Acute Renal Failure in the Intensive Care Unit

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Acute Renal Failurein the Intensive Care Unit

• Ana Lia Graciano, MD
• Pediatric Critical Care
• The University of North Carolina-Chapel Hill

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Basic Renal Physiology
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• nephron
• the functional unit of the kidney
• capable of forming urine
• has two major components
• glomerulus
• tubule
• proximal
• loop of Henle
• distal
• collecting

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structural organization
renal parenchyma cortex medulla nephrons cortical
juxtamedullary
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• renal blood supply
• the kidneys receive 20 of the cardiac output
• vascular supply
• renal arteries
• interlobar arteries
• arcuate arteries
• interlobular arteries
• afferent arterioles
• glomerular capillaries
• efferent arterioles
• peritubular capillaries

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Efferent Arteriole
Afferent Arteriole
renal circulation

• there are two capillary beds arranged in series
• the efferent arteriole helps to regulate the
  hydrostatic pressures in both sets of capillaries

Vasa Recta
C cortex OS outer stripe IS inner stripe IM
inner medulla
IM
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• steps in urine formation
• filtration (glomerular function)
• reabsorption and secretion (tubular function)
• 98 of the ultrafiltrate is reabsorbed
• tubular reabsorption is quantitatively more
  important than tubular secretion in the formation
  of urine, but secretion determines the amount of
  K and H ions that are excreted

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glomerular filtration rate (GFR)

• GFR depends on the interplay between hydrostatic
  and oncotic pressures within the nephron
• hydrostatic pressure is usually higher in the
  glomerulus than within the tubule, forcing
  filtrate out of the capillary bed into the tubule
• oncotic pressure is generated by non-filtered
  proteins it helps to retain fluid in the
  intravascular space
• GFR Kf (hydrostatic pressure - oncotic
  pressure)
• Normal GFR 100 ml/min/1.72m2
• Kf filtration coefficient in the glomerulus

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Adjusting the resistances of the afferent
and efferent arterioles, the kidneys can regulate
both the hydrostatic pressures in the glomerular
and peritubular capillaries, changing the rate of
glomerular filtration and/or tubular reabsorption
in response to homeostatic demands.
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determinants of Glomerular Filtration Rate (GFR)
net filtration pressure hydrostatic colloid
osmotic pressure
Glomerular colloidosmotic pressure
Glomerular hydrostatic pressure
Bowmans capsule pressure
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determinants of renal blood flow (RBF)

• RBF
• renal artery pressure - renal vein pressure
• total renal vasculature resistance

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autoregulation
a feedback mechanism that keeps renal blood flow
(RBF) and glomerular filtration rate (GFR)
constant despite changes in arterial blood
pressure.
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• autoregulation of GFR
• as renal blood flow increases, GFR increases,
  leading to an increase in NaCl delivery to the
  macula densa.
• a feedback loop through the macula densa to the
  juxtaglomerular cells of the afferent arteriole
  results in increased vascular tone, decreased
  renal blood flow and a decrease in GFR.
• NaCl to the macula densa then decreases leading
  to relaxation of the afferent arteriole
  (increasing glomerular hydrostatic pressure) and
  increases renin release from juxtaglomerular
  cells of afferent and efferent arterioles
• renin increases angiotensin I, then converted to
  angiotensin II which constrict efferent arteriole
  increasing hydrostatic pressure returning GFR to
  normal

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Macula densa feedback mechanism for
autoregulation
-

Proximal tubule NaCl reabsorption
afferent arteriolar resistance
afferent arteriolar resistance
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Tubular Function

• proximal tubule
• 70 of Na is reabsorbed in the proximal tubule

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Tubular Function

• loop of Henle
• 20 of Na, Cl and K reabsorbed
• urine concentration and dilution occurs in the
  loop of Henle through an osmotic gradient
  provided by the countercurrent mechanism (vasa
  recta)
• urine flow rate is regulated by NaCl,
  prostaglandins, adenosine and urine volume
  presented to the macula densa

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Tubular Function

• distal tubule
• secretes K and bicarbonate
• proximal segment of distal tubule is impermeable
  to water (urine dilution)
• distal segment (cortical collecting tubule) K
  and bicarbonate secretion

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Tubular Function

• collecting duct
• regulates final urine concentration
• aldosterone receptors regulate Na uptake and K
  excretion
• ADH increases water reabsorption. In the absence
  of ADH, the collecting duct is impermeable to
  water

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major sites of solute and water movement across
the nephron
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Acute Renal Failure (ARF)
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acute renal failure definition ARF is an abrupt
decline in glomerular and tubular function,
resulting in the failure of the kidneys to
excrete nitrogenous waste products and to
maintain fluid and electrolyte homeostasis.
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Azotemia is a consistent feature of acute renal
failure (ARF), oliguria is not. anuria
urine output lt 0.5 ml/kg/h
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acute renal failure pathophysiology Increase in
NaCl delivered to macula densa. Damage to
proximal tubule cells increases NaCl delivery to
distal nephron,. This causes disruption of
feedback mechanism. Obstruction of tubular lumen.
Casts (necrosis of tubular cells and sloughed
basement membrane) clog the lumen. This will
increase the tubular pressure and then GFR will
fall. Backleak of fluid through the tubular
basement membrane.
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• acute renal failure clinical setting in the
  PICU
• postoperative states (especially cardiac surgery)
• shock states
• trauma, burn or crush injuries
• nephrotoxic drugs
• neonatal asphyxia

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• acute renal failure common clinical features
• azotemia
• hypervolemia
• electrolytes abnormalities
• ? K ? phosphate
• ? Na ? calcium
• metabolic acidosis
• hypertension
• oliguria - anuria

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• acute renal failure classification
• Prerenal (hypoperfusion)
• Renal (intrinsic)
• Postrenal (obstructive)

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prerenal

• decreased perfusion without cellular injury
• renal tubular and glomerular functions are intact
• reversible if underlying cause is corrected

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prerenal

• common etiologies
• dehydration
• hypovolemia
• hemodynamic factors that can compromise renal
  perfusion (CHF, shock)
• Sustained prerenal azotemia is the main
  factor that predisposes patients to ischemia-
  induced acute tubular necrosis (ATN)

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Prerenal azotemia and ischemic tubular necrosis
represent a continuum. Azotemia progresses to
necrosis when blood flow is sufficiently
compromised to result in the death of tubular
cells. Most cases of ischemic ARF are reversible
if the underlying cause is corrected.
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postrenal

• obstruction of urinary tract
• important to rule out quickly
• potential for recovery of renal function is often
  inversely related to the duration of the
  obstruction

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renal

• classified according primary site of injury
• tubular
• interstitium
• vessels
• glomerulus

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acute renal failure diagnosis

• History and Physical examination
• Blood tests CBC, BUN/creatinine,
  electrolytes, uric acid, PT/PTT, CK
• Urine analysis
• Renal Indices
• Renal ultrasound (useful for obstructive forms)
• Doppler (to assess renal blood flow)
• Nuclear Medicine Scans
• DMSA anatomy
• DTPA and MAG3 renal function, urinary
• excretion and upper tract outflow

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renal indices
Reabsorption of water and sodium - intact in
pre-renal failure - impaired in
tubulo-interstitial disease and ATN Since
urinary indices depend on urine sodium
concentration, they should be interpreted
cautiously if the patient has received diuretic
therapy
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renal indices
Renal Failure Index (RFI) RFI urine
Na urine creatinine / serum creatinine
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renal indices
Fractional Excretion of Na (FENa) FENa
urine Na/serum Na x 100 urine
creatinine/serum creatinine
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• prerenal azotemia
• Urine sediment hyaline and fine granular casts
• Urinary to plasma creatinine ratio high
• Urinary Na low
• FENa low
• Increased urine output in response to hydration

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• renal azotemia
• Urine sediment brown granular casts and tubular
  epithelial cells
• Urinary to plasma creatinine ratio low
• Urinary Na high
• FENa high

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urine and serum laboratory values
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acute renal failure prevention

• recognize patients at risk (postoperative states,
  cardiac surgery, septic shock)
• prevent progression from prerenal to renal
• preserve renal perfusion
• isovolemia, cardiac output, normal blood pressure
• avoid nephrotoxins (aminoglycosides, NSAIDS,
  amphotericin)

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• hemoglobinuria myoglobinuria
• hemoglobinuria
• transfusion reactions, HUS, ECMO
• myoglobinuria
• crush injuries, rhabdomyolisis
• urine () blood but (-) red blood cells
• ? CPK ? K
• treatment
• aggressive hydration urine alkalinization
• mannitol / furosemide

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acute renal failure management

• treat the underlying disease
• strictly monitor intake and output (weight, urine
  output, insensible losses, IVF)
• monitor serum electrolytes
• adjust medication dosages according to GFR
• avoid highly nephrotoxic drugs
• attempt to convert oliguric to non-oliguric renal
  failure (furosemide x 3)

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acute renal failure fluid therapy

• If patient is fluid overloaded
• fluid restriction (insensible losses)
• attempt furosemide 1-2 mg/kg
• Renal replacement therapy (see later)
• If patient is dehydrated
• restore intravascular volume first
• then treat as euvolemic (below)
• If patient is euvolemic
• restrict to insensible losses (30-35
  ml/100kcal/24 hours) other losses (urine, chest
  tubes, etc)

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sodium

• most patients have dilutional hyponatremia which
  should be treated with fluid restriction
• severe hyponatremia (Nalt 125 mEq/L) or
  hypernatremia (Nagt 150 mEq/L) dialysis or
  hemofiltration

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potassium

• Oliguric renal failure is often complicated by
  hyperkalemia, increasing the risk in cardiac
  arrhythmias
• Treatment of hyperkalemia
• sodium bicarbonate (1-2 mEq/kg)
• insulin hypertonic dextrose 1 unit of
  insulin/4 g glucose
• sodium polystyrene (Kayexalate) 1 gm/kg . Can
  be repeated qh. (Hypernatremia and hypertension
  are potential complications)
• dialysis

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nutrition

• provide adequate caloric intake
• limit protein intake to control increases in BUN
• minimize potassium and phosphorus intake
• limit fluid intake

If adequate caloric intake can not be achieved
due to fluid limitations, some form of dialysis
should be considered