Acute kidney injury (AKI) previously known as acute renal failure (ARF), is an important emergency where prompt and appropriate management is life-saving. AKI usually occurs in patients with previously normal renal function but may occasionally be superimposed on preexisting renal disease (acute-on-chronic renal failure). The incidence of AKI in pediatric intensive care unit (PICU) is around 30–40% with mortality rates of 40–50%.
The Indian Academy of Pediatrics (IAP) has released Standard Treatment Guidelines 2022 for Acute Kidney Injury in Children. The lead author for these guidelines on Acute Kidney Injury in Children is Dr. Mukta Manthan along with co-author Dr. Bipin Jose and Dr. Mihir Sarkar. The guidelines come Under the Auspices of the IAP Action Plan 2022, and the members of the IAP Standard Treatment Guidelines Committee include Chairperson Remesh Kumar R, IAP Coordinator Vineet Saxena, National Coordinators SS Kamath, Vinod H Ratageri, Member Secretaries Krishna Mohan R, Vishnu Mohan PT and Members Santanu Deb, Surender Singh Bisht, Prashant Kariya, Narmada Ashok, Pawan Kalyan.
Following are the major recommendations of guidelines:
Nomenclature and Classification:
Acute kidney injury is defined as an increase in serum creatinine by ≥0.3 mg/dL within 48 hours; or an increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within last 7 days; or a urine volume <0.5 mL/kg/h for 6 hours.
Acute kidney injury is further classified into three stages based on rise of serum creatinine or change in urine volume. It is recommended to use Kidney Disease: Improving Global Outcomes (KDIGO) classification for an early diagnosis of AKI so that measures are taken to prevent the progression of the condition.
TABLE 1: Classification of acute kidney injury (KDIGO classification).
AKI severity
Serum creatinine criteria
Urine output criteria
Stage I
1.5–1.9 times baseline Or
³ 0.3 mg/dL increase
<0.5 mL/kg/h for 6–12 hours
Stage II
Increase ³ 2–2.9 times baseline
<0.5 mL/kg/h for ≥12 hours
Stage III
3.0 times baseline Or
Increase in serum creatinine to ³ 4.0 mg/dL
Or
Initiation of renal replacement therapy Or
In patients <18 years, decrease in eGFR to
<35 mL/min per 1.73 m2
<0.3 mL/kg/h for 24 hours or anuria for 12 hours
(AKI: acute kidney injury; eGFR: estimated glomerular filtration rate; KDIGO: Kidney Disease: Improving Global Outcomes)
Causes:
The etiology of AKI has conventionally been classified as prerenal, intrinsic renal, or postrenal (Box 1). Prerenal AKI occurs due to inadequate systemic and/or renal circulation, due to either systemic hypovolemia or renal hypoperfusion. Both pre- and postrenal categories can, if prolonged, lead to intrinsic renal failure.
BOX 1: Causes of AKI.
Prerenal
Hypovolemia (dehydration, blood loss, and diabetic ketoacidosis)
Third space losses (septicemia and nephrotic syndrome)
Congestive heart failure
Perinatal asphyxia
Drugs (ACE inhibitors, NSAIDs, and diuretics)
Intrinsic
Acute tubular necrosis
Prolonged prerenal insult (see above)
Medications: Aminoglycoside, radiocontrast, and NSAIDs
Exogenous toxins: Diethylene glycol and methanol
Intravascular hemolysis and hemoglobinuria
Snake bite
Tumor lysis syndrome
Hemolytic uremic syndrome: Diarrhea associated (D+) and atypical (D-) forms Glomerulonephritis (GN)
Postinfectious GN
Systemic disorders: SLE, Henoch–Schönlein syndrome and microscopic polyangiitis
Membranoproliferative GN
Interstitial nephritis (drug-induced and idiopathic) Bilateral renal vessel occlusion (arterial and venous)
Postrenal
Posterior urethral valves and urethral stricture
Bilateral pelviureteric junction obstruction
Ureteral obstruction (stenosis, stone, and ureterocele)
Neurogenic bladder
(ACI: angiotensin-converting enzyme; AKI: acute kidney injury; NSAIDs: nonsteroidal anti-inflammatory drugs; SLE: systemic lupus erythematosus)
Clinical Features:
Presenting symptoms of AKI include oliguria with peripheral or pulmonary edema, suggesting fluid overload. Patients may have altered sensorium and convulsions due to advanced uremia, dyselectrolytemia, or hypertensive encephalopathy. The breathing may be rapid and deep due to acidosis. Features that suggest an underlying cause are presented in Table 2. Children with AKI due to acute interstitial nephritis, aminoglycoside toxicity, and perinatal asphyxia are often nonoliguric.
TABLE 2: Clinical features.
Clinical features
Likely diagnosis
Edema, hematuria, and hypertension
Acute glomerulonephritis
Dysentery, pallor, and jaundice
HUS
History of fluid loss with severe dehydration
ATN
Sudden passage of dark urine, pallor, and jaundice
Intravascular hemolysis
Interrupted urinary stream and palpable bladder
Obstructive uropathy
Abdominal colic, hematuria, and dysuria
Urinary tract calculi
Altered sensorium and seizures
Uremic encephalopathy
Acidotic breathing and pulmonary edema
Complications of AKI
(AKI: acute kidney injury; ATN: acute tubular necrosis; HUS: hemolytic uremic syndrome)
Investigations:
Investigations in patients with AKI are given in Box 2.
BOX 2: Investigations in patients with AKI.
Blood
Complete blood counts
KFT
Electrolytes (Na, K, and Ca)
Venous blood gas (pH and bicarbonate)
Urine
Urinalysis; culture (if symptoms of urinary infection)
Sodium, osmolality, fractional excretion of sodium (if available to differentiate prerenal from intrinsic AKI)
Radiology
Chest X-ray (for fluid overload and cardiomegaly)
Ultrasonography (identify obstruction and dilatation)
ECG for hyperkalemia
Investigations to determine cause
Peripheral smear examination, platelet, and reticulocyte count; blood and LDH levels; and stool culture (suspected hemolytic uremic syndrome)
Peripheral smear/RMAT—malaria
Leptospiral serology/microscopic agglutination test (gold standard)—leptospirosis
Blood culture—sepsis
Blood ASO, complement (C3), antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA) (suspected acute and rapidly progressive GN)
Doppler ultrasonography (suspected arterial or venous thrombosis)
Renal biopsy in RPGN or nonresolving AKI
Micturating cystourethrogram (suspected obstruction)
(AKI: acute kidney injury; ASO: antistreptolysin O; ECG: electrocardiogram; GN: glomerulonephritis; KFT: kidney function test; LDH: lactate dehydrogenase; RMAT: rapid malarial antigen test; RPGN: rapidly progressive glomerulonephritis)
Management:
Management of AKI includes the management of complications and treatment of the specific underlying cause (Table 3).
TABLE 3: Management of complications.
Complications
Management
Others
Fluid overload
AKI regimen—insensible losses to be replaced by 5% Dextrose
UO to be replaced by NS
Modify according to Na level
Replace other losses
þ Consider dialysis
þ 0.5–1% weight loss per day
Pulmonary edema
O2/IV furosemide (2–4 mg/kg)
Respiratory support—HFNC/NIV/MV according to the patient condition
Chest X-ray
þ Lung ultrasound—B line
þ IVC assessment and ejection fraction
þ Monitor by CVP line
þ Dialysis (for fluid removal)
Hypertension
Symptomatic
Labetalol infusion @ 0.25–1 mg/kg/h
IV furosemide 2–4 mg/kg
Asymptomatic—oral nifedipine/ amlodipine 0.3–0.5 mg/kg
NTP—0.5–8 µg/kg/min (not to be given for >48 hours due to risk of toxicity)
Maintenance with amlodipine/ hydralazine
Metabolic acidosis
IV or oral NaHCO3
To monitor for fluid overload and hypernatremia
Hyperkalemia
Stop all potassium in IVF and medications
IV 10% Ca gluconate 1 mL/kg over 5–10 minutes if ECG changes
Salbutamol (2.5–5 mg) nebulization. Can be repeated after 20 minutes
Neutralizing glucose insulin drip— dextrose 0.5–1 g/kg and insulin 0.1–0.2 U/kg over 30 minutes. Can be repeated after 30 minutes
NaHCO3—1–2 mL/kg over 15–20 minutes if associated with metabolic acidosis
Potassium binding resins—sodium polystyrene 1 g/kg (oral/NG/rectal)
maximum 30 g
Monitor blood glucose for hypoglycemia
þ Continuous ECG monitoring
þ Repeat potassium level
Anemia
PCV transfusion at 5–10 mL/kg
Monitor for fluid overload
Hyper- phosphatemia
Phosphate binders such as calcium carbonate, and sevelamer hydrochloride (only if significant)
(AKI: acute kidney injury; CVP: central venous pressure; ECG: electrocardiogram; HFNC: high-flow nasal cannula; IV: intravenous; IVC: inferior vena cava; MV: mechanical ventilation; NG: nasogastric; NIV: noninvasive ventilation; NS: normal saline; PCV: packed cell volume; UO: urine output)
Nutrition:
Patients with AKI are usually catabolic and have increased metabolic needs. Adequate nutritional support is desirable with maximization of caloric intake. However, volume restriction necessary during the oliguric phase often imposes limitations. A diet containing 0.8–1.2 g/kg of protein in infants and 0.6–0.8 g/ kg in older children and a minimum of 50–60 Cal/kg should be given. The latter requirement can be met by adding liberal amounts of carbohydrates and fats to the diet. Once dialysis is initiated, dietary fluid and electrolyte restrictions can be made more liberal.
Kidney Replacement Therapy:
Indications of kidney replacement therapy (KRT) are given in Table 4.
TABLE 4: Indications of kidney replacement therapy (KRT).
Indications
Features
Fluid overload
Most common indication
þ Determines the outcome
þ >15% fluid overload resistant to diuretics
Metabolic acidosis
pH<7.2 despite bicarbonate therapy
Refractory hyperkalemia
K+ >6.0 or electrocardiogram (ECG) changes despite medical management
Hyponatremia/hypernatremia
Symptomatic
Uremia
Urea >160–200 mg/dL, encephalopathy
Create space for more fluid
Blood products, drugs, and nutrition
Removal of dialyzable toxins
Salicylate poisoning and phenobarbitone
Acute kidney injury requiring dialysis can be managed with a variety of modalities, including peritoneal dialysis (PD), intermittent hemodialysis (HD), and continuous renal replacement therapy (CRRT) (continuous venovenous hemofiltration or hemodiafiltration). The choice of dialysis modality to be used in managing a specific patient is influenced by several factors, including the goals of dialysis, the unique advantages and disadvantages of each modality, and institutional resources (Table 5). The initial KRT of choice in sick and unstable patients is often PD. It is popular because of the ease of initiation and effectiveness in children of all ages, including neonates.
TABLE 5: KRT modalities.
Modality
Potential setting in AKI
Advantages
Disadvantages
IHD
Hemodynamically stable
Rapid removal of toxins
Reduced exposure to anticoagulants
þ Lower cost than CRRT
Hypotension with rapid fluid removal
þ Dialysis
disequilibrium
CRRT
Hemodynamically unstable
Continuous removal of toxins
þ Hemodynamic stability
Easy control of fluid balance
þ No risk of increased
ICP
Slower clearance of toxins
Need for prolonged anticoagulation
þ Patient
immobilization
Increased cost
PD
Hemodynamically unstable
þ Coagulopathy
þ Difficult access
Under resourced region
Technically simple
þ No anticoagulation
þ Hemodynamic stability
þ Lower cost
No need for vascular access
Poor clearance
þ Protein loss
þ Risk of peritonitis
No control on rate of fluid removal
þ Hyperglycemia
(AKI: acute kidney injury; CRRT: continuous renal replacement therapy; ICP: intracranial pressure; IHD: intermittent hemodialysis; KRT: kidney replacement therapy; PD: peritoneal dialysis)
Reference:
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter. 2012;2:1-138.
Levey AS, Eckardt KU, Dorman NM, Christiansen SL, Hoorn EJ, Ingelfinger JR, et al. Nomenclature for kidney function and disease: report of a Kidney Disease: Improving Global Outcomes (KDIGO) Consensus Conference. Kidney Int. 2020;97(6):1117-29.
Sutherland SM, Kwiatkowski DM. Acute kidney injury in children. Adv Chronic Kidney Dis. 2017;24(6):380-7.
The guidelines can be accessed on the official site of IAP: https://iapindia.org/standard-treatment-guidelines/