Acute kidney injury

    Cards (34)

    • functions of the kidney include:
      • salt and water balance
      • potassium excretion
      • acid-base balance
      • vitamin D metabolism
      • EPO production
    • normal renal structure:
      • glomeruli - filtering units
      • tubules - reabsorption tubes
      • interstitial - comprised of microvascular capillaries that
    • definition of AKI:
      • increase in serum creatinine by >26.5 µmols/l in 48 hours or,
      • increase in serum creatinine by >1.5x baseline creatinine within last 7 days or
      • urine volume <0.5ml/kg/hr for 6 hours
    • AKI staging:
      • AKIN 1 - increased serum creatinine > 26.5 µmol/l in 48 hrs or increased serum creatinine > 1.5 - 1.9 fold over baseline
      • AKIN 2 - increases serum creatinine > 2 - 2.9 fold over baseline
      • AKIN 3 - increased serum creatinine >3 fold over baseline or increased serum creatinine >394 µmol/l or started on dialysis
    • severe AKI is independently associated with adverse renal outcomes:
      • increased incidence of chronic kidney disease
      • increased incidence of end-stage renal disease
    • all patients with significant acute kidney injury must have an ultrasound scan to exclude or demonstrate obstruction to the renal tract
    • renal causes of AKI can be split into:
      • tubulointerstitial (tubules and the bit ‘in between’)
      • glomerular
      • vascular
    • tubulointerstitial causes of AKI:
      • acute allergic interstitial nephritis
      • drug-related (e.g., PPI’s omeprazole, antibiotics, diuretics, NSAID’s)
      • may have an eosinophilia (infiltration of kidneys by eosinophils, may respond to steroids)
      • often respond well to steroids
    • glomerular causes of AKI:
      • rapidly progressive glomerulonephritis (RPGN): immune aetiology and characterised by ‘glomerular crescents’
      • mass of inflammatory cells in the Bowman’s space
    • examples of causes of cresentic rapidly progressive glomerulonephritis:
      • Goodpasture’s syndrome: anti-GBM antibody (targets collagen in GMB)
      • Wegener’s granulomatosis: PR3 antibody (perinuclear pattern, myeloperoxidase
      • Microscopic polyarteritis (MPA): MPO antibody (cytoplasmic pattern, proteinase-3)
      • SLE: anti-nuclear antibody(ANA), anti-dsDNA antibody
    • vascular causes of AKI:
      • haemolytic uraemia syndrome (HUS) (leads to glomerular microvascular thrombosis)
      • E coli related (E coli O157)
      • familial cases (genetic aetiology)
    • acute tubular injury (ATI) is the commonest causes of AKI in hospitals
    • ATI can be caused by:
      • tubular toxin (e.g., gentamicin, cisplatinum, NSAID’s radio-contrast dye)
      • sever prolonged hypotension (sepsis, MI)
      • renal hypoperfusion e.g., elderly patient on ACEI, diuretic who has D&V
    • ATI causes initial oliguria (low urine output) then may exhibit polyureic recovery phase (watch electrolysis)
    • ischaemia is a very important part of the aetiology of patients who have acute kidney injury, nephron is partially hypoxic (medullary area) and thus is very susceptible to ischaemia
    • pathogenesis of AKI:
      • ischaemia insult (haemodynamic injury leading to decreased filtration pressure)
      • systemic inflammation
      • sepsis
    • differential diagnosis of AKI can be split into pre-renal, renal, and post-renal
    • pre-renal differential diagnosis of AKI include:
      • reduced renal or ‘effective’ blood volume
      • hypovolaemic (e.g., bleeding, 3rd space fluid losses, over-enthusiastic diuretic therapy)
      • hypotension e.g., septic/cardiogenic shock, liver failure
      • reduced renal blood supply secondary to severe renovascular disease (± ACEI), dissection of the abdominal aorta etc.
    • renal differential diagnosis of AKI include issues with glomerulus, tubules and interstitial
    • post-renal differential diagnosis of AKI include obstruction at multiple levels (e.g., ureter, bladder etc.)
    • post-renal differential diagnosis of AKI can be caused by:
      • prostate- hypertrophy (common), cancer
      • bladder lesions - tumour
      • ureter - calculi, tumour, extrinsic compression (retroperitoneal fibrosis, tumour)
      • myeloma kidney- internal obstruction of the lumen of the nephron, para protein precipitates in the nephron creating a myeloma cast
    • bilateral obstruction or obstruction of a single kidney transplant is required is order to result in AKI
    • clinical history in AKI:
      • renal history- pre-existing renal disease, diabetes, famiy history
      • urine volume- acute oliguria
      • drug history- new drugs, nephrotic drugs (NSAID’s, ACEI, antibiotics)
      • systemic symptoms- diarrhoea, rashes, etc.
    • clinical examination in AKI:
      • fluid status (JVP, postural BP) dehydration?
      • evidence of infection?
      • rash, joint pathology?
      • arterial burits? underlying reno-vascular disease
      • palpable bladder (obstruction)
      • check drug chart
    • investigations in AKI
      • urine dipstick - simple but important (blood protein)
      • urine culture
      • renal ultrasound - if obstructed then decompress
      • renal biopsy (AKI and normal sized kidney)
      • angiography ± intervention
      • blood tests
      • immunological tests
      • other tests
    • blood tests for AKI investigation include:
      • FBC, blood film, clotting screen
      • biochemistry including calcium, phosphate, LFT’s and albumin
      • creatinine kinase (rhabdomyolysis)
      • blood cultures
      • virology and serology (e.g., Hep B, ASOT)
    • immunological tests for AKI include:
      • IgG’s and serum electrophoresis (myeloma)
      • complement levels (SLE, post strep GN)
      • autoantibodies
    • autoantibodies to check for AKI:
      • anti-nuclear factor (ANA) - SLE
      • anti-neutrophil antibody (ANCA) - vasculitis
      • anti-GBM antibody - Goodpasture’s syndrome
    • other tests to do for AKI:
      • urine: Bence Jones protein = light chains (myeloma)
      • chest X-ray (cardiac size, pulmonary oedema or haemorrhage)
      • ECG especially if hyperkalaemia
    • general treatment for AKI:
      • optimise fluid balance and circulation
      • stop exacerbating factors (e.g., nephrotoxic drugs- check drug chart)
      • appropriate prescribing (check BNF, discuss with pharmacist) e.g., opiates accumulate in AKI
      • supportive treatment (e.g., dialysis, nutrition)
    • specific treatment of AKI:
      • obstruction - drain renal tract
      • sepsis - effective antibiotics
      • RPGN (e.g., SLE) - immunosuppression
      • Goodpasture’s syndrome - plasma exchange
      • compartment syndrome - fasciotomy
    • criteria of initiating haemodialysis:
      • severe ‘uraemia’ (no prospect of immediate improvement/uraemia encephalopathy or seizures/uraemic pericarditis)
      • hyperkalaemia unresponsive to medical treatment (>6.5)
      • fluid overload, especially pulmonary oedema, resistant to treatment with diuretics/fluid restriction
      • severe acidosis (results in myocardial depression and hypotension
    • haemodialysis (long-term dialysis) for AKI can cause vascular access related complications (pneumothorax, infection, bleeding)
    • for haemodialysis anticoagulation may be required which could be problematic in patients with bleeding, and hypotension may be troublesome in some patients (sepsis, IHD, diabetes)
    See similar decks