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Epidemiology
Studies estimate that 2.5 to 15% of ICU patients develop some form of AKI
In a large observational study of 29,269 ICU patients, Uchino et al. observed 5.7% patients
had severe AKI requiring Renal Replacement Therapy or with severe oliguria and uremia.
Overall hospital mortality of these patients with severe AKI was 60.3%, the outcome was not
prognostic factors included older age, male gender, baseline GFR, tachycardia, low UOP,
and presence of co-morbid organ failure.
Stage
GFR** Criteria
Probability
Risk
Injury
SCr increased 2
or
GFR decreased >50%
Failure
SCr increased 3
or
GFR decreased 75%
or
SCr 4 mg/dL; acute rise 0.5 mg/dL
Loss
ESRD*
High specificity
*ESRDend-stage renal disease; **GFRglomerular filtration rate; SCrserum creatinine; UOurine output
Note: Patients can be classified either by GFR criteria or by UO criteria. The criteria that support the most severe classification should be used. The
superimposition of acute on chronic failure is indicated with the designation RIFLE-FC; failure is present in such cases even if the increase in SCr is less
than 3-fold, provided that the new SCr is greater than 4.0 mg/dL (350 mol/L) and results from an acute increase of at least 0.5 mg/dL (44 mol/L).
When the failure classification is achieved by UO criteria, the designation of RIFLE-FO is used to denote oliguria. The initial stage, "risk," has high
sensitivity; more patients will be classified in this mild category, including some who do not actually have renal failure. Progression through the
increasingly severe stages of RIFLE is marked by decreasing sensitivity and increasing specificity.
Oliguria definition
Urine Output < 400 ml/day or or 16ml/hr
Or more commonly <0.5ml/kg/hr (30-60 ml/hr in
70-80 kg adult)
Evaluating AKI
Pre renal urine sodium low (<20mEq), FeNa < 1%,
FeUrea < 35%, UOsm > 500, BUN/Cr ratio of > 20 may
also suggest pre-renal state but none of these are absolute
Intrinsic renal Urine sodium high (>40) FeNa>2%,
FeUrea > 50%, UOsm< 350
However, there is often a mixed picture, so FeNa, Uosm etc. does not
help much.
Pre-renal Causes
Hypovolemia eg diarrhea, vomiting, GIB
Mechanical Ventilation (decreased venous return)
Cardiomyopathy (Decreased LVEF)
Aortic Stenosis
Dissecting Aortic Aneurysm
Drugs that impair renal autoregulation (eg NSAIDS,
ACEI, ARBS)
Sepsis
Renal causes
Usually ATN (50% cases) or AIN caused by:
Circulatory Shock
Severe Sepsis
Multi-organ failure
Surgery (Cardiac and AAA repair)
Drugs and toxins (e.g. aminoglycosides,
amphotericin, cisplatin causing AIN, nephrotoxins
like ethylene glycol)
Myoglobinuria, Radio-contrast dye
Post-renal Obstruction
Distal to the renal parenchyma
Papillary necrosis
Retroperitoneal mass compressing ureters
Urethral Stricture
Prostatic hypertrophy
Bladder stones - if 1 functional kidney
Work up
CVP usually we want this 8-12. If Low i.e. less than 2, pretty sensitive for hypovolemia
BP varying with respirations or collapsing IVC with respirations may benefit from volume
Spot urine protein to creatinine ratio (if UA positive for protein)
Serum osmoles to calculate osmolar gap
Check CPK to evaluate for rhabdomyolysis
Check bladder pressure to evaluate for abdominal compartment syndrome (concerning
if>20)
Check ANCA, cryoglobulins and complements (C3 & C4) to look for MPGN or Wegneners
Urine Microscopy
Hyaline casts suggests pre-renal
Granular casts , muddy brown casts - ATN
Red cell casts, dysmorphic RBCs acute
Glomerulonephritis
Oval fat bodies, maltese crosses Crystals calcium
oxalate (ethylene glycol ingestion)
White cell casts, sterile pyuria Interstitial
nephritis
Eosinophils with Wrights stain AIN,
pyleonephritis, prostatitis, Cholesterol emboli
ATN
Pathophysiology:
Oxidative injury to renal tubular epithelial cells
Sloughing of cells into lumen of renal tubules
Management
Correct underlying cause
Fluid challenge in pre-renal patients
Dont use low dose dopamine makes no difference
Furosemide (Lasix) if they have LV dysfunction with
fluid overload
failure
Contrast-induced nephropathy is considered the third leading cause of
sodium bicarbonate found no differences in the incidence of CIN in patients with mild
CKD
There appears to be insufficient evidence to support the universal use of NAC to
net benefit for NAC in the prevention of CIN. NAC, however, has been reported to
decrease SCr levels in normal volunteers with normal kidney function. This reduction in
SCr was not accompanied by a change in serum cystatin C levels, suggesting an effect
independent of a change in GFR, such as an increase in tubular secretion of creatinine
or a decrease in creatinine production.
In view of its low costs and the high likelihood of absence of harm, there is no objection
against oral NAC administration, but this should never replace adequate fluid loading.
Cho R, Javed N, Traub D, et al. Oral hydration and alkalinization is noninferior to intravenous therapy for prevention of contrast-induced nephropathy in patients with chronic kidney disease. J
Interv Cardiol 2010;23:460466.
Fishbane S. N-acetylcysteine in the prevention of contrast-induced nephropathy. Clin J Am Soc Nephrol2008;3:281287
AIN
In cases of drug-induced AIN, the characteristic signs of a
with rhabdomyolysis.
The culprit is myoglobin, which is released by the injured
muscle and is capable of damaging the renal tubular
epithelial cells after it is filtered through the glomerulus.
The source of cell injury may be the iron moiety in heme ,
which is capable of oxidative cell injury via the production
of hydroxyl radicals
The common causes of rhabdomyolysis are trauma,
infection, immobility (in alcoholics), drugs (e.g., lipid
lowering agents) and electrolyte abnormalities (e.g.,
hypophosphatemia).
Hepatorenal syndrome
Defined as worsening renal dysfunction in a cirrhotic with a
Hepatorenal syndrome
There are 2 major types of HRS:
Type I: defined as doubling Cr in < two weeks may
Pros of Intermittent Hemodialysis: more available ; less bleeding risk, removes toxins and electrolytes
faster, cheaper.
Cons of Intermittent HD: need special staffing, may be limited by patients hemodynamic status
(hypotension, tachycardia), poor fluid control, may achieve lower dialysis dose
CRRT
Pros of CVVH: can be used in more hemodynamically unstable pts, less hypotension and tachycardias,
perhaps associated with a reduced ICU length of stay
Cons: expensive
Prognosis
2013 study in Chest: Severity of Acute Kidney Injury and