Acute Kidney Injury
Anwesha Mukherjee
PGT
ICH
Case presentation
3 month old male child presented with h/o high
grade fever and respiratory distress for 3 days
• Child lethargic
• HR 189/min
• SpO2 83% at room air.
• On day 3 ..urine output <0.5 mL/kg/hr
Investigations
Day 1 Day 3 Day 4
Hb 9.2 8.6 8.4
TLC 15,360 21,250 18,000
CRP 56 121
Urea 56 60
Creatinine 0.29 2.3 1.8
Sodium 136 125 120
Potassium 4.2 5.6 4.8
What is AKI?
Abrupt loss of kidney function
Retention of nitrogenous waste, and inability of
kidney to regulate fluid and electrolyte
homeostasis
The term AKI has replaced “acute renal failure”
Classification of AKI
Risk, Injury, Failure, Loss, End-stage (RIFLE)
criteria in 2004
AKI Network (AKIN) classification in 2007.
In 2012, both were merged resulting in the
Kidney Disease Improving Global Outcomes
(KDIGO) classification.
RIFLE stage RIFLE:Cr RIFLE and KDIGO : Cr AKIN
increase AKIN : increase Stage
Urine
output
Risk(R) 150-200% <0.5 ml/kg/hr >=0.3 mg/dl 1
for 6-12 hrs increase or150-
200%
Injury(I) 200-300% <0.5ml/kg/hr 200-300% 2
for >12hr
Failure(F) >300% <0.3ml/kg/hr >300%; creatinine 3
for >24hr; or >=4mg/dl; initiation
anuria of renal
>12hrs replacement
therapy; or eGFR
<35ml/min/1.73m2
( <18 yr)
Loss(L) Persistent
Failure >4
weeks
ESRD(E) Persistent
failure
>3months
Etiology of AKI
Acute kidney injury
Renal
Prerenal Postrenal
Glomerular Interstitial Tubular Vascular
Prerenal acute kidney injury
Reduction of
Severe fall in cardiac Profound third
extracellular fluid
output space loss
volume
• Acute • Congestive heart • Massive ascites
gasteroenteritis failure • Extensive burns
• Hemorrhage • Cardiogenic shock • Nephrotic
• Renal syndrome
vasoconstriction
• Peripheral
vasodialatation
• Hepatorenal
syndrome
Compensatory mechanism
Decreased renal
perfusion
Renin Vasopressin
Angiotensin II
Aldosterone
Tubular water
reabsorbtion
Renal tubular Na
reabsorbtion
Concentration of urine
Intrinsic acute kidney injury
Vascular Glomerular Tubular
• Renal vein • Acute • Acute
thrombosis glomerulonephritis tubulointerstitial
• Poststreptococcal, nephritis
• Renal arterial
obstruction other infections, • Acute tubular
crescentic GN necrosis
• HUS
• HSP
• Polyangitis
• Vasculitis
Pathophysiology of ATN
Postrenal cause of AKI
Clinical examination
BP: Hypo/Hypertension
Skin:
Palpable purpura- Systemic vasculitis
Maculopapular rash- allergic interstitial nephritis
Eyes:
Uveitis-interstitial nephritis and necrotising vasculitis
Ear:
• Hearing loss- Alports disease and aminoglycoside toxicity
Respiratory system:
• Rapid and deep breathing-metabolic acidosis
Basal crepts- volume overload
CVS-
• Pericardial rub- uremic pericarditis
Gallop rhythm, pitting edema- CHF, Volume overload
Abdomen-
• Renal angle tenderness, distended bladder
Prerenal Vs Intrinsic renal failure
Pre- renal failure Intrinsic renal failure
Urinary sodium(mEq/L) <20 >40
Urinary osmolality >500 <300
(mOsm/kg)
Blood urea-creatinine >20:1 <20:1
ratio
Urine- plasma osmolality >1.5 <0.8-1.2
ratio
Fractional excretion of <1 >1
sodium (%)
Biomarkers in AKI
Indications of renal biopsy
Etiology of AKI not identified
Unremitting AKI >2-3 weeks
Suspected drug induced AKI
Management
• Goals of management –
o Treatment of life threatening complications
o Maintenance of fluid and electrolyte balance
o Specific management of underlying disorder
o Nutritional management
Management of complications
• Fluid restriction-insensible losses
(300mL/m2/d) with urine output and other
Fluid overload losses
• 5% dextrose for insensible losses; N/2 for
urine output
• Oxygen
Pulmonary • Frusemide 2-4mg/kg IV
edema
• Symptomatic-Sodium nitroprusside
infusion,frusemide, nifedipine-oral or
Hypertension sublingual
• Asymptomatic-Nifedipine, amlodepine
prazosin, labetalol, clonidine.
Metabolic • Sodium bicarbonate (IV or oral) if bicarbonate levels
<18
acidosis
• Calcium gluconate(10%) 0.5-1mL/kg over 5-10 min IV
• Salbutamol 5-10 mg nebulized
• Sodium Bicarbonate (7.5%) 1-2 mL/kg over 15min IV
Hyperkalemia • Dextrose (10%) 0.5-1 g/kg and insulin 0.1-0.2 U/kg IV
• Calcium or sodium resonium
• Fluid restriction
Hyponatremia • Na correction
• Packed red cells 3-5 mL/kg;
Severe anemia consider exchange transfusion
• Phosphate binders( calcium
carbonate, acetate,aluminium
Hyperphosphatemia hydroxide)
Supportive management
Diet
o 1.2-2g/kg of protein in infants and 0.8-1.2g/kg in older children
o 60-80 Cal/kg
o If on dialysis-protein, fluid and electrolyte intake should be
increased
• Infections
o Maintaining asepsis
o Avoiding long term catheterisation of bladder
o Specimen for culture and initiation of antibiotics
• Medications
o Avoiding nephrotoxic drugs
o Dose and dosing interval of other drugs to be modified
• Dopamine
o No beneficial effect on the outcome of AKI
Indications of dialysis
Anuria / oliguria
Uremia (encephalopathy, pericarditis, neuropathy)
Hyperkalemia- K+ >6 mEq/L or ECG changes
Hyponatremia: Na+ ,120 meq/l if symptomatic
Fluid overload: resistant to diuretics, CCF, HTN
Metabolic acidosis: pH<7.2 despite sodium
bicarbonate therapy
Hypercatabolic states-marked tissue injury, burns,
sepsis, crush syndrome
Types of dialysis
• Intermittent Peritoneal Dialysis
o Requires minimal equipment and infrastructure
o Ease of initiation and effectiveness in children of
all ages
• Continuous renal replacement therapy
o Require expensive equipment and expertise
o Patient’s cardiac output provides the driving
force for the hemofilter.
o Used in hemodynamically unstable patients with
multiorgan failure.
Monitoring
• Accurate record of intake and output.
• Careful physical examination.
• Relevant laboratory investigations.
Thank you
