss of circulatory volume due to whole blood loss

External bleeding
○ Easy to see!
○ Usually controlled but not always

Internal bleeding
○ Hard to estimate whether controlled

24
Q

Internal cause of haemorrhage

A

Haemoabdomen (idiopathic or peri-parturient)

Haemothorax (trauma)

Loss from internal organs
○ Intestinal blood loss (masses/diarrhoea with mucosal loss)
○ Renal or urethral blood loss
○ Pulmonary haemorrhage (associated with exercise)

Drug related
○ Phenylephrine administration (major or minor vessel bleed)

25
Q

Haemoabdomen on ultrasound

A

Internal haemorrhage
○ Hyperechoic swirls
○ Effusion
○ Ventral abdomen

26
Q

How to recognise haemorrhagic shock

A

Similar to acute colic

Marked hypovolaemia results in tachycardia and tachypnoea

Pale mucous membranes

Prolonged capillary refill times

Profuse sweating

Depression or anxiety

Reluctance to move

Weakness

27
Q

Haematological and biochemical changes in haemorrhagic shock

A

Poor general tissue perfusion
○ Lactate concentration increased

Poor renal perfusion
○ Pre-renal azotaemia - elevated creatinine and urea
○ Small volume of concentrated urine produced or may be anuric - this is one reason why we check USG in our inpatients after surgery or medical treatment for colic

28
Q

Pre-renal azotaemia

A

With hypovolaemic shock from colic, or colitis, the reduction in circulating volume is SLOWER than moderate or life-threatening haemorrhage

This precipitous drop in blood pressure and circulating volume affects kidneys early on, so azotaemia recognised alongside only moderate signs of shock otherwise

If you find an elevated creatinine, in a dull, vaguely unwell horse, check for internal haemorrhage

29
Q

Haematological and biochemical changes in pre-renal azotaemia

A

Total protein concentration - drops slowly over 12-24hrs

Packed cell volume (PCV) - splenic contraction ruins any value in assessing PCV in most cases of haemorrhagic shock for approx. 24hrs

30
Q

Splenic reserves

A

Catecholamine release due to tissue hypoxia results in splenic contraction

Spleen holds a vast reserve supply of RBC

This provides advantageous good oxygen carrying capacity when exercising/running from a predator

Will counteract the natural loss of RBC from haemorrhage so that the PCV will not drop reliably for at least 24hr after major haemorrhage

Do not let a ‘normal’ PCV mislead you into ruling out haemorrhage

31
Q

Causes of acute tubular necrosis

A

Ischaemia - sustained or severe hypoperfusion of the kidney

‘nephrotoxins’
○ Aminoglycosides
○ Tetracyclines
○ NSAIDs
○ Pigments (myoglobin/haemoglobin)
○ Bisphosphonates
○ Plants
§ Oak/acorn

32
Q

NSAIDs causing AKI

A

Most common sick horses receiving IV NSAIDs

Also possible, though rarer, if oral doses of NSAIDs

Might see haematuria

COX-2 selectivity makes no real difference (COX-2 is expressed in the kidneys)

So consider giving NSAIDs when dehydration corrected FIRST

Consider language used
○ “Adverse reaction” or “adverse event”
○ Do not use the terminology “toxicosis” or overdose or hypersensitivity
○ Because this is not correct, misleading and infers blame which would be misplaced

33
Q

Aminoglycosides causing AKI

A

Concentration dependent antimicrobials

A small percentage of every dose accumulates in the proximal tubular epithelial cells - localised into vacuoles

Impaired organelle function -> tubular epithelial cell death
○ Accumulation when shorter intervals between doses

Other risk factors
○ Hypovolaemia
○ Co-administration of other potentially nephrotoxic drugs
○ Concurrent pigmentiuria

Increased dosing intervals are protective

Trough concentration is important

Therapeutic drug monitoring - trough probably more important to check than peak levels

34
Q

Bisphonates causing AKI

A

Reduce osteoclastic activity in bone

Tiludronate/tiludronic acid (Tildren, Equidronate)

Clodronate/clodronic acid (Osphos)

NSAIDs should not be used concurrently with TILDREN. Concurrent use of NSAIDs with TILDREN may increase the risk of renal toxicity and acute renal failure

Adequate access to drinking water should be provided when using the product.

35
Q

Pigment nephropathy

A

Myoglobin
○ Muscle injuries
○ Hypoglycin A toxicity
○ Exertional myopathy
○ PSSM

Haemoglobin
○ Haemolysis - IMHA, neonatal isoerytholysis

Might not have pigmenturia at the time of renal injury - don’t guess - check bloods

36
Q

Haematuria

A

presence of blood in the urine

RBC - whole blood - can be seen under the microscope

Haemoglobin - massive IV haemolysis overspills via kidney to urine

37
Q

Pigmentiuria

A

change from the usual pigment of the urine

Usually as a result of myoglobin

Care if only seen in wood shavings bed - metabolites in urine oxidise and turn red

38
Q

Pigmentiuria - mechanisms of injury

A

Not well understood

Could be tubular obstruction, oxidative stress, vasoconstriction?

Be aware that dipstick ‘positive’ for haemoglobin could be (Arguably more likely to be) myoglobin

39
Q

Acute glomerular nephritis

A

Rare

Nephrotic syndrome
○ Might have haematuria/oliguria

Might see with other autoimmune diseases e.g. purpura haemorrhagica

Diagnosis with biopsy

Histopathology - demonstration of immune complexes

40
Q

Acute interstitial nephritis

A

Rare

Rapid increase in urea and creatinine

Biopsy - interstitial oedema and infiltrate

Unknown aetiology

Corticosteroids but a poor prognosis

41
Q

AKI diagnosis

A

Biochemistry
○ Low sodium, low chloride, azotaemia

Urinalysis
○ USG - concentrated and small volumes
○ Casts

Enzymuria (GGT:Creatinine ration in urine)

42
Q

Treatment of AKI

A

All about the primary risk factors - NSAIDs (not swap, just stop), haemorrhage - blood transfusion, treat colic or colitis

Replace deficit, meet maintenance requirements and ongoing losses - IVFT

BUT now need to ‘flush obstruction’?

Frusemide - might reduce metabolic demands on the cell (Na/K ATP ase pump is massive drain on energy in cells)

43
Q

Chronic kidney disease

A

Gradual loss of renal concentrating ability

Retention of nitrogenous waste and other products

Retention of Na and Ca

Maybe acid base derrangements

Vit D and erythropoietin might be affected

44
Q

Clinical signs of CKD

A

Weight loss

Inappetance

PUPD

Oedema (due to hypoalbuminaemia)

Lethargy/poor performance

Rough retained hair coat

Uraemic syndrome - halitosis, dental tartar, encephalopathy

45
Q

Congenital CKD

A

Young

Often no history

46
Q

Acquired CKD

A

Insidious onset

Probably don’t know what the original cause was - it has been missed, subclinical etc.

No one notices a problem until overt clinical signs of failure by which time irreversible change

47
Q

Glomerulonephritis

A

Immune-mediated
○ Deposition of immune complexes on the glomerulus basement membrane
○ Haematuria and proteinuria

Was considered rare, but might be subclinical disease

53% of CKD in one study

48
Q

Diagnosis of CKD

A

Persistent isosthenuria
○ USG 1.008 - 1.014

Azotaemia - often really marked

Mild anaemia

Hypoalbuminaemia

High potassium, low sodium and chloride, hypercalcaemia

49
Q

Treatment of CKD

A

Try to biopsy if they’ll let you - referral not an ‘in the barn’ job

Prognosis dreadful once thin due to low albumin

Palatable diet

Try to control calcium intake?

Add Na bicarb

50
Q

Idiopathic renal haemorrhage

A

Spontaneous, severe haemorrhage

Try to find out if another cause

Might respond to steroids

Could be unilateral and consider nephrectomy

Equine II (28 decks)

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