Acute kidney injury

• Haemodynamic (pre-renal) AKI

  Arguably not true AKI - kidney not directly damaged just reduced blood supply.

  Anything that affects renal blood flow locally or systemic hypotension will contribute.

  Common causes:

  • Hypovolaemia
  • Anaesthesia
  • NSAIDs (prostaglandin inhibition)

  Causes pre-renal azotaemia due to reduced clearance.
• Intrinsic (renal) AKI - Ischaemic

  Hypovlaemia, distributive, obstructive and Cardiogenic shock.

  Deep/ prolonged anaesthesia.

  Thrombosis/ DIC

  Hyperviscocity/ polycythaemia

  NSAIDs
• Intrinsic (renal) AKI - primary renal disease

  Infectious:

  • UTI (e.coli/ gram negative most common).
  • Pyelonephritis
  • Lepto

  Immune mediated e.g. Glomerulonephritis, SLE

  Neoplasia e.g. lymphoma
• Intrinsic (renal) AKI - secondary renal disease

  Infectious e.g. FIP, Leishmania

  Malignant hypertension

  Hepatorenal syndrome in cirrhosis (rare)

  Sepsis - endothelial glyocalyx damage, vascular leak, microcirculatory disruption, S-AKI
• Intrinsic (renal) AKI - nephrotoxins

  NSAIDs

  Ethylene Glycol

  Lillies (cats)

  Vitamin D toxicity

  Aminoglycoside antibiotics
• Post-renal AKI - Urinary obstruction

  Ureteral obstruction:

  • Ureterolithiasis is becoming more common in cats
  • Iatrogenic post spay

  Urethral obstruction (blocked bladder)

  Prolonged -> intrinsic renal damage from pressure.
• Post-renal AKI - urinary leakage

  Ureter/ bladder/proximal urethra damaged -> uroabdomen

  Distal urethra leak can damage soft tissue around penis/ caudo ventral abdomen (male dogs).

  If bacterial UTI can -> septic peritonitis
• Intrinsic damage - Phase 1 initiation (insult) phase

  Asymptomatic initially

  Towards the end azotaemia begins to develop and urine output drops.
• Intrinsic damage - Phase 2 propagation phase

  Hypoxia and inflammatory responses propagate renal damage (proximal tubule and loop Henle worst affected as is very metabolic cells).

  Usually oliguria/ anuria
• Intrinsic damage - Phase 3 static phase

  Up to three weeks

  Polyuria or oliguria/ anuria possible.
• Intrinsic damage - Phase 4 recovery phase

  Weeks to months

  Na+ often lost -> severe polyuria which can lead to hypovolaemia and by extension recurrent AKI (hypoxia).
• Diagnosing AKI - history clues

  Has the best prognosis if caught early and treated.

  Presence of predisposing factor (e.g. anaesthesia, toxin exposure).

  <1 week history of anorexia, vomiting, PUPD, lethargy, diarrhoea.
• Diagnosing AKI - clinical exam clues

  Causal signs:

  • Signs of concurrent (causal) illness (e.g. sepsis)
  • Jaundice - Lepto.

  Direct AKI signs:

  • Renal pain +/- palpable enlargement
  • Uremic halitosis and oral ulceration (relatively rare)

  Secondary signs:

  • Dehydration/ hypovolaemia (fluid loss).
• Diagnosing AKI - biochemistry

  Azotaemia

  Hyperphosphataemia (relatively marked)

  Hyperkalaemia - can be dangerously high and need urgent correction - IVFT glucose +/- insulin or Ca2+ Gluconate).

  Hypokaleamia possible - if severe polyuria as have urinated out all the potassium.

  Hypocalcaemia

  Elevated liver enzymes (lepto)
• Diagnosing AKI - urinalysis

  Inappropriate USG (can be hyper isosthenuric) - caution as there could be possibly residual normal urine in bladder.

  Proteinuria

  Glucosuria

  If suspect infectious cause remember to sample for C&S.
• Diagnosing AKI - Ultrasound imaging

  Kidneys normal or enlarged (in AKI)

  • Normal dogs - 5.5 -9.1 x Aortic diameter)
  • Normal cats - 3-4.3cm long).

  Peri-renal free fluid possible if with Lepto (dogs) or lymphoma (cats)

  Hydronephrosis possible if obstruction or pyelonephritis

  Can do guided FNA if suspicious of lymphoma.

  Can do true cut biopsy but take care because o the risk of bleeding.
• Diagnosing AKI - radiography/CT

  If suspect obstructions

  • Intravenous contrast studies may help

  Care - avoid further damage.
• Leptospirosis - presentation

  Very commonly causes renal insult (99.6%)

  Hepatic damage less common (26%)

  Dyspnoea often present (76.7%)

  • Leptospira pulmonary haemorrhage syndrome (LPHS)

  DIC (18.2%)

  Can only vaccinate for 4 of the strains.
• Leptospirosis - diagnostics

  Clinpath findings consistent with hepatic damage.

  Thoracic radiographs - possible interstitial/alveolar patterns.

  Abdominal ultrasound - hepatomegaly, splenomegaly, abdominal free fluid, mild lymphadenomegaly.
• Leptospirosis - definitive diagnosis

  SNAP lepto antibody test (needs antibodies so early false negatives)

  External lab - PCR or MAT (microscopic agglutination test).
• Treating AKIs - fluid therapy

  Aim is to maintain fluid status/ renal perfusion but also avoid volume overload.

  Requires close monitoring with regular rate adjustments.

  Match losses:

  • Severe polyuria needs high fluid rates.
  • Lower urine output titrate down to avoid volume overload.

  Don’t go over the target weight (reassess your target weight daily)
• Treating AKIs - loop diuretics

  E.g. Furosemide

  • No good evidence for improved outcomes in AKI
  • May be justified to prevent fluid overload and allow nutrition.
  • Ensure well hydrated (Furosemide is nephrotoxic if not).
• Treating AKIs - osmotic diuresis

  E.g. Mannitol

  • No good evidence for improved outcomes through theoretical benefits.
  • Potentially can cause AKI itself.
• Treating AKIs - dopamine

  Increases afferent renal blood flow, bit not GFR

  No evidence for improving outcomes.
• Treating AKIs - Ca2+ channel antagonists

  Diltiazem

  Causes afferent renal Vasoldilation

  Some none significant findings supporting improved resolution of azotaemia and urine output.
• Treating AKIs - renal replacement therapy (Dialysis)

  Indicated in acute toxicities or if non-responsive to IVFT

  Peritoneal dialysis - the first opinion option

  • Peritoneal catheter is placed.
  • Dialysate solution (glucose containing) is infused
  • Drained after 20 minutes to a few hours (allows for diffusion)
  • Repeat as needed
  • Complications - moderate (including iatrogenic septic peritonitis)
  • Moderately improved outcomes.
• Prognosis of AKId

  Success depends on the owners finances, willingness and the facilities of the practice in providing 24 hour care.

  Prognosis - survival rates for treated patients (without dialysis)

  • Obstructive (cats) - 91%
  • Infectious - 82%
  • Metabolic/haemodynamic - 66%
  • Other - 50%
  • Toxin - 43-69%