ACUTE KIDNEY INJURY IN CHILDREN

1. ACUTE KIDNEY INJURY IN CHILDREN (AKI) Presenter Dr. Beatrice Kyomugisa Paediatrician Fort Portal Regional Referral Hospital

2. Outline • Definition • Staging • Epidemiology • Classification of AKI • Causes of AKI • Risk factors • Clinical features • Complications • Investigations • DDx • Management • Prevention • Prognosis

3. Definition Abrupt loss of kidney function that results in a decline in glomerular filtration rate (GFR), retention of urea and other nitrogenous waste products, and dysregulation of extracellular volume and electrolytes. AKI is defined as any of the following: • Increase in Serum Creatinine (SCr) by ≥0.3 mg/dl (≥ 26.5 umol/l) within 48 hours OR • Increase in SCr of ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days OR • Urine volume <0.5 ml/kg/h for 6 hours.

4. Staging • KDIGO, 2012 proposed a combined definition for AKI in children & adults combining aspects of AKIN, pRIFFLE and RIFFLE

5. Staging of acute kidney injury in children: Kidney Disease Improving Global Outcomes (KDIGO) criteria

6. AKI or NOT • Change of 0.7mg/dL within 24 hours • Fold change of 2 using the repeat creatinine (Stage 2) • What is the baseline value? • Use the value from follow-up • Estimate baseline • 2 year old • Creatinine on admission: • 0.6mg/dL or 53 umol/L • Repeat creatinine: • 1.3mg/dL or 106.1 umol/L

7. Limitations of creatinine AKI definitions • Serum creatinine (SCr) is highly affected by muscle mass, age and altered by malnutrition • SCr is affected by volume status, where volume overload can dilute SCr concentrations, leading to a potential masking of SCr increase • Definitions are based on baseline SCr which is usually unknown • SCr and/or urine output changes late in the pathophysiology of AKI; up to 72 h after injury has occurred

8. Epidemiology • Globally, 85% of acute kidney injury (AKI) cases occur in low-and-middle-income countries. • KDIGO criteria: 11-59% • Uganda: 35-46%

9. Etiological classification of AKI

10. Etiopathogenesis of AKI

11. Clinical features • Edema • Hypertension • Acute weight gain • Decreased or no urine output • Gross and microscopic hematuria • Poor urinary stream History • A short duration of vomiting, diarrhea, or decreased oral intake associated with decreased urine output suggests prerenal AKI • History of bloody diarrhea 3 to 7 days prior to the onset of oliguria suggests hemolytic uremic syndrome

12. Cont….. • History of pharyngitis or impetigo a few weeks prior to the onset of gross hematuria or edema suggests poststreptococcal glomerulonephritis. • History of drug use: nephrotoxic medications(NSAIDs, aminoglycosides) or prolonged periods of hypotension are associated with intrinsic AKI. • A diligent search for all drugs and medications ingested is especially important, even when another obvious cause for AKI is evident. • Systemic complaints of fever, joint pains, and rash i.e Henoch-Schönlein purpura, systemic lupus erythematous • Burns , bleeding and surgery

13. Physical examination • Measure blood pressure e.g hypo or hypertension • Assess for edema • Weigh the patient to determine weight gain • Rash: Henoch-Schönlein purpura, systemic lupus erythematous • Joint tenderness or swelling: Henoch-Schönlein purpura, SLE) • Poor urinary stream • Palpably enlarged bladder • Palpably enlarged kidneys: Polycystic/multicystic kidney disease, Renal vein thrombosis • Assess for shock

14. Complications • Chronic kidney disease • Electrolyte abnormalities e.g hyperkalemia, hyperphosphatemia • Metabolic acidosis • Uremic encephalopathy (seizures) • Uremic gastritis and bleeding • Uremic pericarditis and pleuritis • Complications of dialysis

15. Investigations • Urinalysis: urinalysis in children with prerenal AKI is typically normal. Glomerulonephritis (RBC or WBC casts); ATN (granular casts); acute interstitial nephritis (eosinophilia) • Complete blood count: Leucopenia (SLE , sepsis), thrombocytopenia (sepsis, HUS), anaemia(dilutional or hemolytic e.g. HUS, SLE) • RFTs (blood urea nitrogen (BUN) and creatinine) and electrolytes (K, Na, phosphate, Ca, Mg) • Blood gas: metabolic acidosis, compensated or not • Complement studies e.g C3, C4, hypocomplementemia is seen in patients with poststreptococcal glomerulonephritis (PSGN)

16. Cont…… Autoimmune work-up: ANCA, ANA, C3 and C4 for glomerulonephritis Renal ultrasound: Increased echogenicity, kidney size/ number/ structure, hydronephrosis/ hydroureter Renal vessel Doppler study: increased resistive indices with ATN and thrombosis Computed tomography/magnetic resonance: trauma, stones Radionucleotide scan: determine level of obstruction and assess function Voiding cystourethrogram (vCUG): diagnose obstruction (esp posterior urethral valves)

17. Differential diagnosis • Chronic kidney disease • Heart failure • Acute malnutrition (edematous) • Nephrotic syndrome • Liver cirrhosis • Acute tubular necrosis • Acute glomerulonephritis • Hemolytic uremic syndrome

18. General principles of management of (AKI) • Fluid management: Assess fluid status, if edematous give diuretics(IV Furosemide 2-5mg/kg/dose) if hypovolemic give fluids (N/saline), if euvolemic give maintenance fluids. • Renal replacement therapy: Dialysis (when all measures fail) • Adjustment of drug dosing: withhold or adjust nephrotoxic drugs • Nutritional support: Restrict all K+ containing foods (fruits/juices, packed foods) and salt intake • Electrolyte management: Manage hyperkalemia, hyperphosphatemia • Specific pharmacologic therapies: Treat HTN and specific RX of the underlying cause (Malaria: antimalarials) • Supportive measures: Fluid input and output/ prescription, daily dipstick, RFTs and electrolytes, measure TPR,SPO2, BP and weight .

19. Management of hyperkalemia by severity

20. Management of hypocalcaemia and hperphosphatemia • Hypocalcemia • Managed with calcium supplements • Vitamin D • 1 alpha or 1,25 hydroxycholecalciferol (this is especially important in CKD) • Hyperphosphatemia • Phosphate binders; Calcium carbonate available on market

21. Prevention of acute kidney injury Multidisciplinary approach • Identify the patients at risk of AKI eg DKA, shock, sepsis, malaria • Avoidance and substitution of nephrotoxic drugs eg gentamycin , NSAIDs • Avoidance of hypovolemia by fluid administration egDiarrhoea and vomiting • Avoid hypotension • Perform RFTs and electrolytes early.

22. Differences between AKI and CKD in children

23. Follow-up • Evaluate patients 3 months after AKI for resolution, new onset, or worsening of pre-existing CKD.

24. Prognosis • AKI in hospitalized children is associated with increased mortality • ICU setting mortality rates associated with AKI are higher: up to 30 to 44% • Highest mortality rates are seen in infants, patients with multiorgan failure and those on renal replacement therapy (KRT) • Children with AKI are at long-term risk for developing CKD • Patients with moderate to severe AKI should be followed annually to detect signs of CKD (eg, hypertension and proteinuria).