Paediatric nephrology

1. ACUTE KIDNEY
INJURY
BY: DR ENOBONG RUNCIE
LECTURER/CONSULTANT PAEDIATRIC NEPHROLOGIST
UNIVERSITY OF UYO TEACHING HOSPITAL

2. OUTLINE
• Introduction
• Epidemology
• Classification
• Etiology
• Pathophysiology
• Clinical features
• Investigations
• Management
• Prognosis
• prevention

3. INTRODUCTION
• AKI is the sudden deterioration of the renal function due to injury to the
kidney
• Can be mild, moderate or severe
• The kidneys become unable to perform its functions of adequately excreting
nitrogenous waste, maintaining fluid and electrolyte homeostasis
• This can manifest as increase in creatinine + reduction in urine volume

4. EPIDEMOLOGY
• Global problem
• Associated with severe morbidity and mortality
• Death is more in children
• In developed countries, 1.5-2% of all paediatric inpatients at major hospital, about
20% in ICU
• In developing countries, the true prevalence is not known in most African countries
but some reports give a prevalence of 6.6-11.7% of renal diseases in tertiary
institution

5. CLASSIFICATION
• Anatomical location
-pre-renal
-intrinsic
-post-renal
• Urine output
-oliguric: <1ml/kg/hr (infants), <0.5kg/kg/hr for >6hrs in children
-non-oliguric: >1ml/kg/hr (neonates), >0.5ml/kg/hr (infants and children)
-polyuric : >4ml/kg/hr
-anuric: <1ml/kg/day
• Clinical setting: Hospital acquired or Community acquired

6. CLASSIFICATION
• Decline in renal function- RIFLE criteria
- The pRIFLE criteria is used in children
- A reduction in GFR is calculated as a change in estimated creatinine clearance (eCCI) using
Schwartz formula
- Schwartz formula ml/min = K x ht(cm) x serum creatinine(mg/dl)
- K = 0.33 –LBW, 0.45- term babies and children <1yr, 0.55- children and adolescent girls,
0.7- adolescent boys
- Serum creatinine in mg/dl=88.4x serum creatinine in mmol/l
- Unknown baseline serum creatinine are assumed to have eGFR=100ml/min/1.73m2

7. Paediatric RIFLE criteria

8. ETIOLOGY

9. PATHOPHYSIOLOGY OF AKI
• Approx 25% of cardiac output gets to the kidney
• This is filtered by the glomeruli as ultrafiltrate
• Secretion and absorption processes leads to urine formation
• Ultimate goal is removal of nitrogenous waste, control of water, electrolyte and acid
balance, contribute to calcium and phosphate metabolism, produce erythropoietin
• Ischemic, nephrotoxic, septic insults to the kidney leads to damage of the
endothelium of intrarenal vessels, production of inflammatory mediators and this
further damages the kidney.

10. PATHOPHYSIOLOGY CONT
• Kidney tries to maintain perfusion but auto regulation is impaired.
• The resultant effects are
- Decreased urinary output
- Fluid retention
- Accumulation of metabolic waste
- Increase serum creatine
- Increase BUN
- Hydrogen and potassium not excreted
- Phosphate retention with calcium depletion

11. CLINICAL PRESENTATION
• HISTORY: this brings out the probably risk factors for AKI
- Diarrheoa ( Bloody- HUS)
- CHD
- Haemorrhage
- Burns
- Drugs
- Pharyngitis or impetigo
- Urine output (oliguric, anuric, polyuric)
- Body swelling

12. - Uremic symptoms ( anorexia, vomiting puritus)
- Generalised weakness
- Seizures
- Coma
- Blood loss
- Known CKD patient
- Drug hx
- Fever ( infection)
- Joint pain (autoimmune disease)

13. CLINICAL PRESENTATION
• PHYSICAL EXAMINATION
- Volume depletion ( signs of dehydration)
- Hypertension
- Pallor
- Rash
- Tender enlarged palpable kidney (RVT)
- Audible renal bruits (RAT)
- Enlarged bladder ( obstructive uropathy)
- CCF

14. INVESTIGATIONS
• To confirm the presence of AKI
• To determine the underlying cause
• To assist in management

15. INVESTIGATIONS
• URINE
- Urinalysis ( maybe normal especially in pre- renal AKI), note the specific
gravity (high >1.020 in pre-renal AKI)
- Urine MCS
- Fractional excretion of sodium: this measures the percentage of sodium
filtered by the kidney that is excreted in the urine. It can be used to
differentiate between pre-renal AKI and intrinsic AKI due to ATN.

17. INVESTIGATION
• BLOOD
- Serum creatinine
- BUN ( increased in AKI)
- Serum electrolytes ( maybe normal or deranged)
- Serum phosphate (maybe normal or increased)
- Serum calcium ( maybe decreased or normal)
- FBC: leucocytosis (infection), leucopaenia and thrombocytopenia (SLE or TTP), anaemia ( microangiopathic
haemolytic anaemia with thrombocytopenia in HUS)
- Blood film for malaria parasite
- Blood culture

18. INVESTIGATIONS
• RADIOLOGY
- Abdominal USS: kidney (number, size, parenchyma), obstructive uropathy
- Abdominal Xray
- CT scan
- MRI
- MCUG
• RENAL BIOPSY: consider this when a non-invasive evaluation cannot establish an
intrinsic cause of AKI

19. INVESTIGATIONS
• NEW BIOMARKERS FOR DIAGNOSING AKI
- Serum cystatin C
- Neutrophil Gelatinase- Associated Lipocalin (NGAL)
- Kidney injury molecule 1
- IL-18

20. MANAGEMENT OF AKI
• BASIC PRINCIPLES
- Maintenance of haemodynamics and renal perfusion
- Maintenance of fluid and electrolyte balance
- Control of blood pressure
- Treatment of underlying cause
- Pharmacological management
- Treatment of anaemia
- Provision of adequate nutrition
- Surgical treatment when necessary
- RRT when indicated

21. MAINTENANCE OF HAEMODYNAMICS
AND RENAL PERFUSION
• FLUID MANAGEMENT: this depends on if the child is hypovolaemic, euvolaemic or
hypervolaemic
• Fluid challenge can be therapeutic or diagnostic
• Hypovolaemic patient
- Fluid: 10-20ml/kg of NS or RL over 30mins. May be repeated twice. Lack of improvement
suggests an intrinsic renal cause. This is contraindicated in patients with overt fluid overload.
- Diuretics: IV frusemide 1-2mg/kg/dose. This can be repeated. If no diuresis occurs within
2 hrs, discontinue. Note that diuretics are given in the early stage of oliguria to induce
diuresis to convert oliguric AKI to non-oliguric form thereby aiding in fluid mgt.

22. • FLUID MANAGEMENT
• Euvolaemic patient: ongoing loses( insensible fluid loss + urine +GI losses)
are replaced by fluids
• Hypervolaemic patient: restrict fluid to insensible loss + previous day output.
If patient is markedly hypervolemic or anuric, dialysis is indicated.
• Polyuric patient: fluid is replace volume for volume.

23. CORRECTION AND MAINTENANCE OF
ELECTROLYES
• Hyperkalemia: serum potassium>5.5mmol/l
- Stop potassium containing fluid, medication and food
- Treat >6.0mmol/l, presence of ECG findings such as peaked T waves, widened QRS complex and small
indiscernible P wave
- Stabilize the myocardium: IV 10% calcium gluconate 0.5-1ml/kg slowly over 10min
- Shift potassium into the cells: IV sodium bicarbonate 1-2mmol/kg over 5min OR Soluble insulin 0.1 iu/kg +
50% dextrose 1ml/kg over 1hr OR Salbutamol 4ug/kg IV or 2.5mg (<25kg), 5mg (>25kg) nebulized
salbutamol
- Eliminate potassium from the body: Sodium polystyrene sulfonate (Kayaxelate) 1g/kg given orally or by
enema.
- Dialysis

24. CORRECTION AND MAINTAINCE OF
ELECTROLYTE
• Acidosis: oral or IV sodium bicarbonate 1-2mg/kg in moderate to severe
cases
• Hyponatraemia: if severe give hypertonic sodium chloride 6-12ml/kg over
30-90mins with caution
• Hyperphosphatemia: give oral phosphate binders-calcium carbonate
• Hypocalcemia: if tetany or convulsions are present give calcium gluconate.

25. MANAGEMENT OF AKI
• BASIC PRINCIPLES
- Maintenance of haemodynamics and renal perfusion
- Maintenance of fluid and electrolyte balance
- Control of blood pressure
- Treatment of underlying cause
- Pharmacological management
- Treatment of anaemia
- Provision of adequate nutrition
- Surgical treatment when necessary
- RRT when indicated

26. INDICATIONS FOR DIALYSIS IN AKI
• Symptomatic volume overload
• Hyperkalemia: serum potassium >6.5mmol/l with ECG changes and unresponsive to non-dialytic therapy
• Pulmonary edema
• Refractory hypertension
• Severe uremia: uremic encephalopathy, pericarditis, pleuritis
• Severe metabolic acidosis unresponsive to medical management
• Hypercatabolic state e.g. burns, sepsis, TLS
• Severe hyponatraemia
• Refractory hyperphosphataemia

27. COMPLICATIONS
• Fluid overload: pulmonary oedema, CCF
• Cardiovascular: HTN, pericardial effusion, CCF
• Electrolyte imbalance: hyperkalaemia, hyponatraemia, metabolic acidosis
• neurologic: seizures, confusion, coma
• Infection
• GI: ileus, haemorrhage
• Haematologic: Anaemia, platelet dysfunction

28. PROGNOSIS
• Depends on age, etiology, presence of pre existing renal disease, time of onset vs
presentation, need for dialysis and resourses.
• Poor prognostic factors
- Young age
- Multi system failure
- Oliguria
- Certain etiology such as RPGN, malignancies
• Mortality – 20-60% in developing countries
• Follow up for HTN, proteinuria, decreased GFR should be for up to 5 years

29. PREVENTION
• 5 LEVELS OF PREVENTION