Paediatric Acute Kidney Injury

Introduction

• In developed countries, aetiology has shifted from primary glomerular disease to hospital-acquired causes
• Nephrotoxins are a common cause of AKI in children
  • Aminoglycosides, vancomycin, PipTaz, antivirals, contrast, ACEi, tacrolimus, NSAID’s
• Pre-renal is the most common form due to volume depletion
• Community-acquired usually pre-renal volume depletion
• Hospital-acquired usually multifactorial in setting of critical illness

pRIFLE

• Paediatric modification of RIFLE criteria utilising Schwartz modification of creatinine clearance to take into account somatic growth

Normal serum creatinine by age

• Newborn 27-88micromol/L
• Infant 18-35
• Child 27-62
• Adolescent 44-88

History

• Short duration vomiting/diarrhoea or reduced oral intake – Pre-renal AKI
• Bloody diarrhoea 3-7 days before oliguria – HUS
• Pharyngitis or impetigo weeks prior followed by haematuria and oedema – PSGN
• Hospitalised – Nephrotoxic medications or ischaemic ATN
• Fever, joint complaints, rash seen in autoimmune intrinsic AKI, vasculitidies (HSP) or SLE

Examination

• Volume depletion – Pre-renal AKI
• Oedema – Nephrotic syndrome, glomerulonephritis
• HTN – Glomerulonephritis
• Rash – HSP, interstitial nephritis, acute onset SLE
• Enlarged palpable kidneys – Acute renal vein thrombosis
• Enlarged bladder – Urethral obstruction

Investigations

Urinalysis

• Muddy brown granular casts – ATN
• Red cell casts – GN
• Dysmorphic red cells – Nephritic urinary sediment
• Pyuria – Tubular or interstitial disease or UTI
• Heme positive dipstick without red cells – Haemolysis, rhabdo

FENa

• <1% = Pre-renal
• >2% = ATN
• However, in neonates, sodium reabsorption is less effective so:
  • <2% = Pre-renal
  • >2.5% = ATN

FBC

• Microangiopathic haemolytic anaemia – HUS
• Eosinophilia – Interstitial nephritis

Further tests

• Low C3/normal C4 = PSGN
• Streptococcal serology/ASOT/Anti-DNAse B – PSGN
• Renal USS in all kids with AKI of unclear aetiology

HUS

• Classic triad of microangiopathic haemolytic anaemia, thrombocytopaenia and acute kidney injury
• All paediatric cases show triad
• Rare if over 5yo
• One of the most common causes of ARF in children
• Primary form generally related to complement disorders or Cobalamin C metabolism disorders (rare)
• Secondary form due to Shiga-toxin E. coli 0157:H7 in 90% of cases, Shigella, S. pneumoniae, HIV, drug toxicity (particularly in transplant patients), malignancy, pregnancy, scleroderma and antiphospholipid syndrome

Typical HUS

• E.coli 0157:H7 most commonly
• Antibiotics increase likelihood of HUS by 17x
• Antimotility agents also increase risk
• Fever only seen in 1/3 of cases
• Classically, 2-3 days after onset of watery diarrhoea and abdominal pain get bloody diarrhoea and worsened pain
• High-risk of progressing to oliguric AKI and dialysis
• CNS involvement in 1/3 that can progress to seizures (suggests TTP – although need ADAMTS13 <10% to diagnose?)
• Anaemia can be profound

Diagnosis of HUS

• Microangiopathic haemolytic anaemia
  • Hb <80, negative Coombs, schistocytes >10% and helmet cells
• Platelets <140 (usually around 40)
• AKI (severe in 50% of cases)
• Typically raised LDH, unconjugated bilirubin and low haptoglobin

Differential of HUS

• DIC
  • Have abnormal coagulation profile with elevated fibin degradation products and D-dimer
• TTP
  • Due to deficiency of vWF cleaving protease due to mutation in ADAMTS13 or acquired anti-ADAMTS13 antibodies (activity <10%)
• Systemic vasculitis
  • Typically have rash, arthralgia and no prodromal diarrhoeal illness

TTP

• Treatable with plasmapheresis (decreases mortality to 10%) + steroids
  • Avoid transfusion unless life-threatening haemorrhage
  • Daily check platelets until >150 and LDH normal for 2-3 days
  • Rituximab (monoclonal anti-CD20 antibody against B cells mostly)
• HUS triad + neurological dysfunction and fever
• Significant renal impairment is less common than in HUS
• Risk factors
  • Infection (EHEC)
  • Drugs (tacrolimus, cyclosporine, clopidogrel, ticlopidine)
  • Pregnancy
  • SLE
  • GVHD
  • HIV-1
  • Connective tissue disorders
  • Malignancy

Last Updated on November 10, 2021 by Andrew Crofton