Kidney disease Flashcards
Urine collection
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
pH of equine urine
Usually alkaline due to the forage they eat
Isosthenuria
1.008-1.014
Hyposthenuria
More dilute
<1.008
Hypersthenuric
More concentrated
>1.014
Microscopy of equine urine
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)
Polydipsia in horses
Polydipsia: >100ml/kg/day intake
○ >70ml/kg/day poss more relevant
○ Maintenance: 4-60ml/kg/day
Polyuria
> 50ml/kg/day
Hard to measure
Most common cause of polydipsia in horses
Psychogenic PD
Or less likely PPID
Or CKD
Creatinine in kidney disease
byproduct of muscle activity continually produced
Concentration proportional to glomerular filtration rate
Becomes increased once approx. 75% function of kidney gone
Urea in kidney disease
nitrogenous waste product from liver
Not very sensitive
Affected by diet, prolonged exercise etc.
SMDA in kidney disease
symmetric dimethylarginine
Endogenous arginine released into bloodstream during usual protein catabolism - excreted unchanged form in urine unless in kidney failure
Blood biochemistry in AKI
Hyponatraemia, hypochloraemia, hypocalcaemia, hypokalaemia, hyperkalaemia, and hyperphosphataemia all reported
Blood biochemistry in CKD
Hypercalcaemia (67%), hyponatraemia (65%), hyperkalaemia (56%), hypophosphataemia (47%), and hypochloraemia (46%)
Hypercalcaemia in CKD
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
Acute kidney injury
Reduction in glomerular filtration rate
Failure to excrete nitrogenous waste
Cannot maintain acid-base
Failure to maintain fluid homeostasis
AKI classification
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)
Oligouria
Reduction in production of urine
Anuria
Lack of production of urine
Signs of AKI
Many have no overt signs
Vague - dull, inappetant
Oliguric more likely than anuria
Think about AKI if severe profound conjunctival oedema with little inflammation
Pre-renal AKI
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
Hypovolaemia vs dehydration
Hypovolaemia - loss of water from the circulation
Dehydration - loss of body water
Can occur together if losses have been going on long enough
Haemorrhagic shock
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
Internal cause of haemorrhage
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)
Haemoabdomen on ultrasound
Internal haemorrhage
○ Hyperechoic swirls
○ Effusion
○ Ventral abdomen
How to recognise haemorrhagic shock
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
Haematological and biochemical changes in haemorrhagic shock
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
Pre-renal azotaemia
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
Haematological and biochemical changes in pre-renal azotaemia
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
Splenic reserves
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
Causes of acute tubular necrosis
Ischaemia - sustained or severe hypoperfusion of the kidney
‘nephrotoxins’
○ Aminoglycosides
○ Tetracyclines
○ NSAIDs
○ Pigments (myoglobin/haemoglobin)
○ Bisphosphonates
○ Plants
§ Oak/acorn
NSAIDs causing AKI
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
Aminoglycosides causing AKI
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
Bisphonates causing AKI
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.
Pigment nephropathy
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
Haematuria
presence of blood in the urine
RBC - whole blood - can be seen under the microscope
Haemoglobin - massive IV haemolysis overspills via kidney to urine
Pigmentiuria
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
Pigmentiuria - mechanisms of injury
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
Acute glomerular nephritis
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
Acute interstitial nephritis
Rare
Rapid increase in urea and creatinine
Biopsy - interstitial oedema and infiltrate
Unknown aetiology
Corticosteroids but a poor prognosis
AKI diagnosis
Biochemistry
○ Low sodium, low chloride, azotaemia
Urinalysis
○ USG - concentrated and small volumes
○ Casts
Enzymuria (GGT:Creatinine ration in urine)
Treatment of AKI
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)
Chronic kidney disease
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
Clinical signs of CKD
Weight loss
Inappetance
PUPD
Oedema (due to hypoalbuminaemia)
Lethargy/poor performance
Rough retained hair coat
Uraemic syndrome - halitosis, dental tartar, encephalopathy
Congenital CKD
Young
Often no history
Acquired CKD
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
Glomerulonephritis
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
Diagnosis of CKD
Persistent isosthenuria
○ USG 1.008 - 1.014
Azotaemia - often really marked
Mild anaemia
Hypoalbuminaemia
High potassium, low sodium and chloride, hypercalcaemia
Treatment of CKD
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
Idiopathic renal haemorrhage
Spontaneous, severe haemorrhage
Try to find out if another cause
Might respond to steroids
Could be unilateral and consider nephrectomy
