Acute Kidney Injury (ARF)

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Acute Kidney Injury (ARF)

• By Dr. Hatim Ahmed Hassan
• Senior Registrar PICU

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Objective

• Introduction and background
• Definition
• Epidemiology
• Physiology
• Etiology
• Clinical presentation
• Diagnosis
• management

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INTRODUCTION

• AKI is defined as the abrupt loss of kidney
  function that results in a decline in GFR,
  retention of urea and other nitrogenous waste
  products, and dysregulation of extracellular
  volume and electrolytes.
• The term AKI has largely replaced (ARF), as it
  more clearly defines renal dysfunction as a
  continuum rather than a discrete finding of
  failed kidney function.
• Pediatric AKI presents with a wide range of
  clinical manifestations from a minimal elevation
  in serum creatinine to anuric renal failure,
  arises from multiple causes, and occurs in a
  variety of clinical settings .

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Background

• Acute kidney injury (previously known as acute
  renal failure) covers a wide spectrum of injury
  to the kidneys, not just kidney failure
• Up to 18 of all hospital admissions have AKI
• Inpatient AKI-related mortality is between 25 and
  30
• Between 20 and 30 of cases of AKI are
  preventable. Prevention could save up to 12,000
  lives each year
• NHS costs related to AKI are between 434 and
  620 million per year

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Definition

• AKI is defined as a decrease in glomerular
  filtration rate (GFR), which traditionally is
  manifested by an elevated or a rise in serum
  creatinine.
• However, serum creatinine is often a delayed and
  imprecise test as it reflects GFR in individuals
  at steady state with stable kidney function, and
  does not accurately estimate the GFR in a patient
  whose renal function is changing. For example, a
  child in the early stages of severe AKI with a
  markedly reduced GFR may have a relatively normal
  or slightly elevated creatinine, as there has not
  been sufficient time for creatinine accumulation..

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Definition

• In addition, creatinine is removed by dialysis,
  and it is not possible to assess renal function
  using serum creatinine once dialysis is
  initiated.
• Despite these limitations, elevated or a rise in
  serum creatinine continues to be the most widely
  used laboratory finding to make the diagnosis of
  AKI in children

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Definition
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Definition
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EPIDEMIOLOGY

• The precise incidence and prevalence of pediatric
  acute kidney injury (AKI) are not known, largely
  due to the lack of a consensus definition in
  published studies. The incidence varies based on
  the definition used and potentially geographic
  location

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Epidemiology of AKI

• Community acquired AKI seen in 1 of all
  hospitalized patients on admission.50 of those
  patients have underlying CKD.
• Development of AKI in hospitalized patients is
  common and carries independent mortality risk.
• In patients with normal renal function, the
  incidence of AKI is about 5.
• In patients with underlying CKD, the incidence is
  about 16

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Epidemiology of AKI

• Hospital acquired AKI
• 40 is due to ATN
• 15 related to medication associated AKI.
• 10 due to contrast induced nephropathy.
• AIDS associated AKI account for 5.

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PHYSIOLOGY
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Types of AKI

• AKI
• AKI/CKD
• Anuric (lt50ml of urine output/day)
• Oliguric (lt400 ml/day)
• Non-oliguric (gt400 ml/day)

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ARF Pirouz Daeihagh, M.D.Internal
medicine/Nephrology Wake Forest University
School of Medicine. Downloaded 4.6.09
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Etiology of AKI

• Prerenal
• Renal hypoperfusion, no structural damage to
  the kidneys, Cr normalizes in 24-72 hours with
  correction of hypoperfused state.
• Post-renal
• Obstruction to the urine flow, either
  unilateral/bilateral, intra-ureteral or
  extra-ureteral or bladder neck or intra-pelvis
  (renal pelvis).
• Intra-renal
• Damage or inflammation within the kidney, may
  be primary renal or part of systemic disease.

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Prerenal AKI
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Prerenal AKI
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Intrarenal hemodynamic changes
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Intrarenal AKI

• Vascular
• Glomerular
• Interstitial
• Tubular

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Vascular causes of Intrarenal AKI

• Large and Medium size vessels
• Renal artery thrombosis or emboli
• Renal vein thrombosis
• Polyarterial nodosa
• Small vessel disease
• Atheroembolic phenomenon
• Microangiopathies like TTP, HUS, HELLP and
  malignant HTN.

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Glomerular causes of Intrarenal AKI

• Nephritis
• Hematuria
• Proteinuria (1-2gm/d)
• ARF
• May present as Rapidly progressive
  Glomerulonephritis
• Renal Biopsy to diagnose

• Nephrosis
• Minimal hematuria
• Massive proteinuria(gt3gm/d)
• Uncommon to present as ARF
• Renal Biopsy not needed to diagnose.

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Interstitial causes of Intrarenal AKI

• Focal/diffuse edema and infiltration of the renal
  interstitium with inflammatory cells.

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Tubular causes of Intrarenal AKI, Acute Tubular
Necrosis

• Ischemia induced
• Shock
• Hemorrhage
• Sepsis
• Trauma
• Pancreatitis

• Nephrotoxin induced
• Drugs like IV contrast, Aminoglycosides, Ampho B,
  pentamidine, Acyclovir, Ehtylene Glycol etc.,
• Endogenous Toxins in the case of Rhabdomyolysis,
  Hemolysis, uric acid nephropathy

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Postrenal AKI

• Intra Ureteral
• Stones, Clots, Pyogenic debris, Sloughed
  papillae in analgesic nephropathy, sickle cell
  disease etc.,
• Extra Ureteral
• Malignancy, Retroperitoneal fibrosis,
  accidental ligation etc.,
• Bladder neck/Urethral
• Autonomic neuropathy with urinary retention,
  Urethral stricture, Blood clots/bladder stones.

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CLINICAL PRESENTATION 

• (Symptoms of acute renal failure depend largely
  on the underlying cause.)
• Fever
• Rash
• Bloody diarrhea
• Severe vomiting
• Abdominal pain
• Hemorrhage
• No urine output or high urine output
• History of recent infection
• Pale skin

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CLINICAL PRESENTATION 

• History of taking certain medications
• History of trauma
• Swelling of the tissues
• Inflammation of the eye
• Detectable abdominal mass
• Exposure to heavy metals or toxic solvents

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Evaluation of ARF

• Careful History and tabulation of data including
  u.o, weights, vitals, medications etc.,.
• Physical Examination findings including signs of
  vol. depletion etc.,
• Urinalysis
• Urinary indices(Urine sodium, creatinine, FeNa,
  FeUrea etc.,)

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Mortality associated with AKI

• ICU associated AKI along with respiratory failure
  requiring hemodialysis, the mortality is gt90.
• ICU associated AKI with out respiratory failure
  or hemodialysis, it is 72
• Non-ICU renal failure associated mortality is
  around 32.

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Urinary Indices

• Prerenal
• High SpGr
• No proteinuria/hematuria
• U.Na lt20
• U.Cr/P.Cr gt40
• U.Osm gt500
• FeNa lt1
• FeUrea lt35

• ATN
• Sp Gr 1.010
• Variable proteinuria
• U.Na gt40
• U.Cr/P.Cr lt20
• U.Osm lt350
• FeNa gt1
• FeUrea gt50

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Urinalysis and Urine Sediment

• UA positive for heme and proteinuria seen in
  Glomerular and Interstitial renal failure.
• Urine eosinophils are seen in AIN, Atheroembolic
  disease etc.,
• Urine sediment positive for red cell casts seen
  in Glomerulonephritis.
• UA bland in Post Renal ARF.

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Laboratory Data

• .Hypocomplementemia seen in SLE, MPGN,
  Atheroembolic disease etc.,
• Elevated ESR seen in Atheroembolic disease.
• Serologies positive in glomerular diseases, like
  ANA, ANCA, Anti GBM, Hepatitis, HIV
• Elevated LDH seen in RVT.

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Laboratory Data (contd)

• Thrombocytopenia with microangiopathic hemolysis
  seen in TTP, HUS etc.,
• Low Haptoglobin, High retic count seen in
  microangiopathic states.
• Schistocytes (red cell fragmentation).
• CPK, uric acid levels etc., to evaluate for
  rhabdomyolysis, uric acid nephropathy.
• Evidence of hepatic insufficiency in diagnosing
  hepatorenal syndrome.

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Imaging

• Ultrasound
• Useful in Post renal AKI.
• Early obstruction may not show significant
  hydronephrosis.
• External obstruction encrasing the whole urinary
  system may not show hydronephrosis, for e.g.,
  retroperitoneal fibrosis.
• U/S doppler useful in diagnosing Renal vein
  thrombosis.

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Imaging (contd)

• CT scan
• Useful for detecting stones, location of the
  obstruction, Tumours etc.,
• Isotope renography
• To evaluate the function significance of
  obstruction.
• Done with lasix and Mag3 isotope for evaluatine
  obstruction.

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Imaging (contd)

• Cystoscopy and Retrograde Pyelography
• To evaluate patients with high clinical suspicion
  of obstruction esp., in unique cases of calculi,
  pyogenic debris, blood clots, bladder cancer
  etc.,
• Renal Angigraphy
• In emergent cases of anuria with suspicion of
  renal embolization.

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Renal Biopsy

• Only in patients with no clear etiology.
• In patients with active urinary sediment (RBCs,
  red cell casts etc., )
• RPGN (rapidly progressive glomerulonephritis).
• Refractory ATN with out recovery despite no
  further renal insults.
• Acute Interstitial nephritis.

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Management of AKI

• Volume repletion with isotonic fluids to improve
  renal perfusion pressures in prerenal states.
• CVP/ PEWS monitoring.
• Supportive measures for sepsis with pressors,
  antibiotics etc.,
• Colloidal substances like blood products in
  hemorrhagic shock.
• Management of heart failure by improving cardiac
  output.

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Children and young people ongoing hospital
assessment

• Consider a paediatric early warning score (PEWS)
  to identify children and young people at risk of
  acute kidney injury
• Record physiological observations at admission
  and then according to local protocols for given
  PEWS
• Increase the frequency of observations if
  abnormal physiology is detected
• Use PEWS with multiple-parameter or aggregate
  weighted scoring systems that allow a graded
  response and include
• heart rate
• respiratory rate
• systolic blood pressure
• level of consciousness
• oxygen saturation
• temperature
• capillary refill time

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Management (contd)

• Drugs need to be dosed according to the renal
  clearance.
• Electrolyte and acid base correction.
• Renal diet, if K high.
• Diuretics in overt fluid overload states.
• Foley catheterization in bladder neck
  obstruction/prostatic obstruction.

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Management (contd)

• Avoid nephrotoxic agents like Contrast dye,
  NSAIDs, Aminoglycosides etc.,
• Also avoid ACEI unless the underlying problem is
  decompensated heart failure.
• Nutritional support with parenteral or enteral
  feeding.

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Management (contd)

• Renal replacement therapy
• Modes of dialysis
• IHD (Intermittent Hemodialysis)
• Quick removal of solutes over 3-4 hours,
  possible hemodynamic instability. ICU,
  hypotensive patients are probably not the best
  candiadtes for this type of HD.
• CRRT (Continuous renal replacement therapy).
• Modality of choice in critically ill patients.

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Management (contd)

• Vascular access needed for Hemodialysis.
• Peritoneal dialysis uncommonly used for managing
  ARF
• It may be used in locations where IHD or CRRT are
  not available.

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Any Questions?