acute renal failure\injury

3.  Primary unit of the kidney is the nephron
 1 million nephrons per kidney
 Composed of a glomerulus and a tubule
 Kidneys receive 20% of cardiac output.

4. • Aorta  Renal artery  interlobar
arteries  interlobular arteries 
afferent arterioles  glomerulus 
efferent arterioles
• In the cortex  peritubular
capillaries
• In the juxtamedullary region vasa
recta
• Back to the heart through the
interlobular  intralobar  renal
veins

5. Hydrostatic pressure in the glomerulus
is higher than in the tubule, so you get a
net outflow of filtrate into the tubule.
Oncotic pressure in the glomerulus is
the result of non-filterable proteins.
Greater oncotic pressure as you
progress through the glomerulus
GFR =
Kf (hydrostatic – oncotic pressure)
Determined by:
the hydrostatic and oncotic pressure within the
nephron.

7. • Foot processes of the podocytes
form filtration slits that :
 Allow for ultrafiltrate passage
 Limit filtration of large negatively charged
particles
►Less than 5,000 daltons = freely filtered
►Large particles (albumin 69,000 daltons)
not filtered
 The capillary endothelium is surrounded by
a basement membrane and podocytes

8. Proximal
• Most of reabsorption occurs here
• Fluid is isotonic with plasma
• 66-70% of sodium presented is
reabsorbed
• Glucose and amino acids are
completely reabsorbed

9. Loop of Henle
• Urine concentration and dilution
via changes in oncotic pressure in
the vasa recta
• Descending tubule – permeable to
water, impermeable to sodium
• Ascending tubule – actively
reabsorbs sodium, impermeable to
water

10.  Medullary thick ascending limb – critical for
urinary dilution and most often damaged in ARF
• ADH stimulates Na re-absorption in
this area
• Most sensitive to ischemia
• Low oxygen tension, high oxygen
consumption
• Lasix use here inhibits the Na-K-2Cl
ATPase which in the face of ARF,
may decrease oxygen consumption
and ameliorate the severity of the
ARF

11. Distal Tubule
• Re-absorption of another ~12% of
NaCl
• Proximal segment – impermeable
to water
• Distal segment is the cortical
collecting duct and secretes K and
HCO3

12. Collecting Duct
• Aldosterone acts here to increase
Na reuptake and K wasting
• ADH enhances water re-absorption
• Urea re-absorption to maintain the
medullary interstitial concentration
gradient

13. • Inability of kidney to maintain
homeostasis leading to a buildup of
nitrogenous wastes
• Different to renal insufficiency
where kidney function is deranged
but can still support life
Renal failure
is defined as the cessation of kidney function with
or without changes in urine volume

14. Anuria – no urine output or less
than 100mls/24 hours or UOP <
0.5 cc/kg/hour
Oliguria - <500mls urine output/24
hours or <20mls/hour or UOP
“more than 1 cc/kg/hour
Polyuria - >2.5L/24 hours.

15. • 70% Non-oliguric , 30% Oliguric
• Non-oliguric associated with better
prognosis and outcome
• “Overall, the critical issue is
maintenance of adequate urine
output and prevention of further
renal injury.”
Our main role here as doctors
is not to convert non-oliguric
ARF to oliguric.!!!

16. Lab definition
• Increase in baseline creatinine of
more than 50%.
• Decrease in creatinine clearance of
more than 50%.
• Deterioration in renal function
requiring dialysis.

17. Usual causes
• Hypo-perfusion and ischemia
• Toxin mediated
• Inflammation
“Damage is caused mostly by renal
perfusion problems and tubular
dysfunction”

18. • Renal vasoconstriction is a well
documented cause of ARF.
• Renal vasodilation does not
consistently reduce ARF once
established
• Although renal hemodynamic
factors play a large role in initiating
ARF, they are not the dominant
determinants of cell damage

19. • Overall, renal vasoconstriction is
the major cause of the problems
in ARF
►Suggested ARF be replaced
with vasomotor nephropathy
• Insult to tubular epithelium
causes release of vasoactive
agents which cause the
constriction.
• Angiotensin II, endothelin, NO,
adenosine, prostaglandins, etc.

22. • Pre-renal (functional)
• Renal-intrinsic (structural)
• Post-renal (obstruction)

23. • Pre-renal:
- Inadequate perfusion
►check volume status
• Renal:
- ARF despite perfusion & excretion
►check urinalysis, CBC &
autoimmune screen
• Post-renal:
- Blocked outflow
►check bladder, catheter &
ultrasound

26.  Pre-renal:
• Decrease in RBF constriction
of afferent arteriole which serves
to increase systemic blood
pressure by reducing the “shunt”
through the kidney, but does so
at a cost of decreased RBF.
• At the same time, efferent
arteriole constricts to attempt to
maintain GFR

27.  Pre-renal (cont.):
•As GFR decreases, amount of filtrate
decreases. Urea is reabsorbed in the
distal tubule, leading to increased
tubular urea concentration and thus
greater re-absorption of urea into the
blood.
•Creatinine cannot be reabsorbed,
thus leading to a BUN/Cr ratio of > 20

28.  Acute tubular necrosis (ATN)
• Ischaemia
• Toxin
• Tubular factors
 Acute interstitial Necrosis (AIN)
• Inflammation
• oedema
 Glomerulonephritis (GN)
• Damage to filtering mechanisms
• Multiple causes as per previous
presentation

29. BUN/Cr >20 <20
FENa <1% >2%
Renal Failure Index
UNa UCr/PCr
<1% >1%
UNa <20 mEq/L >40 mEq/L
Specific Gravity >1.020 <1.010
Uosm >500 mOsm/L <350 mOsm/L
Uosm/Posm >1.3 <1.3

30. Intra-renal Obstruction
• Acute uric acid nephropathy
• Drugs (e.g., acyclovir)
Extra-renal Obstruction
-Renal pelvis or ureter
(e.g., stones, clots, tumors, papillary
necrosis, retroperitoneal fibrosis)
-Bladder (e.g.,neuropathic bladder)
-Urethra (e.g., stricture)

31. Urinary sediment.
Urinary indices:
•Urine volume
•Urine electrolytes
Radiologic studies

32. Bland
• Pre-renal azotaemia.
• Urinary outlet obstruction
RBC casts or dysmorphic RBCs
• Acute glomerulonephritis.
• Small vessel vasculitis.
WBC Cells and WBC Casts
•Acute interstitial nephritis
•Acute pyelonephritis

33. Anuria (< 100 ml/24h)
• Acute bilateral arterial or venous
occlusion
• Bilateral cortical necrosis
• Acute necrotizing
glomerulonephritis
• Obstruction (complete)
• ATN (very rare)

34. Oliguria (<500 ml/24h)
• Pre-renal azotemia
• ATN
Non-Oliguria (> 500 ml/24h)
• ATN
• Obstruction (partial)

35. Urinary Indices:
FeNa =
urine Na x plasma Cr
𝒑𝒍𝒂𝒔𝒎𝒂 𝑵𝒂 𝒙 𝒖𝒓𝒊𝒏𝒆 𝑪𝒓
FeNa <1%
FeNa 1%-2%
FeNa >2%

36. 1. PRERENAL
- Urine Na < 20. Functioning tubules
reabsorb lots of filtered Na
2. ATN (unusual)
- Postischemic dz: most of UOP comes
from few normal nephrons, which
handle Na appropriately
- ATN + chronic prerenal dz (cirrhosis,
CHF)
3. Glomerular or vascular injury
-Despite glomerular or vascular injury, pt
may still have well-preserved tubular
function and be able to concentrate Na
FeNa <1%

37. FeNa 1%-2%
FeNa >2%

38. Other helpful indices:

39. Ultrasound
•Structural anomalies – polycystic,
obstruction, etc.
•ATN –
- poor corticomedullary differentiation
- Increased Doppler resistive index
- (Systolic Peak – Diastolic peak) / systolic
peak
Nuclear medicine scans
-DMSA – Static - anatomy and scarring
- DTPA/MAG3 – Dynamic – renal function,
urinary excretion, and upper tract
outflow

40. Immediate treatment of pulmonary edema and
hyperkalaemia
Remove offending cause or treat offending
cause
Dialysis as needed to control hyperkalaemia,
pulmonary edema, metabolic acidosis, and
uremic symptoms
Adjustment of drug regimen
Usually restriction of water, Na, and K intake, but
provision of adequate protein
Possibly phosphate binders and Na polystyrene
sulfonate

41. Nutrition management
- Initially very catabolic
Goals:
 Adequate calories
 Low protein
 Low K and Phos
 Decreased fluid intake

42. Peritoneal Dialysis
Acute Intermittent Hemodialysis
Continuous Hemofiltration
CAVH
SCUF
CVVH, CVVHD
And others….

43. Advantages Disadvantages
• Simple to set up &
perform
o Unreliable ultrafiltration
o Slow fluid & solute removal
• Easy to use in infants o Drainage failure & leakage
• Hemodynamic
stability
o Catheter obstruction
• No anti-coagulation o Respiratory compromise
o Hyperglycemia
• Bedside peritoneal
access
o Peritonitis
• Treat severe
hypothermia or
hyperthermia
o Not good for hyperammonemia
or intoxication with dialyzable
poisons

44. Advantages Disadvantages
• Maximum solute clearance of 3
modalities
o Hemodynamic
instability
• Best therapy for severe
hyperkalemia
o Hypoxemia
• Limited anti-coagulation time o Rapid fluid and
electrolyte shifts
o Complex equipment
• Bedside vascular access can
be used
o Specialized personnel
o Difficult in small
infants

45. Advantages Disadvantages
Easy to use in PICU Systemic
anticoagulation
(except citrate)Rapid electrolyte correction
Excellent solute clearances
Frequent filter
clottingRapid acid/base correction
Tolerated by unstable pts
Vascular access in
infants
Controllable fluid balance
Early use of TPN

46. Oliguria/Anuria
Hyperammonemia
Hyperkalemia
Severe acidemia
Severe azotemia
Pulmonary Edema
Uremic complications
Severe electrolyte abnormalities
Drug overdose with a filterable
toxin
Anasarca
Rhabdomyolysis
Still evolving….Generally accepted

47. Remember to:
 Think about who might be
vulnerable to acute renal failure.
 Think twice before initiating
therapy that may cause ARF.
 Think about it as a diagnosis –> it
happens rapidly, you won’t see/
find signs