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