35. Acute kidney diseases in dogs and cats Flashcards

1
Q

General clinical signs of renal diseases?

A

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

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2
Q

Types of azotaemia & Kidney injury?

A

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

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3
Q

Acute Nephrosis & Nephritis?

A

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

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4
Q

Phases of AKI?

A

PHASES OF AKI

  1. Initiation: Kidney injury
  2. Extension: Inflammation, vasoconstriction,

coagulopathy, microvascular obstruction, ↑ ROS

(reactive oxygen species)

  1. Maintenance: Differentiation, migration &

proliferation of new cells → Death of the animal often

happens in this phase

  1. Recovery: Redifferentiation & repolarisation →

Complete regeneration/partial regeneration → Leads

to chronic kidney disease (CKD)

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5
Q

General pathophysiology of AKI?

A
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6
Q
A
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7
Q

Clinical signs and diagnosis of AKI?

A

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

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8
Q

Treatment Of Acute kidney injury?

A

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

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9
Q

Prognosis of AKI?

A

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

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10
Q

Pathogenesis of ethylene glycol poisoning?

A
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11
Q

Ethylene glycol toxicosis?

A

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

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12
Q

Haemoglobin Nephrosis + Leptosporosis?

A

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

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