Paediatrics chapters
Acute kidney injury in children
Sudden loss of kidney function in a child: prerenal, intrinsic and postrenal causes, how urine tests and FENa separate them, and how to manage fluids, hyperkalaemia, acidosis and dialysis.
- AKI is a sudden fall in GFR with retention of waste and loss of fluid and electrolyte control; oliguria is under 0.5 mL/kg/hour in children (under 1 mL/kg/hour in infants).
- Causes are prerenal (commonest: dehydration), intrinsic (ATN, HUS, GN, nephrotoxins) and postrenal (posterior urethral valves); urine sodium, osmolality and FENa separate prerenal from ATN.
- Treat the cause, give insensible losses (400 mL/m²/day) plus output, treat hyperkalaemia (calcium, shift, remove), and dialyse for refractory overload, potassium, acidosis or uraemia.
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Overview
Acute kidney injury (AKI), formerly called acute renal failure, is a sudden fall in glomerular filtration rate (GFR) and tubular function. Waste products (urea, creatinine) build up, and the child loses control of water, sodium, potassium and acid. In children it is often reversible if the cause is found early, but the complications (hyperkalaemia, fluid overload, acidosis) can kill quickly.
Definition and staging
Urine output
| Group | Oliguria |
|---|---|
| Neonates and infants | Under 1 mL/kg/hour |
| Children | Under 0.5 mL/kg/hour |
AKI can also be non-oliguric (normal or high urine output), typically with nephrotoxins such as aminoglycosides or contrast. It is harder to recognise but usually recovers better.
Staging (Akbar)
AKIN stages severity by the rise of serum creatinine over baseline: stage 1 more than 1.5 times, stage 2 more than 2 times, stage 3 more than 3 times.
Paediatric RIFLE (pRIFLE):
| Stage | Estimated creatinine clearance | Urine output |
|---|---|---|
| Risk | Falls by 25% | Under 0.5 mL/kg/hour for 8 hours |
| Injury | Falls by 50% | Under 0.5 mL/kg/hour for 16 hours |
| Failure | Falls by 75% or below 35 mL/min/1.73 m² | Under 0.3 mL/kg/hour for 24 hours or anuria for 12 hours |
| Loss | Failure persisting over 4 weeks | |
| End-stage | Failure persisting over 3 months |
R-I-F-L-E climbs in steps of a quarter: 25, 50, 75% loss of clearance.
Causes
| Category | Mechanism | Examples |
|---|---|---|
| Prerenal | Kidney is underperfused but structurally normal | Dehydration (diarrhoea, vomiting), haemorrhage, burns, diabetic ketoacidosis, septic shock, heart failure, nephrotic syndrome, drugs that cut renal blood flow (ACE inhibitors, ARBs, ciclosporin) |
| Intrinsic (renal) | Damage to tubules, glomeruli, interstitium or vessels | Acute tubular necrosis (ATN) from prolonged hypoperfusion or sepsis; nephrotoxins (aminoglycosides, contrast, myoglobin from crush injury, haemoglobin); haemolytic uraemic syndrome; acute glomerulonephritis; acute interstitial nephritis; tumour lysis (uric acid crystals); renal vein thrombosis |
| Postrenal | Obstruction of both kidneys (or a single kidney) | Posterior urethral valves, bilateral pelviureteric or vesicoureteric junction obstruction, neurogenic bladder, stones, tumour |
Dehydration is the commonest cause of prerenal AKI, and untreated prerenal failure turns into ischaemic ATN. Tubular injury is the commonest intrinsic group.
Haemolytic uraemic syndrome (HUS) in brief
- Triad: microangiopathic haemolytic anaemia, thrombocytopenia and acute kidney injury; an important cause of AKI under 5 years.
- Diarrhoea-associated (typical) HUS: Shiga-like (vero) toxin from E. coli O157:H7; in our subcontinent also Shigella dysenteriae type 1. Bloody diarrhoea is followed about a week later by pallor, lethargy, petechiae, oliguria and hypertension.
- Blood film: schistocytes (fragmented cells), raised reticulocytes, high LDH; Coombs test negative; clotting times normal.
- Treatment is supportive: fluids and electrolytes, blood pressure control, red cell transfusion, early dialysis (about half need it). Avoid platelets unless bleeding, and avoid antibiotics and antidiarrhoeals (they may increase toxin release).
- Over 95% survive the acute phase (Nelson); a minority are left with chronic kidney damage. Atypical HUS (no diarrhoea; complement defects, pneumococcus) is more severe; eculizumab is used.
In pneumococcal HUS the Coombs test is usually positive, and plasma infusion is avoided.
Clinical features
- Reduced or absent urine, puffiness, oedema, breathlessness from pulmonary oedema.
- Hypertension, headache, seizures or confusion (uraemia, hypertension, low sodium or calcium).
- Deep rapid breathing from metabolic acidosis.
- Clues to the cause:
| Clue | Points to |
|---|---|
| Diarrhoea, vomiting, dry mucosa, shock | Prerenal or ATN |
| Bloody diarrhoea, pallor, petechiae | HUS |
| Oedema, haematuria, hypertension after a sore throat | Acute GN |
| Dark red urine with pallor and jaundice | Intravascular haemolysis (e.g. malaria) |
| Poor stream, palpable bladder in a boy | Posterior urethral valves |
| Colicky flank pain, haematuria | Stones |
| Complete anuria | Obstruction, bilateral renal vein thrombosis, cortical necrosis, severe GN |
| Short stature, rickets, anaemia, small kidneys | Acute-on-chronic disease |
Investigations
- Urea, creatinine, electrolytes, blood gas daily: typical pattern is high potassium, low sodium, low calcium, high phosphate, high uric acid, metabolic acidosis.
- Full blood count and film: anaemia; schistocytes and low platelets in HUS.
- Urinalysis in every child: bland in prerenal; red cell casts in GN; muddy brown granular casts and tubular cells in ATN; eosinophils in interstitial nephritis.
- C3, ASO titre, throat swab if acute GN is suspected.
- Ultrasound: size, hydronephrosis, stones, bladder; small kidneys suggest chronic disease.
- ECG: watch for hyperkalaemia.
- Chest X-ray: cardiomegaly, pulmonary oedema.
- MCUG for suspected valves or reflux; renal biopsy only if the cause is unclear or AKI does not settle in 2 to 3 weeks (e.g. crescentic GN).
Urinary indices (Nelson)
| Index | Prerenal (child) | Prerenal (neonate) | ATN (child) | ATN (neonate) |
|---|---|---|---|---|
| Urine sodium (mEq/L) | Under 15 | Under 20 to 30 | Over 40 | Over 50 |
| FENa | Under 1% | Under 2.5% | Over 2% | Over 2.5% |
| Urine osmolality (mOsm/L) | Over 500 | Over 350 | About 300 | About 300 |
| Urinalysis | Normal, high specific gravity | Normal | Casts, cells, protein | Same |
| Ultrasound | Normal | Normal | Bright cortex, poor corticomedullary distinction | Same |
Postrenal AKI shows variable indices and hydronephrosis on ultrasound.
FENa (%) = (urine Na ÷ plasma Na) ÷ (urine creatinine ÷ plasma creatinine) × 100
Child A: urine Na 10, plasma Na 140, urine creatinine 100, plasma creatinine 1.0
FENa = (10/140) ÷ (100/1.0) × 100 = 0.07% → prerenal (kidney still saving sodium)
Child B: urine Na 80, plasma Na 140, urine creatinine 40, plasma creatinine 2.0
FENa = (80/140) ÷ (40/2.0) × 100 = 2.9% → acute tubular necrosis
A concentrated urine with low sodium and FENa under 1% means the tubules are working and the kidney is just underperfused: give fluid.
Management
General
- Secure IV access, strict intake and output chart, daily weight, blood pressure regularly, cardiac monitoring.
- Treat the cause: rehydrate, stop nephrotoxic drugs, relieve obstruction (catheter for a palpable bladder).
- Avoid aminoglycosides, NSAIDs, contrast, ACE inhibitors and ARBs; adjust doses of renally cleared drugs.
Fluids
| Situation | Action |
|---|---|
| Dehydrated or shocked | Normal saline 20 mL/kg quickly (Akbar: within half an hour), reassess; continue rehydration; if well hydrated but no urine, furosemide (Akbar: 2 mg/kg IV, may repeat once) |
| Fluid overloaded | No IV fluid; furosemide 1 to 2 mg/kg (Nelson) and fluid restriction |
| Euvolaemic, oliguric | Insensible loss (about 400 mL/m²/day) plus urine and other losses; Akbar suggests 15 mL/kg plus output in infants |
Add about 10% more fluid for each 1 °C of fever. Use glucose-containing fluid without potassium. Give at least 300 kcal/m²/day mainly as carbohydrate and fat, and restrict protein (Akbar: 0.5 g/kg/day, more in infants).
Body surface area 0.6 m², urine output yesterday 200 mL
Insensible loss = 400 × 0.6 = 240 mL
Today's allowance = 240 + 200 = 440 mL (plus any vomit or stool losses)
Hyperkalaemia
Hyperkalaemia (potassium above 6 mEq/L; act urgently above 7 or with ECG change) is the commonest killer. Treat in three steps:
| Step | Drug | Point |
|---|---|---|
| 1. Protect the heart | 10% calcium gluconate 0.5 to 1 mL/kg IV, diluted, slowly over about 10 minutes with ECG monitoring | Works in minutes; does not lower potassium |
| 2. Shift K into cells | Sodium bicarbonate 1 to 2 mEq/kg IV; glucose with insulin; nebulised salbutamol | Short-lived (a few hours) |
| 3. Remove K | Sodium polystyrene sulfonate (Kayexalate) 1 g/kg by mouth or rectum; loop diuretic; dialysis | Dialysis is the definitive method |
Also stop all potassium intake.
"C BIG K, then Dialyse": Calcium, Bicarbonate, Insulin with Glucose, Kayexalate, then Dialysis.
Other problems
- Acidosis: partial correction with sodium bicarbonate (Akbar: dose = 0.3 × weight × (12 − serum bicarbonate)), then oral bicarbonate.
- Hypocalcaemia and high phosphate: oral calcium and calcitriol; IV calcium gluconate for tetany or seizures.
- Hyponatraemia: usually dilutional; fluid restriction; hypertonic saline only if sodium is very low with symptoms and no overload.
- Hypertension: diuretic, calcium channel blocker (nifedipine), vasodilators; sodium nitroprusside for a crisis.
- Seizures: diazepam; correct sodium, calcium and blood pressure.
- Anaemia: transfuse packed cells slowly if haemoglobin falls below about 7 g/dL.
Child 15 kg, serum bicarbonate 8 mEq/L, aim 12
NaHCO3 needed = 0.3 × 15 × (12 − 8) = 18 mEq, given slowly
Indications for dialysis
| Indication | Notes |
|---|---|
| Fluid overload not responding to restriction and diuretics | Pulmonary oedema, heart failure, uncontrolled hypertension |
| Hyperkalaemia not responding to medical treatment | |
| Metabolic acidosis not responding to medical treatment | |
| Uraemia | Encephalopathy, pericarditis, bleeding; no single urea level |
| Others (acute dialysis) | Some poisonings, hyperammonaemia |
Peritoneal dialysis is simple, safe and widely used in children; haemodialysis and continuous renal replacement therapy are alternatives.
"AEIOU": Acidosis, Electrolytes (potassium), Intoxication, Overload, Uraemia.
Phases and prognosis
- In ATN the oliguric phase usually lasts 7 to 10 days, followed by a diuretic (recovery) phase with brisk urine and risk of losing water, sodium and potassium.
- Oliguria lasting more than 3 weeks, or complete anuria, makes simple ATN unlikely.
- Outlook is good (about 90% full recovery) in ATN, typical HUS and prerenal failure; it is poor in rapidly progressive GN, bilateral renal vein thrombosis and cortical necrosis.
- Even after apparent recovery, a past AKI raises the later risk of chronic kidney disease.
Prevention
- Prompt rehydration in diarrhoea.
- Careful use of nephrotoxic drugs; hydrate before contrast.
- Hydration and allopurinol before chemotherapy to prevent tumour lysis.
- High suspicion in sepsis, after cardiac surgery and in ventilated children on inotropes.
Expect: oliguria cut-offs (0.5 mL/kg/hour in children, 1 in infants); dehydration as the commonest prerenal cause and HUS (E. coli O157:H7 or Shigella toxin) as a classic intrinsic cause in young children; posterior urethral valves as the postrenal cause in boys; prerenal versus ATN by urine sodium, osmolality and FENa (under 1% versus over 2%); muddy brown casts in ATN; daily fluid of 400 mL/m² plus output; the order of hyperkalaemia treatment with calcium gluconate first; avoiding ACE inhibitors and nephrotoxins; and the indications for dialysis.
Quick revision
- AKI: abrupt fall in GFR; oliguric or non-oliguric.
- Oliguria: under 0.5 mL/kg/hour (child), under 1 (infant).
- Prerenal (dehydration) → ATN if untreated; intrinsic (ATN, HUS, GN, toxins); postrenal (valves).
- Prerenal: urine Na under 15, FENa under 1%, osmolality over 500; ATN: Na over 40, FENa over 2%.
- HUS: haemolysis with schistocytes, low platelets, AKI after bloody diarrhoea; supportive; no platelets or antibiotics.
- Fluids: shock gets 20 mL/kg saline; oliguric child gets 400 mL/m²/day plus output.
- Hyperkalaemia: calcium gluconate, then bicarbonate, insulin-glucose, salbutamol, then resin or dialysis.
- Dialysis: refractory overload, potassium, acidosis, uraemia.
- ATN oliguria about 7 to 10 days, then a diuretic phase.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
How can I quickly tell prerenal failure from acute tubular necrosis?
In prerenal failure the urine is concentrated with low sodium and FENa under 1% in a child; in ATN the urine is isotonic (about 300 mOsm/L) with sodium over 40 and FENa over 2%, often with muddy brown casts.
Why is calcium gluconate given first in hyperkalaemia?
It stabilises the heart muscle membrane within minutes and prevents arrhythmia, but it does not lower potassium, so shifting and removal measures must follow.
Should antibiotics be given in diarrhoea-associated HUS?
No. Antibiotics and antidiarrhoeal drugs may increase toxin release and worsen the disease; treatment is supportive with dialysis when needed.
Can a child recover completely from AKI?
Yes, most children with ATN, prerenal failure or typical HUS recover full function, but they need follow-up because a past AKI increases the later risk of chronic kidney disease.