Parvez Quadri, PGY-3.

Acute Kidney Injury Network(AKIN) Criteria:

An abrupt( within 48 hrs) increase in the
serum creatinine concentration > 0.3 mg/dl
above baseline
A percentage increase in the serum
creatinine concentration of > 50%
Oliguria less than 0.5 ml/kg/hr for more than
6 hours

True volume depletion- GI losses, renal losses,

skin/respiratory losses, third spacing
Hypotension- of any etiology; post treatment of
severe hypertension
Edematous states-heart failure, cirrhosis and
nephrotic syndrome
Selective renal ischemia- bilateral renal artery
stenosis( worsened by ACEIs and ARBs) and
hepatorenal syndrome
Drugs affecting autoregulation- may be
preglomerular( NSAIDs and calcineurin
inhibitors) and post glomerular( ACEIs and ARBs)

Vascular disease
Glomerular disease
Tubular and interstitial disease

The major vascular disease is vasculitis,

e.g.Wegeners granulomatosus.
Less common etiologies include:
Thromboembolic disease
TTP/HUS
Malignant hypertension
Scleroderma

There are numerous idiopathic and secondary

renal disorders that produce glomerular disease.
Two patterns are recognised:
Nephritic: inflammation on histology, active urine
sediment with red cells, white cells, granular and
often other cellular casts, variable degree of
proteinuria.
Nephrotic: not associated with inflammation on
histology, associated with nephrotic range
proteinuria and an inactive urinary sediment.

Acute tubular necrosis- usually in

hospitalized patients
Acute interstitial nephritis- drug induced
Cast nephropathy- multiple myeloma
Acute phosphate nephropathy- following the
administration of phosphate containing
bowel prep
Tumor lysis syndrome

Post Ischemia: all causes of severe pre-renal

disease, particularly hypotension
Nephrotoxins- drugs and exogenous toxins,
including
Aminoglycosides
Amphotericin B
Cisplatin
Radiocontrast media
Pentamidine
Foscarnet
IVIG
Heme pigments

Drugs- NSAIDs, beta lactam antibiotics, rifampin,

sulfonamides, ciprofloxacin, allopurinol, PPIs,5-amino
salicylates
Infection-Legionella,Leptospira, CMV, streptococcus
Autoimmune disorders- SLE, Wegeners, Sjogrens
syndrome, sarcoidosis
Physical exam- fever, rash, back/flank pain
Labs/other-abnormal UA with eosinophils,casts;
eosinophilia, FeNa>2, uptake on gallium/indium scan,
biopsy
Remember to order urine eosinophils in suspected cases.

Obstruction can occur anywhere from renal

pelvis to urethra
Usually bilateral or unilateral with a single
obstructing kidney
Prostate disease( hyperplasia or cancer)
Metastatic cancer

A report from Madrid analyzed 748 cases of AKI at

13 tertiary hospital centers:
ATN-45%
Pre-renal -21%
Acute on CKD-13%( mostly ATN and pre-renal)
Urinary tract obstruction-10%
Glomerulonephritis/vasculitis-4%
Acute interstitial nephritis-2%
Atheroemboli-1%
Data from PICARD study evaluated 618 pts in 5 ICUs
in the US:
70% of causes due to ischemic ATN
Pre-renal,nephrotoxic ATN,cardiac, liver and
multifactorial etiologies made up the remainder.

Signs and symptoms resulting directly from

alterations in kidney function, including decreased
or no urine output, flank pain, edema, HTN,
discolored urine
Lab findings, including elevation in plasma
creatinine, hyperkalemia and abnormal UA.
Symptoms and signs of renal failure- weakness and
easy fatigability( from anemia),anorexia, vomiting,
edema, AMS/seizures
Systemic symptoms-fevers, arthralgias and
pulmonary findings, suggestive of systemic process
such as vasculitis
Incidental findings( renal cyst/mass) on
radiographic tests performed for some other
reason.

Assessment of kidney function by

estimation of GFR, initially by measurement
of the plasma creatinine concentration.
Careful examination of the urine, by both
qualitative chemical tests and microscopic
examination, since the urinary findings
narrow the differential.

Estimation of the GFR gives an approximate

measure of the number of functioning nephrons.
Methods to estimate GFR include serum creatinine
concentration, the creatinine clearance, and
equations based on serum creatinine concentration
such as the Cockrauft-Gault equation and the
MDRD equation.
GFR estimation is only useful in patients with
STABLE kidney function.
In AKI, the GFR is initially markedly reduced but
there is not enough time for the serum creatinine to
accumulate.
It is important to know in a patient with kidney
disease if the GFR is changing or is stable

Serum creatinine
( mg/dl)
1
2
4
8
16

GFR (ml/min)
100
50
25
12.5
6.25

Microscopic examination of the urinary

sediment is the most important non-invasive
test in the diagnostic evaluation of kidney
disease
UA could be normal or near normal in prerenal,
obstruction, cast nephropathy ,hypercalcemia,
acute phosphate nephropathy, tumor lysis
syndrome and in some cases of ATN.
Urine is also tested via dipstick for protein, pH,
concentration, glucose, hematuria and pyuria.

The urine is rendered virtually sodium free in

the presence of volume depletion and normal
renal function.
Measurement of urine sodium concentration is
helpful in distinguishing ATN from pre-renal
etiology.
Fractional excretion of sodium ( FeNa):
FeNa, percent= UNa X PCr
---------- X 100
PNa X UCr
A value below 1 % indicates pre-renal disease, 12% could be either ATN/prerenal, a value above
2 % usually indicates ATN.

FeUrea: U urea nitrogen X P Cr

-------------------- X 100
BUN
X
U Cr
Only utility is in pts on diuretics.
Value < 35% - Pre renal
Value 50-65%- ATN

Kidney ultrasound: All pts presenting with

AKI of unknown etiology, should undergo
ultrasound to assess for possible
obstruction.
Also gives information on cystic disease of
the kidneys, and possible masses/tumors.
CT scan: Non-contrast CT is the gold
standard for diagnosis of nephrolithiasis.
Also useful for diagnosis of cystic disease,
neoplastic lesions, renal vein thrombosis.

A renal biopsy is obtained when noninvasive

evaluation has been unable to establish a
correct diagnosis.
Major indications:
Isolated glomerular hematuria with
proteinuria
Nephrotic syndrome
Acute nephritic syndrome
Unexplained acute or rapidly progressive
renal failure

Oliguria is defined as urine output less than

500 ml/day
Normal urine output is 0.5-1.0 ml/kg/hour, and
oliguria is UOP less than 0.5 ml/kg/hour.
Anuria : urine output < 50ml/day
Causes of anuria include shock, complete b/l
urinary tract obstruction, rarely HUS, renal
cortical necrosis, bilateral renal artery
obstruction and crescentic RPGN.
Non oliguric pts have higher GFR than oliguric
pts, or reabsorb less in the tubules.

Intermittent bolus doses of loop diuretics

are sometimes used in acute renal failure.
Most common indications for use include
pulmonary edema, rhabdomyolysis, major
surgery, cardiogenic shock and sepsis.
There is experimental and anecdotal
evidence in early oliguric AKI.
Proposed mechanism- protect against
cellular injury and washing out obstructive
intracellular casts.

No evidence of benefit after 3-4 days of

ESTABLISHED oliguric AKI.
No change in duration of AKI, decreased
requirement of dialysis or improved
survival.
Increase in UOP due to decreased tubular
reabsorption in remaining functional
nephrons, not due to recruitment of
previously non functioning nephrons.

 Acid-base

disturbance: metabolic acidosis

Electrolyte disorder-Hyperkalemia( > 6.5) or
rapidly rising K levels
Intoxication- methanol, ethylene
glycol,lithium, salicylates
Overload of volume- refractory CHF
Uremia- pericarditis, neuropathy or
unexplained decline in mental status

Step 1
History
Chart review-recent events( surgery ,
procedures),medications, vitals, I&O, body
weight, recent labs
Physical exam
Urinary bladder catheterization( if
oligoanuric)
Urinalysis

Consider urinary diagnostic studies-UNa,

FeNa, FeUrea
Exclude bladder obstruction- kidney US,
CT/MRI
Assess intravascular volume, cardiac output
status-Central line/Swan-Ganz
Additional blood tests-vasculitis, drug
screen, plasma cell disorders
Evaluation of renal vascular status- Doppler,
isotope scans

Selected therapeutic trials

Volume expansion- fluids, albumin
Diuretics
Ureteric stents/nephrostomy

Empiric therapy for suspected diagnosis

Steroids for suspected Acute Interstitial
Nephritis
Renal biopsy

Nurse on 9EW pages Intern A at 0200, saying her pt has

decreased UOP, about 150 ml in last 8 hours. He was
admitted with shortness of breath.
On exam, pt is in moderate respiratory distress, has JVD,
crackles on lung exam, and S3 gallop. You notice a bag of
NS running at 60 ml/hr. Review of labs shows Na 130, BNP
264. ECHO done earlier shows 35% EF.
What would you do next?
A. Call your senior
B. Administer a 500 ml bolus
C. Stat nephrology consult
D. Give a dose of iv lasix
E. Discontinue iv fluids and give a dose of iv lasix

You are cross-covering in the ICU, as your senior is

evaluating a floor pt. Nurse calls you at 0300 and says pt in
bed 17 has decreased UOP, only 30 cc in last 2 hrs. He
received 2.5 litres in boluses in the ER, and is now on
maintenance fluids at 150/hr. Pt has PMH of CHF, with EF
40%, admitted for septic shock from pneumonia. He is
intubated, has a right IJ , but not on pressors.
What is your response?
A. Let me call my senior, this is my first ICU rotation.
B. Page the nephrologist
C. 40 mg iv lasix, he must be fluid overloaded.
D. Go evaluate the pt, check his CVP.
E. 500 ml bolus, let me now if his UOP picks up.

Nurse pages you at 0130, informing you that Mr.Robinson in

8E, has decreased urine output over the last shift. He is a
73 yo gentleman admitted 3 days ago for chest pain. Pt
underwent cardiac cath with stent placement 2 days ago.
Review of his labs reveals a rising trend in BUN and
creatinine, decreased UOP to 200 ml over last shift. Review
of meds reveals he is on metformin for diabetes. What is
the most likely etiology of his deteriorating renal function?
A. Volume depletion
B. Obstructive uropathy
C. Ischemic ATN
D. Nephrotoxic ATN
E. Allergic interstitial nephritis

64 year old nursing home resident presents to ED for

evaluation of altered mental status. He has no other comorbidities. Pt was recently discharged a week ago with
creatinine of 1.06. He now presents with creatinine of 3.4.
UA reveals increased specific gravity,bacteria,leucocytes,
L.esterase+. Urine sodium is 7. FeNa is 0.14%.
On exam, he has dry mucus membranes, decreased skin
turgor. He is febrile at 38.9C,BP is 70/40.
What would you do next to improve his renal function?
A. Lasix 40 iv
B. Emergent hemodialysis
C. Fluid bolus, atleast 2-3 litres
D. Treat his UTI with Zosyn.

21 yo female admitted to ICU after consuming 60 pills of

ASA 81 mg, after a fight with her boyfriend. She received
activated charcoal in the ER. An hour later, she complains
of severe shortness of breath, drops O2 sats to the
80s.Lung exam reveals bibasilar crackles. CXR shows b/l
opacities, which are new. Stat salicylate level is 106 mg/dl.
What is the next best step in management of this pt?
A. Start the pt on bicarb drip at 250 ml/hr.
B. Give another dose of activated charcoal.
C. Alert nephrology and vascular surgery for possible
hemodialysis
D. Give her a dose of ativan for anxiety.
E. Stat cardiology consult.