35. Acute kidney diseases in dogs and cats Flashcards
General clinical signs of renal diseases?
GENERAL CLINICAL SIGNS OF RENAL DISEASE
§ Anorexia § Vomiting
§ Weight loss § Poor coat
§ Immunosuppression § Anuria
§ Blindness (BP-associated) § Oedema
§ CNS Symptoms § Weakness
§ Uraemic pneumonia § PU/PD
§ Uraemic coma § Oedema
§ Respiratory signs § Anaemia
§ Dehydration
Remember that historical & physical findings can be non-specific
When considering a renal diagnosis, always use the “Three-legged chair”:
I. Blood test
II. Imaging (Ultrasound)
III. Urinalysis
Blood pressure measurement may also be included
Assessing glomerular function
GFR (Glomerular filtration rate) –“Kidney function analysis”
§ Urea, creatinine & SDMA measurement
§ Clearance testing:
§ Endogenous: Creatinine
§ Exogenous: Creatinine; Inulin; Ionexol; Isotopes
Urinary Protein
§ Dipstick; Sulfosalycylic acid; UPC ;Microalbuminuria;
Sediment
UPC Parameters:
§ Physiological: <0.2
§ Borderline: 0.2 → 0.4 (0.5 in Ca.)
§ Proteinuria: >0.4 (0.5 in Ca.) (Pathological)
Assessing Tubular Function
Specific Gravity → Measured using a refractometer
§ Isosthenuria: 1008 → 1012
§ Hyposthenuria: >1030 (>1035 in Fe.)
§ Hyposthenuria: <1007 (Pathological)
Cats can concentrate urine even if they have a renal disease
Urine sediment; glycosuria; proteinuria
Urinary biomarkers: GGT/Creatinine; ALKP/Creatinine
Used to diagnose early proximal tubular damage
Clinical syndromes associated with renal disorders
§ Kidney disease
§ Azotaemia ≠ Renal failure
§ Uraemia (end-stage injury; ≠ azotaemia)
§ Renal failure ≈ Disease injury
Types of azotaemia & Kidney injury?
TYPES OF AZOTAEMIA & KIDNEY INJURY
Prerenal/Extrarenal Azotaemia:
Haemodynamic, transient & fluid-responsive
§ Very common & curable
§ ↓ GFR due to dehydration
§ Aetiology: Heart failure; diuretic/vasodilator use;
preanalytical
Long term (>1 day) → Kidney injury
Renal Azotaemia:
§ Infectious, ischaemic & toxic causes → AKI
§ Direct nephron injury → Nephron death
Postrenal Azotaemia (Lower urinary tract)
Obstruction/leakage into abdomen
§ Diagnosis:
§ Imaging
§ Abd. fluid creatinine:Blood creatinine = > 2:1;
§ Abdominal fluid K > Blood K
Treatable
§ Prerenal Azotaemia
§ Postrenal Azotaemia
§ AKI because of these
Non-Treatable
§ CKD & prerenal/postrenal cause
§ CKD & end-stage kidney failure
Acute Nephrosis & Nephritis?
Acute Nephrosis & Nephritis
Acute tubular cell injury & death → Nephron Dysfunction
(↓ GFR & AKI)
Nephrotoxic causes
§ Abx (Gentamycin) § Ethylene Glycol
§ Lilies (Fe. only) § Myoglobin
§ IV Xray contrast fluid § Heavy metals
§ Hypercalcaemia § Anaesthetic
§ Haemoglobin § Grapes/Raisins
§ Chemotherapy §
Ischaemic causes
§ Hypotension § Sepsis
§ Hypercalcaemia § Trauma
§ Hypovolaemia § NSAIDS
§ Deep anaesthesia § Hypothermia
§ Hyperthermia § Burns
Ways to avoid renal ischaemia:
§ IVFT during GA (to prevent hypotension & hypothermia)
§ Ø NSAIDS → Opioids instead ✓
Infectious causes
§ Pyelonephritis
§ Leptospirosis
Obstructive causes: Ureteric obstruction
Phases of AKI?
PHASES OF AKI
- Initiation: Kidney injury
- Extension: Inflammation, vasoconstriction,
coagulopathy, microvascular obstruction, ↑ ROS
(reactive oxygen species)
- Maintenance: Differentiation, migration &
proliferation of new cells → Death of the animal often
happens in this phase
- Recovery: Redifferentiation & repolarisation →
Complete regeneration/partial regeneration → Leads
to chronic kidney disease (CKD)
General pathophysiology of AKI?
Clinical signs and diagnosis of AKI?
CLINICAL SIGNS
§ Lethargy § Anorexia
§ Diarrhoea § Dull consciousness
§ Dehydration § Hyperhydration
§ Oliguria § Anuria
§ Painful kidneys § Halitosis
§ Vomiting § Polyuria
§ Seizures § Uraemic ulcers
§ Hypertension
DIAGNOSIS
Lab. D
Biochemistry: Hypovolaemia; Hypervolaemia; Metabolic
acidosis; Hyperkalaemia; Toxic metabolic products
Bloods: Azotaemia (↑Urea/↑Creatinine); Haemoconcentration
Urine: Iso/hyposthenuria; Sediment; Glucosuria; Proteinuria
Ultrasound: Negative; Cortical hypertrophy
Early Dx: Urine production; USG; Sediment; Plasma creatinine
trending
Treatment Of Acute kidney injury?
TREATMENT
Aim: Maintain adequate perfusion; ↑GFR; Avoid nephrotoxins;
Maintain urine output; Acid-base balance; Electrolyte balance; Treat
underlying disease; Optimise nutrition
Fluid therapy
After rehydration & treatment of shock → Individual fluid therapy
Fluid for rehydration (ml) = % Dehydration x BW x 10 (over 2-4 hrs)
Shock bolus: ¼ dose in 15 mins
Aspect of fluid therapy: Urine production; Sensible losses
(diarrhoea/vomiting); Insensible losses; Body weight changes
Daily insensible losses: Panting & metabolic processes =
22ml/kg/24hr
Daily sensible losses: Urine; Faeces; Vomiting etc.
Too much Cl-
: Hyperchloraemic acidosis; Renal
vasoconstriction; ↓GFR
Overhydration: Interstitial oedema in kidneys → ↓ perfusion &GFR; Higher morbidity
Monitoring urine volume: Urinary catheter & urine collection;
Measuring litter/patient pads
Oliguria/Anuria
§ Mannitol: Osmotic diuretic; Rehydrated animals only
§ Furosemide: Loop diuretic; Ø diuresis
Acid-Base Balance
Tx of metabolic acidosis
Mild cases → Infusion therapy
HCO3: <16mmol/l → Sodium hydrogen carbonate supplement
Hyperkalaemia
§ Mild: K+ free or low-K+ concentration infusion
§ Moderate: Glucose infusion + insulin; Alkalisation
§ Severe: Both treatments above + calcium gluconate →
Cardiac protection & ↓ arrhythmia effect
Hypotension: Norepinephrine
Hypertension: Amlodipine
Dialysis
Peritoneal or haemodialysis
Indications: Anuria; Hyperkalaemia; Fluid overload; Severe
metabolic acidosis
Prognosis of AKI?
PROGNOSIS OF AKI
§ Grade I → II: After a few days of treatment, normal
kidney function may return
§ Grade III → V: After a few weeks of treatment, normal
kidney function may return
§ Grade IV → V: The animal may die, despite adequate
treatment within a few days
§ Toxicosis has a worse prognosis than infection
Pathogenesis of ethylene glycol poisoning?
Ethylene glycol toxicosis?
Ethylene Glycol Toxicosis
Antifreeze/car radiator fluid; Absorbed quickly: 40-60min
CLINICAL SIGNS
Phase I
30 min – 12 hours
§ Depression
§ Vomiting
§ Salivation
§ PU/PD
Phase II
12-24 hours
§ Acidosis
Phase III
12-24 hours for cats; 36-72 hours for dogs
§ AKI
§ Oliguria
§ Anuria
§ Painful kidneys
DIAGNOSIS
Anamnesis/CSx
Lab. D
Haematology: Ethylene glycol levels; ↑Serum osmolality;
Metabolic acidosis; Hypokalaemia; Hypocalcaemia; Azotaemia
Urine Examination: Measured ethylene glycol concentration;
Isosthenuria; Calcium oxalate monohydrate crystals can appear
from 6 hrs
Ultrasound: Echogenic renal cortex; “Halo” sign in
corticomedullary region
TREATMENT
§ Early dx is essential
§ Prognosis is better within 8hrs of ingestion
§ Within the first 1-2hrs → Emesis; Gastric lavage;
Activated charcoal
§ Tx of any resultant AKI; Haemodialysis
Antidotes
§ Fomepizole (see pathogenesis above)
§ Ethyl alcohol (20% ethanol)
If azotaemia is present → Poor prognosis
Haemoglobin Nephrosis + Leptosporosis?
Haemoglobin Nephrosis
Haemolytic disorders; IMHA or haemolytic anaemia caused by Babesia
Babesia
§ CSx: Fever; Dark urine; Vomiting; Anorexia; AKI; Liver
failure
§ Tx: Imidocarb; Tx of any AKI
Leptospirosis (Zoonotic)
Acute interstitial nephritis
