Acute kidney injury

Question 1

What is an acute kidney injury?

Answer 1

Acute refers to hours to days, rather than weeks to months.

Acute on chronic, refers to an acute injury suffered in addition to pre-existing chronic renal disease – the injury may or may not be related to the cause of pre-existing disease.

Acute injury is classically split into three categories:
* Haemodynamic i.e. volume responsive (pre-renal azotaemia)
* Intrinsic Renal i.e. actual damage to the kidneys
* Postrenal i.e. urethral obstruction

Question 2

What is a haemodynamic acute injury?

Answer 2

• It could be argued this isn’t a true AKI i.e. it’s simply reduced renal blood supply.
• Anything that affects renal blood flow locally or systemic hypotension will contribute to this, common causes being hypovolaemia, anaesthesia, use of NSAIDS (prostaglandin inhibition).
• This produces a pre-renal azotaemia due to reduced clearance that is rapidly resolved by correcting the underlying cause (often fluid therapy to restore renal perfusion).
• If this is not corrected – progression to intrinsic renal damage occurs – ischaemia and hypoxia.

Question 3

What are causes of instrincic renal acute injuries?

Answer 3

Ischaemic
* Hypovolaemia, distributive, obstructive, cardiogenic shock
* Deep / prolonged anaesthesia
* Thrombosis / DIC
* Hyperviscosity / polycythaemia
* NSAIDs

Primary renal disease
* Infectious
* UTI (e.coli / gram negative most common) – pyelonephritis
* Lepto
* Immune mediated e.g. glomerulonephritis, SLE
* Neoplasia e.g. lymphoma

Secondary disease
* Infectious e.g. FIP, Leishmania
* Malignant hypertension
* Hepatorenal syndrome in cirrhosis (rare)
* Sepsis – endothelial glycocalyx damage, vascular leak, microcirculatory disruption – S-AKI

Nephrotoxins
* NSAIDs
* Ethylene Glycol
* Lillies (cats)
* Vitamin D toxicity
* Aminoglycoside antibiotics

Question 4

What are causes of post-renal AKI?

Answer 4

Urinary obstruction
* Ureteral obstruction
* Ureterolithiasis is becoming more common in cats
* Iatrogenic post spey
* Urethral obstruction (blocked bladder)
* Prolonged obstruction will lead to intrinsic renal damage

Urinary leakage
* Ureteral, bladder or proximal urethra damage leading to uroabdomen
* Distal urethra leading to tissue leakage
* If a UTI is present, septic peritonitis can develop

Resolves with treatment of the underlying problem

Question 5

What are the 4 phases of intrinsic AKIs?

Answer 5

Phase 1 – Asymptomatic phase of the initial insult, towards the end of this phase Azotaemia begins to develop and urine output drops.

Phase 2 – hypoxia and inflammatory responses propagate renal damage, particularly proximal tubule and loop of Henle (highly metabolic cells).

Phase 3 – can last up to three weeks, urine output may be increased or decreased.

Phase 4 – recovery phase, can last weeks to months. During this period, sodium may be lost and severe polyuria – this can result in hypovolaemia, causing recurrent damage through hypoxia.

Question 6

Describe diagnostic approach to AKIs

Answer 6

Aim is to identify as soon as possible – unfortunately this is probably missed most of the time considering Phase 1 can be relatively asymptomatic or subtle.

History:
* Presence of a predisposing factor e.g. anaesthesia, toxin exposure
* <1w history – anorexia, vomiting, PUPD, lethargy, diarrhoea.

Clinical exam:
* Signs associated with fluid loss – dehydration/hypovolaemia.
* Signs associated with concurrent illness e.g. sepsis
* Specific signs:
* Renal pain +/- palpable enlargement
* Uremic halitosis and oral ulceration
* Jaundice - Lepto

Biochemistry
* Azotaemia
* Hyperphosphataemia (relatively marked)
* Hyperkalaemia – to a possibly dangerous level
* Hypokalaemia possible
* Hypocalcaemia
* Elevated hepatic parameters in Lepto

Urinalysis
* Inappropriate USG
* Proteinuria
* Glucosuria
* Get a sample for culture and sensitivity

Ultrasound – POCUS!
* Kidneys may appear normal or enlarged
* Dogs – 5.5 - 9.1x Aortic Diameter
* Cats – 3 – 4.3cm in length
* Peri-renal free fluid may be seen with Lepto in dogs, or lymphoma in cats
* Hydronephrosis – obstruction or pyelonephritis
* Allows for FNA (may allow rapid diagnosis of lymphoma on cytology) or Biopsy (risk of bleeding)

Radiography/CT
* Identification of obstructions
* Intravenous contrast studies elucidate better

Question 7

What findings are consistent with leptospirosis?

Answer 7

• Thrombocytopaenia
• Anaemia
• Electrolyte disturbances

Imaging may reveal interstitial/alveolar patterns, hepatomegaly, splenomegaly, abdominal free fluid, mild lyphadenomegaly.

Question 8

How would you treat AKIs?

Answer 8

Treat any concurrent/underlying/causative disease

Fluid therapy:
The goal is to maintain volume status and renal perfusion, but avoid volume overload – close monitoring is key, and regular alterations in fluid rates to maintain normal volume status in the face of either polyuria, oliguria or anuria.

Monitoring – ins/outs and body weight

Match the losses – this means in severe polyuria you may need high fluid rates, but if losses are less, titrate down to avoid volume overload as damaged kidneys can’t get rid of it– don’t go over the target weight and reassess your target weight daily.

Loop diuretics e.g. furosemide – no good evidence for improved outcomes in AKI, however may be justified to prevent fluid overload and allow increased volumes of e.g. nutrition (tube feeding). Furosemide is nephrotoxic in the poorly hydrated patient.

Osmotic diuresis – mannitol – no good evidence for improved outcomes despite many theoretical benefits, may also cause AKI itself.

Dopamine– increases afferent renal blood flow, but not GFR, no evidence for improving outcomes.

Fenoldopam – increases urine output, no evidence for improved outcomes yet.

Ca2+ channel antagonists – diltiazem – afferent renal vasodilation; some none significant findings supporting improved resolution of azotaemia and urine output, other study showing no significant increase in GFR or UO.

Renal Replacement Therapy – Dialysis
Indicated for the non-responsive patient to fluid therapy or acute poisoning e.g. lilly/ethylene glycol toxicity in cats.

Peritoneal dialysis – the first opinion option.
* Peritoneal catheter is placed
* Dialysate solution (glucose containing) is infused, left anywhere from 20 minutes to a few hours, to allow for diffusion, then drained.
* Repeated as needed
* Complications are moderate, including causing a septic abdomen.
* Moderately improved outcomes.

Haemodialysis – the referral option.
* Requires dialysis machine and specific training
* Improved outcomes

Suspected urinary tract infection – Amoxy-Clav is a good first line choice for e.coli, Doxycycline for Lepto.

Metabolic acidosis – Hartmann’s (Careful if considering sodium bicarbonate, could worsen hypernatraemia if present, and if lung function is impaired can paradoxically cause CNS acidosis)

Tachyarrythmias – ECG for VTACH and consider lidocaine

Hyperkalaemia – Glucose, insulin, bicarbonate or beta agonist.

Hypertension – not uncommon and further damages the kidneys – amlodipine. Avoid ACE inhibitors which reduce afferent renal blood flow.

**Nutrition **– catabolic disease; feeding tube.

Question 9

What is the prognosis for patients with AKIs?

Answer 9

Prognosis without dialysis:
* Obstructive (cats) – 91%
* Infectious – 82%
* Metabolic/haemodynamic – 66%
* Other – 50%
* Toxin – 43-69%

Realistically – in the non-obstructive, non-infectious case, there is a 50/50 chance for a good outcome.