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Home | Articles | Renal | Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI)

Last updated 25th September 2024

Definition (KDIGO Clinical Practice Guideline)

  1. AKI is defined as any of the following:
    • Increase in serum creatinine by ≥26.5 micromol/L within 48 hours; or
    • Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
    • Urine volume <0.5ml/kg/h for 6 hours
  2. AKI is staged for severity according to the following criteria (see table below):
    StageSerum Creatinine CriteriaUrine Output
    11.5 - 1.9 times baseline OR >26.5mmol/L increase in 48 hours<0.5ml/kg/hr for 6-12 hours
    22.0 - 2.9 times baseline0.5ml/kg/hr for 12 hours
    33.0 times baseline OR increase in creatinine to 354mmol/L OR initiation of renal replacement therapy<0.3ml/kg/hr for >24 hours or anuria for >12 hours
  3. Baseline can be defined as the lowest creatinine within the last 12 months (although be wary of spurious results, or falsely low creatinine when patients have received a lot of IV fluids) or the most recent creatinine preceding the acute admission/deterioration.

  4. Note that patients with low baseline creatinine (eg frailty, very low BMI, alcohol related liver disease) can have a significant AKI with a creatinine or eGFR within the ‘normal’ reference range on the reported labs.

  5. Changes in urine output may occur before changes in serum creatinine. Do not be falsely reassured by unchanged bloods in these circumstances.

  6. eGFR is not used to define AKI, as the formula to calculate eGFR assumes a steady state of creatinine, and is therefore inaccurate in AKI.

Risk Factors for Developing AKI

  1. Age >60 years
  2. Pre-existing chronic kidney disease (eGFR<60)
  3. Co-morbid conditions including:
    • Diabetes
    • Heart failure
    • Liver failure
    • Vascular disease
  4. Presence of sepsis, hypovolaemia and/or hypotention
  5. Perioperatively (especially vascular surgery)
  6. Myeloma
  7. Radiocontrast media
  8. Prescription of certain medications including: ACEi/ARBs/NSAIDs/Diuretics/PPIs

Classification and Causes of AKI

ClassificationCause
Pre-renal AKI
(Urinalysis - usually bland)
- Shock/hypotension (profound vs relative)/hypoperfusion
- Hypovolaemia
- Sepsis
- Cardiac or liver failure
- Drugs which exacerbate hypoperfusion or block compensatory mechanisms (e.g. diuretics, ACEIi, ARBs)
Renal or intrinsic AKI
(Urinalysis - significant blood and protein in glomerular disease, bland in interstitial nephritis)
Think anatomy:
- Glomeruli - glomerulonephritis and vasculitis
- Tubules - acute tubular necrosis (ATN), cast nephropathy
- Interstitium - acute interstitial nephritis (often secondary to drugs e.g. antibiotics, NSAIDs, PPI)
Post-renal AKI
(Urinalysis - blood in cases of renal stones or luminal malignancies, bland in extrinsic obstruction)
Obstruction at any level:
- In the lumen - ureteric stone, clot retention, blocked catheter
- In the luminal wall - tumour of the bladder or ureter
- Extrinsic - BPH, gynaecological malignancy, constipation

80% of AKI in hospitalised patients is caused by pre-renal causes and ATN

For the investigation and management of AKI in renal transplant recipients, much of this advice is still relevant, but please also refer to the separate guidelines on kidney transplantation.

Clinical Assessment

  1. Signs of sepsis or infection
  2. Volume status – peripheral oedema, chest auscultation, JVP, mucus membranes, skin turgor, axillary sweat, peripheral veins
  3. Renal angle tenderness
  4. Palpable bladder
  5. Pericardial rub as sign of uraemic pericarditis
  6. Evidence of rashes, rheumatological disorders or other systemic illness

Urinalysis

  1. Urine dip (with documented result) in all cases is a MUST!
  2. Send for both urine protein:creatinine ratio, and urine albumin:creatinine ratio if proteinuria present
  3. Consider culture if clinical concern of infection
  4. Consider urine electrolytes to help distinguish between pre-renal AKI and ATN

Bloods

All patients should have U&Es, bicarb, bone profile, FBC, LFTs, CRP and VBG.

Also consider:

  1. Coagulation screen – if sepsis, hypotension, clinical concern of bleeding, or being considered for haemodialysis or kidney biopsy
  2. CK – if on statin or fall with long lie
  3. Glomerulonephritis screen (ANA, RhF, complement, ANCA, Anti-GBM ab, ESR) – if blood or protein on urinalysis
  4. Myeloma screen (serum electrophoresis, urine Bence Jones protein) – if blood or protein on urine dip, significant anaemia, hypercalcaemia or bone pain.
  5. Haemolysis screen (LDH, blood film, reticulocytes, haptoglobin) – if rapid change in haemoglobin or thrombocytopaenia
  6. Blood cultures – if clinical concern of infection or febrile

Patients with AKI can have significant changes in electrolyes and renal function without symptoms and should have regular blood testing.

Imaging

  1. Urgent USS should be performed if cause of AKI unclear or clinical concern of obstruction ideally within the 12 to 24-hours.
  2. CT KUB more helpful if concern about stone disease, and can be done OoH without IV contrast.
  3. Bladder scan can be used to look for urinary retention, or significant post-void residual volume.

Management

This will largely be guided by treating the underlying cause of AKI. Here are some common treatments to consider:

  1. Fluid balance monitoring, and consider urinary catheter.
  2. IV fluid resuscitation if clinically dry and/or history of volume loss (eg D&V, poor oral intake, polyuria) with goal of achieving euvolaemia – see guidelines on volume status and replacement in AKI.
  3. Diuretics if fluid overloaded (nephrotic syndromes, cardiac failure).
  4. Treat infection – review antibiotics choice and dose based on renal function (CrCl). Some medications will be ineffective in AKI e.g. nitrofurantoin, whereas other may worsen renal function e.g. trimethoprim, gentamycin, co-trimoxazole.
  5. Relieve any obstruction (may require urology/radiology input).
  6. Review medications – stop nephrotoxic or nephromodulatory medications (NSAIDs, ACEi, ARBs, SGLT2i), reduce dose or adjust preparation (opioids, gliclazide), review medications that could cause or worsen hyperkalaemia (potassium supplements, potassium sparing diuretics).
  7. Treat hyperkalaemia – see separate guideline.
  8. Assess bleeding risk – uraemia is associated with platelet dysfunction, and many causes of AKI are associated with coagulopathy. Review antiplatelet and anticoagulants.
  9. Nutritional support – loss of appetite is common, and AKI is a catabolic state. Consider early nutritional support (e.g. Ensures/Fortisip etc or NG feeding) and dietitian referral.

Consider Specific Therapies

These will often be guided by the renal team, and may require renal biopsy to confirm the diagnosis.

  1. No specific treatment for ATN other than restoring renal perfusion and time.
  2. Steroids for interstitial nephritis.
  3. Steroids and Rituximab ± Cyclophosphamide ± Plasma Exchange for systemic vasculitis.
  4. Plasma exchange with FFP for aHUS/TTP.
  5. Organ support in critical care maybe required for shock, sepsis, respiratory failure, or cardiac failure if appropriate based on the patients co-morbidities and premorbid functional status. Early referral for senior review, including critical care teams, can be essential especially in hypotensive patients with AKI.

Indications for Dialysis

  1. Hyperkalaemia refractory to medical management– especially if K+ >6.5 mmol/L in oliguric patient.
  2. Pulmonary oedema refractory to medical management – especially in patients with oliguria.
  3. Severe metabolic acidosis – especially if serum bicarbonate <10mmol/L and hypotensive.
  4. Uraemic complications – encephalopathy or pericarditis.
  5. Certain medication overdoses – e.g. lithium.

When to Refer to Renal Team

(32177 during working hours and oncall consultant via switchboard our-of-hours).

  1. Stage 3 AKI
  2. Considering acute haemodialysis (including helping decide whether this would be a suitable treatment option)
  3. AKI in renal transplant patients
  4. Suspected intrinsic AKI
  5. · Diagnostic uncertainty, poor response to treatment

Follow up

Patients who have significant AKI are at twice the risk of developing end stage kidney disease (even if their renal function made a complete recovery). These patients may be suitable for follow up in the renal clinic particularly if:

  1. Young patient
  2. Pre-existing CKD and not known to the renal services
  3. AKI from intrinsic cause
  4. Stage 3 AKI or multiple episodes of AKI

Content by Robert Ker & Thalakunte Muniraju