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Oliguria and Acute Renal

Failure in the ICU


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

significantly changed by use of RRT.

The most common cause was septic shock.
Other studies cite overall mortality up to 78% in patients requiring RRT.
Its believed that up to 9% of AKI in critically ill patients is 2 to ATN.
The PICARD study - an observational study of 618 ICU patients demonstrated bad

prognostic factors included older age, male gender, baseline GFR, tachycardia, low UOP,
and presence of co-morbid organ failure.

What is the definition of Acute Kidney Injury (AKI)?

Table 1. RIFLE Classification System for Acute Kidney Injury)


GFR** Criteria

Urine Output Criteria



SCr increased 1.5

GFR decreased >25%

UO < 0.5 mL/kg/h 6 h

High sensitivity (Risk >Injury



SCr increased 2
GFR decreased >50%

UO < 0.5 mL/kg/h 12 h


SCr increased 3
GFR decreased 75%
SCr 4 mg/dL; acute rise 0.5 mg/dL

UO < 0.3 mL/kg/h 24 h

anuria 12 h


Persistent acute renal failure: complete loss of kidney function >4 wk


Complete loss of kidney function >3 mo

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.

Post renal (10%) Urine sodium high (>40) FeNa>4%,

Acute Pre-renal picture

Chronic Post-renal picture

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,


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

Evaluating renal causes

Break intrinsic renal causes up anatomically within nephron:
glomerular, tubular, interstitial, collecting system, vascular
Glomerular: glomerulonephritis nephrotic vs. nephritis
Tubular Acute tubular necrosis is the most common cause of AKI in
the ICU

Ischemic most common cause in ICU is septic shock

Toxic contrast, pigment, meds; osmotic agents (IVIG), Cisplatin, Amphotericin,

Interstitial: Acute Interstitial Nephritis

Collecting System: crystals (phosphate, ethylene glycol, acyclovir, sulfa

antibiotics, megadose Vitamin C, MTX, indinavir), stones (uric acid)

Vascular: TTP/HUS, DIC, Sickle Crisis/Papillary Necrosis,
Polyarteritis Nodosa, Atheroembolic Disease (after catherization),
renal artery or vein thrombosis

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

Check ANCA, cryoglobulins and complements (C3 & C4) to look for MPGN or Wegneners

associated with Hepatitis B and C respectively

HIV viral load to estimate activity of disease

Urine Microscopy
Hyaline casts suggests pre-renal
Granular casts , muddy brown casts - ATN
Red cell casts, dysmorphic RBCs acute

Oval fat bodies, maltese crosses Crystals calcium
oxalate (ethylene glycol ingestion)
White cell casts, sterile pyuria Interstitial
Eosinophils with Wrights stain AIN,
pyleonephritis, prostatitis, Cholesterol emboli

Oxidative injury to renal tubular epithelial cells
Sloughing of cells into lumen of renal tubules

obstruction that increases pressure in proximal

Decreases filtration pressure decrease in GFR
Termed tubulo-glomerular feedback

ATN muddy brown cast

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

Other renal disorders: Contrast nephropathy

Iodinated radiocontrast agents can produce acute renal injury and renal

Contrast-induced nephropathy is considered the third leading cause of

acute renal failure in hospitalized patients

Look for rising serum creatinine within 72 hours after the procedure.
Predisposing conditions : diabetes, hypertension, CKD, CHF, osmolality

and volume of iodinated contrast agent used during the procedure.

Most cases resolve within 2 weeks, and few require hemodialysis.
The mechanism of renal injury is multifactorial, and includes hyperosmolar

injury to the endothelium of small vessels in the kidney, and oxidative

injury to the renal tubular epithelial cells.

Prevention CIN Contrast induced nephropathy

ERBP position statement:
We recommend volume expansion with either isotonic sodium chloride
or sodium bicarbonate solutions, rather than no volume expansion, in
patients at increased risk for CIN. (1A)
We suggest using the oral route for hydration, on the premise that

adequate intake of fluid and salt are assured. (2C)

We suggest that, when oral intake of fluid and salt is deemed

cumbersome in patients at increased risk of CIN, hydration should be

performed by intravenous route. (2C)
We recommend not using oral N-acetylcysteine (NAC) as the

only method for prevention of CIN. (1D)

European Renal Best Practice (ERBP) Position Statement on the Kidney Disease Improving Global
Outcomes (KDIGO) Clinical Practice Guidelines on Acute Kidney Injury

Prevention CIN Contrast induced nephropathy

A prospective randomized trial comparing i.v. fluids with oral hydration with or without

sodium bicarbonate found no differences in the incidence of CIN in patients with mild
There appears to be insufficient evidence to support the universal use of NAC to

prevent CIN despite its ease of administration.

To date, 7 out of the 11 meta-analyses that have been published on this subject found a

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

In cases of drug-induced AIN, the characteristic signs of a

hypersensitivity reaction (e.g., fever, rash, eosinophilia) may not be

The onset of renal injury usually occurs within 2 weeks after starting the
drug, but delayed reactions occurring months after the onset of drug
therapy have been reported.
The presence of eosinophils and leukocyte casts on urine microscopy are
the most characteristic diagnostic findings. A renal biopsy can secure the
diagnosis, but is rarely obtained.
In suspected cases of AIN, any possible offending agents should be
Oral prednisone at a dose of 0.5 to 1 mg/kg daily for one to four weeks
may help to speed recovery.
Complete resolution can take months.

Common culprits of AIN


CNS Drugs Diuretics

Aminoglycosides Carbamazepine Acetazolamide
Amphotericin B Phenobarbital Furosemide
Cephalosporins Phenytoin
Fluoroquinolones NSAIDs
Sulfonamides Ibuprofen
ACE Inhibitors
Vancomycin Ketorolac
Iodinated dyes

Myoglobinuric Renal Failure

Acute renal failure develops in about one-third of patients

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.,

Myoglobinuric Renal Failure

The risk of renal failure is not related to any single

abnormality, but is more likely when there is a combination

of abnormalities.
For example, one study of trauma victims with
rhabdomyolysis revealed that the best predictor of acute
renal failure was the combination of a serum creatinine >1.5,
a creatine kinase (CPK) >5,000 IU/L, a base deficit =4, and
myoglobin in the urine .
The serum creatinine is not an accurate index of renal
function in rhabdomyolysis because the enhanced
creatine release from skeletal muscle adds to the
serum creatinine.

Management: Myoglobinuric Renal Failure

The plasma levels of potassium and phosphate must be

monitored carefully in rhabdomyolysis because these

electrolytes are released by injured skeletal muscle
Aggressive volume resuscitation to prevent
hypovolemia and maintain renal blood flow is one of the
most effective measures for preventing or limiting the renal
injury in rhabdomyolysis.
Alkalinizing the urine can also help to limit the renal injury,
but this is difficult to accomplish and is often not necessary.
About 30% of patients who develop myoglobinuric renal
failure will require dialysis

Hepatorenal syndrome
Defined as worsening renal dysfunction in a cirrhotic with a

serum Cr >1.5, after adequate fluid resuscitation with albumin,

being off diuretics > 2 days, absence of shock, signs of renal
parenchyma disease: i.e., bland urine sediment <500 mg
protein, < 50 RBCs, absence of nephrotoxic drugs, normal
kidneys on renal US.
The pathophysiology involves splanchnic vasodilation

causing a decreased venous return to the heart and thus

decreased cardiac output and high renin-angiotension tone
causing an intense afferent arteriolar vasoconstriction leading
to an irreversible pre-renal state for an otherwise normal

Hepatorenal syndrome
There are 2 major types of HRS:
Type I: defined as doubling Cr in < two weeks may

resolve spontaneously after resolution of infection

or inciting factor or may progress to ESRD
Type 2: defined as a slower, more chronic
decompensation of renal function in a cirrhotic;
Type 2 HRS may benefit from simultaneous kidney
and liver transplant because can be hard to
distinguish HRS from ATN and often have both
processes concurrently in same patient

What are indications for dialysis in ICU?

This can be very specific to patients, nephrologist and

hospital factors, however general indications can be

remembered by the mnemonic: A, E, I, O, U:
Acid-base: acidemia pH < 7
Electrolytes: K > 6.5 acutely (in non- CKD patient); Na >
155 or < 120, severe, toxic hyperphosphatemia or magnesium
Intoxicants: Lithium, ethylene glycol, methanol, etc.
Overload: fluid overloaded state, pulmonary edema,
anasarca, etc.
Uremic complications: pericarditis, neuropathy, myopathy,

Options for renal replacement therapies

There are two major types of renal replacement therapy:
Intermittent hemodialysis vs. continuous RRT (Continuous veno-venous hemofiltration
i.e. CVVH is the most common type currently)
Most studies show NO MORTALITY DIFFERENCE between CVVH vs. HD.
Although some initial studies showed better results in patients receiving CVVH this was
found to be because they were able to achieve better dialysis dose (better clearance).
However if one adequately doses intermittent hemodialysis by adjusting goals and dry
weight on the severity of illness in patient can similar results can be achieved.

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


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

2013 study in Chest: Severity of Acute Kidney Injury and

Two-Year Outcomes in Critically Ill Patients

Chart review of 15,048 patients, 12,399 (82.4%) survived 60 days
from ICU admission
45.7% didnt develop during ICU admission, whereas 54.3% did.
Acute Kidney Injury Network (AKIN) criteria AKIN 1, AKIN 2,
and AKIN 3 developed in 37.0%, 13.0%, and 4.3%, respectively
Patients with AKIN 3 had a 61% higher mortality risk at 2 years
from ICU discharge vs. patients without AKI.
They conclude that even 2 years after ICU admission, pts with
AKI have significantly increased risks of death that
extend beyond their high ICU mortality rates.
Chest. 2013;144(3):866-875. doi:10.1378/chest.12-2967