Acute kidney failure

AKI is the entire spectrum of disease (mild -> severe), and can be defined as an abrupt (1 to 7 days) and sustained (more than 24 hours) decrease in kidney function
Mortality of critically patients with acute renal failure is high (50%–60%)
Renal recovery in survivors may be as high as 90% but as many as 50% of survivors do not return to baseline function
Increases risk of CKD and vice-versa
Consider underlying risk factors, minimse use of NSAIDs/nephrotoxics in CKD patients
Triggers may include
- Hypovolaemia – sepsis, critical illness, circulatory shock, burns, trauma
- Drugs – NSAIDS, PPI, Abx
- Vasculitis/rheum – ?rash/arthralgia
- Kidney stones
- Contrast
- LUTS obstruction
- Poisonous animals
- Heatwave

Casues

Pre-renal
- volume responsive AKI -> monitor haemodynamics and challenge with volume
- sepsis-induced AKI
- hypotension – manage aggressively
- renovascular disorders
Renal
- nephrotoxins
  — allopurinol, aminoglycosides, amphotericin, frusemide, NSAIDS, ACE-I, organic solvents, contrast, sulfondamides, thiazides, herbal medicines, heavy metals, pentamidine, paraquat
- glomerular disease
- HUS
- crystal nephropathy
- tubulointerstitial disease
- rhabdomyolysis
Post-renal
- obstruction at any post-renal site (e.g. tumour, clot, papillary necrosis, foreign body, post-surgical, blocked IDC)
- abdominal compartment syndrome

Diagnosis
- Increase serum creatiin > 26.5umol within 48 hours OR
- Acute increase creatinine > 1.5 times from baseline OR
- Significant reduction in urine output
- May need to repeat UECs to confirm if AKI or deterioation of CKD

Wokrup

History
- Review Medications (new or increased dose)
- Trauma or myalgias – Rhabdomyolysis Causes
Symptoms: Severe Kidney Injury
- Fatigue
- Anorexia
- Nausea or Vomiting
- Weight gain
- Edema
- Confusion (uremic encephalopathy)
Assess fluid status
- Dehydration
  - Gastroenteritis
  - Diuresis
  - Diabetic Ketoacidosis
  - Hemorrhage
  - Burn Injury
- Third spacing (e.g. Ascites in Cirrhosis)
- Fluid Overload (e.g. edema in CHF)
Look for signs of Infections
- Interstitial Nephritis
Look for signs systemic ilness
Urine MCS- red cell morphology, casts
ACR/PCR
Renal USS
Bloods for any underlying suspected pathology – consider C3/4, ANA. ENA. Anti-DsDNA, ANCA, srum electrophoresis, serum free light chains

Management

Remove risks
Fluid assessment and medication review
Consult Nephrology early in course
- Most patients with Acute Kidney Injury require hospitalization (except mild cases with known reversible cause)

Sick-day advice

Identify medications with risk of
- Hypoperfusion
- dangerous accumulation
- toxicity
- exacerbating hyperkalaemia.
some high-risk medications – ‘SADMANS’
- sulfonylureas
- ACE inhibitors
- Diuretics
- Metformin
- ARBs
- NSAIDs
- SGLT2 inhibitors
Others prone to acute accumulation in the setting of AKI
- Antivirals
- Aminoglycosides (e.g., Gentamicin, Amikacin)
- Antiarrhythmics
- Analgesics
- sedative medications
- Lithium
- NOACs (e.g., Apixaban, Dabigatran)
- Digoxin
- Allopurinol
Instruct patients to withhold such medications when they experience vomiting, diarrhoea, reduced oral intake or other serious illness.
Provide permission and instruction to seek prompt medical attention, because
- acute illness, including AKI, may paradoxically produce hypertension and hyperglycaemia, warranting an escalation of specific therapies
- vulnerable patients often need further medical interventions on ‘sick days’.
Advice should balance the risks and benefits of briefly stopping medications; be individualised; include translation, written instructions or visual aids; consider existing strategies for chronic medications (eg Webster Packs); and involve carers and other clinicians, including pharmacists

Analgesic nephropathy

Paracetamol most important cause
- Worse when combined with aspirin or codeine
NSAIDS don’t cause increased risk of CKD – but can cause acute renal failure/ AKI

Acute Tubular necrosis

necrosis tubular cells due to prolonged ischaemia or toxicity (heavy metals, solvents, glycols, NSAIDs, contrast, antibiotics, pesticides)
extreme oliguria
presence of “muddy casts” on urinalysis
if cause removed recovery likely

Acute interstitial nephritis