ACUTE KIDNEY INJURY

Dr. Villaflor
Notetakers: AKBC, DKD
January 15, 2014

Definition of Acute Kidney Injury (AKI) based on Acute Kidney
Injury Network LATEST definition
Stage Increase in Serum
Creatinine
Urine Output
1 1.5-2 times baseline or
0.3mg/dl increase from
baseline
<0.5ml/kg/h for >6h
2 2-3 times baseline <0.5 ml/kg/h for
>12h
3 3 times baseline or 0.5
mg/dl increase if baseline
>4mg/dl
or any RRT given
<0.3ml/kg/h for
>24h or anuria for
>12h
Few years back, AKI is not the term given for this condition. It
was Acute Renal Failure. Only at late 2000s that there was a
discussion regarding acute kidney function. Now, when we talk
about acute kidney injury, we are pertaining to the 3 stages
above.
Considerations:
1. Change in the serum creatinine
2. Urine output
3. Time interval that oliguria tract of urine output has
occurred
*Stage 3 the stage which any renal replacement therapy will
now be instituted
*Just remember that the percent change in the baseline and the
hours the oliguria and anuria has occurred, then classify them to
the 3 stages.

RIFLE criteria for diagnosis of AKI based on the Acute Dialysis
Quality Initiative PREVIOUS definition
Increase in S
cr
Urine
output
Risk of renal
injury

Injury to the
kidney

Failure of kidney
function
0.3mg/dl incease


2x baseline


3x baseline or
>0.5mg/dl increase
if Scr >=4mg/dl
<0.5ml/kg/h
rfor >6h

<0.5ml/kg/h
r for >12h

Anuria for
>12h
Loss of kidney
function


End-stage
disease
Persistent renal
failure for >4 weeks

Persistent renal
failure for >3months

This criteria represents the risk of renal injury, the injury itself,
failure of the kidney, loss of kidney and end-stage. In this stage,
the loss of kidney function and end-stage disease require the
renal replacement therapy or dialysis labelled as stage 3 on
the latest classification. They have modified it because probably
the loss of kidney function is temporary or is it persistent, but
because we are considering acute renal injury on top of chronic
renal disease, sometimes this acute episode would not allow the
return to insufficiency stage and then bring them to permanent
loss of kidney function or progress to end-stage renal injury.
Hence, this last stage explains that when only one acute injury
has happened, it will bring them to permanent loss of kidney
function.
Increase in Creatinine without AKI
Any increase in creatinine is not always associated with a
drop in renal function. Thats why review of history and
charts is important because these conditions are associated
with an increase in creatinine without necessarily a drop in
the GFR and renal function. These drugs compete with the
receptor in the secretion of tubular secretion of creatinine,
thats why you can have elevation of creatinine from the
baseline. So in pxs wherein you have a risk of injury, make
sure that these drugs are not there to confuse you. Or if
inevitable, you can change the drug which has the same
action and observe the ternd of the creatinine.
Inhibition of tubular creatinine secretion (trimethoprim,
cimetidine, probenecid)
Medical conditions of the patients can interfere with the
creatinine assays in the lab (false elevation): glucose,
acetoacetate, ascorbic acid, cefoxitin, flucytosine
Make sure that these false positive conditions are not
present in the px

Increase in BUN without AKI
Increased production
o GI bleeding
o Catabolic states(prolonged ICU stay)
o Corticosteroids
o Protein loads (TPN-Albumin infusion)
These conditions can also increase BUN without
necessarily proceeding to AKI.

New Biomarkers in AKI Alternatives to Serum Creatinine
When dealing with acute injury, these biomarkers are the
new ones used. Old biomarkers include urinalysis, urine
microscopy, urine electrolytes, and fractional excretion of
Na and urea. How do you compute for the fractional
excretion of Na and urea? Importance: A normal tubule
can still retain its reabsorptive function. VS a necrosed
tubule will have lost its function already. These
biomarkers can lead us to identify whether the elevation
of creatinine is prerenal or really ATN. Example, in a state
of dehydration, your creatinine level has increased or
guba lang gd ya ang tubules mo kay nag-injury ka na or
ATN.
In dehydration the kidneys tend to reabsorb NA and water,
so when we check for urine electrolytes, Na will be less than
20, converting it to fractional excretion of Na, you will have
a value <1%. And if the values are >20 Na, and its F
e
Na
values are >3%, it supports more of the ATN.
With regards to the fractional excretion of urea, the sodium
levels in the urine can be influenced by the use of diuretics
which are commonly given to pxs with AKI. Because in
oliguria, we often give a challenge of diuretics and because
of the diuretic load to our pxs, the F
e
of urea can be >3%.
However, in real sense, Fe BUN or Fe urea is not influenced
by the use of the diuretics. So if you have 3% Fe urea, it is
still prerenal but if it is >3% ang value, yes it is already ATN.
Urine microscopy the presence of blood urine will really tell
us tubules are still okay. But in ATN, you can now appreciate
granular casts and hyaline casts. The more cast we
appreciate, the more likely the patient is developing ATN,
and not prerenal state.
Newer biomarkers used in determining whether theres
really AKI or not. Their importance comes into play when we
want to predict an outcome or screen pxs contemplated to
be put in a study. Note: double rise in creatinine reflects
more than 50% drop in the function.
These new biomarkers are actually LMW proteins.
Urinary Neutrophil Gelatinase-Associated Lipocalin (NGAL)
Urinary Interleukin 18
Urinary Kidney Injury Molecule 1 (KIM-1)
New biomarkers in determining if the injury is present or not

Major Disease Categories Causing AKI

Prerenal Azotemia
Any condition that can decrease the renal perfusion to the
kidney; the most common cause to progress to ATN
Sometimes the loss is not evident
Adequate fluid body, relative hypovolemia bcoz of
inadequate circulating fluids, they are in a different
compartment
Intravascular volume depletion
o Bleeding, GI loss, renal loss, skin loss, third
space loss
Decreased cardiac output
o CHF
o Fluid tends to pool peripherally in the right
side, resulting to a drop in CO
Renal vasoconstriction
o Liver disease, hepatorenal syndrome, sepsis,
hypercalcemia constrict renal arteries that can
lead to volume depletion
Pharmacologic impairment of autoregulation and GFR
in specific settings
o ACEi in bilateral RAS constrict efferent and drop the
GFR, NSAIDs in any renal hypoperfusion setting
constrict the afferent and reduce the perfusion.
Okay lang kung temporary, kay kung when you
withdraw the drug, ma-dilate liwat ang
ginaconstrict nila
o Review the mechanism of how these drugs actally
decrease GFR and may be cause ATN

Intrinsic Renal Azotemia
Large Renal Vessel Disease
o thrombo-embolic disease
Renal Microvasculature and Glomerular Disease
o inflammatory: glomerulonephritis, allograft
rejection
o vasospastic: malignant hypertension,
scleroderma crisis, pre-eclampsia, contrast
o Hematologic: HUS-TTP, DIC
Acute Tubular Necrosis
o Ischemic
o Toxic
Tubulo-interstitial Disease
o Brought about by drugs, chemical
o Acute interstitial nephritis (AIN), acute cellular
allograft rejection, viral (HIV, BK virus),
infiltration (sarcoid)
Intratubular Obstruction
o Crystal formation along the tubules brought
about by these
o Myoglobin in hazing, haemoglobin in bleeding,
myeloma light chains in MM, uric acid, tumor
lysis syndrome, drugs (indinavir, acyclovir,
foscarnet, oxalate in ethylene glycol toxicity)

Postrenal Azotemia
Anything that obstructs from the calyses down;
obstruction can be luminal or extraluminal
Stones
Blood clots
Papillary necrotic tissue
Urethral disease
o Anatomic: posterior valve
o Functional: anticholinergics, L-DOPA have
effect on the sphincter
Prostate disease
Bladder disease
o Anatomic: cancer, schistosomiasis
o Functional: neurogenic bladder

Initial Diagnostic Tools in AKI
History and Physical Exam impt! Diarrhea for 2days -
prerenal to ATN, coz bal-an mo na nga may fluid loss xa.
Detailed review of the chart, drugs administered,
procedures done, hemodynamics during the
procedures - common among pxs confined in ICU or
those who have undergone surgical procedures, drugs
administered are potentially nephrotoxic. During
introduction of anesthesia, was there episode of
hypotension? And what was the length of time of
hypotension? Amount of blood loss during operation
Risk factors for AKI
Urinalysis
o SG, pH, protein, blood, crystals, infection
Disease Category Incidence
Prerenal azotemia caused by acute renal
hypoperfusion
55-60%
Intrinsic renal azotemia cause by acute diseases
of renal parenchyma:
- Large renal vessels disease
- Small renal vessels and glomerular dse
- ATN (ischemic and toxic)
- Tubule-interstitial dis
- Intratubular obstruction
35-40%





*>90%*
Postrenal azotemia caused by acute obstruction
of the urinary tract
<5%
Urine microscopy
o Casts, cells (eosinophils) if + imply elevated
crea allergic interstitial nephritis or
tubulointerstitial nephritis
Urine electrolytes Na, BUN, compute for the fractional
excretion of Na
Renal imaging
o US - impt: looking for the size, if N can be
acute and no underlying CKD, can also r/o
obstruction, Mag-3 scan, retrograde pyelogram
- ff up dx tool in evaluation of kidney function,
not necessarily impt on initial approach
Markers of CKD
o PTH, size <9cm, anemia, high phosphate, low
bicarbonate support that may be there is
underlying CKD in the px
Renal Biopsy
o Seldom but for therapeutic intervention
o To further evaluate glomeruli and tubules

Likelihood ratio (LR) of ATN vs pre-renal azotemia on the basis of
the number of granular casts in urinary sediment
Granular casts/hpf LR for ATN LR for pre-renal
0 0.23 4.35
1-5 2.97 0.34
6-10 9.68 0.1
The more active the sediments are, chances are ATN xa. If Blood
prerenal azotemia. Impt bcoz urine microscopy can now give
us a clue if ATN or preranl azotemia lang











Cast follow the shape of the tubule.

Treatment of AKI
Treatment is largely supportive in nature! Except if
cause is inflammatory
Pharmacologic treatments under study:
o Dopamine: no benefit
o Atrial Natriuretic Peptide (ANP) or ANP-
analogue (Anaritide): promising
o Human Insulin-like Growth Factor 1: no benefit
Renal Replacement therapy remains the cornerstone of
management of minority of patients with severe AKI
Gold standard: if its Prerenal, upon hydrating the px
normalize creatinine
o Hydration-1st support in px with AKI
Next, dopamine at lower doses, indeed dilate renal
artery increasing renal perfusion; but, in terms of
improving the morbidity and mortality of the pxs who
were given dopa, no benefit
If prerenal hydrate only!
If ATN, hindi na mag-give dopa bcoz no benefit in the
px!
Role of ANP promote natriuresis, not definite results
and need more reliable studies
If there is frank and acute kidney injury that px will not
respond to hydration cornerstone of mngmt renal
replacement therapy (dialysis/ultrafiltration)

Is there a role for Dopamine in prevention or treatment of AKI
in ICU setting?
Clinical Outcomes
No effect on mortality
No effect on the need for or incidence of Renal
Replacement Therapy (RRT)
Renal Physiologic Outcomes:
Diuretic effect and increased creatinine clearance on
the first day which was not significant on the following
days
Adverse Effect:
On the immune, respiratory, and endocrine system

Is there a role for Fenoldepam in prevention or treatment of
AKI in ICU setting?
Dopamine-1 receptor agonist, lack of Dopamine-2, and
alpha-1 receptor effect, make it a potentially safer drug
than Dopamine!
Reduces in-hospital mortality and the need for RRT in
AKI
Reverses renal hypoperfusion more effectively than
renal dose Dopamine
(Vs dopa) advantage no constriction in higher doses
Results initially are good but need more trials to be
recommended
So far so good specifically in cardiothoracic ICU patients
awaiting more powered trials in other groups!

Is there a role for diuretics in the treatment ofAKI in ICU
setting?
PICARD study:
o Cohort study of 552 px in 4 UC hospitals
In-hospital mortality (1.77)*
Non-recovery of renal function
(1.68)*
*odds ratio
o Improved urine output and shorter duration of
RRT (none has clinical relevance in ICU
patients)
o But diuretics continue to be used for volume
control in AKI in ICU setting!
Diuretics improve volume of urine output, but not
overall mortality and morbidityfor volume control
only in AKI.

Results of individual RCTs comparing CRRT to IHD in AKI in ICU
Study n n Primar
y
endpoi
nt
Mortali
ty
Mortali
ty
Persistent
RRT
requirem
ent

CRR
T
IH
D
CRRT IHD CRRT IH
D
Mehta et
al
84 82 Icu
mortali
ty
59.5 41.5 14 7
Augustin
e
40 40 In-
hospit
al
mortali
ty
67.5 70 61.5 66.
7
Uehlinge
r
70 55 In-
hospit
al
mortali
ty
47 51 2.7 3.7
Vinsonne
au
175 18
4
60-day
mortali
ty
67.4 68.5 1.8 0
Lins 172 14
4
In-
hospit
al
mortali
ty
58.1 62.5 16.9 25.
5
Dialysis exchange of solutes
Aki depend on the timing and dose of dialysis impt!
CRRT (continuous renal replacement therapy) chronic
renal replacement therapy pwede nga fluid lang,
more of ultrafiltration (vs clearance)
IHD (intermittent hemodialysis) fluid and toxins ang
ginakuha, but intermittent only!

CRRT vs SLED (Sustained Low-Efficiency Dialysis)
SLED became popular because of CRRT
disadvantages(expensive, continuous, pt
immobilization, need for specialized machines and pre-
mixed commercial solutions, and anticoagulation)
Only 2 small studies compared these 2 in
hemodynamically unstable patients with AKI
They did not see significant differences in
hemodynamic parameters and solute clearance
They did not look at any patient-relevant outcomes, so
the jury is still out there
Sled can actually perform in the usual dialysis
Sustained low efficiency dialysis
Not concerned with clearance
Crrt - needs a speciql machine
No significant difference in hemodialysis and solute
clearance; very expensive, prolonged therapy, loose a lot of
blood

Results of RCTs comparing benefits of the intensity of RRT (high
vs low dose dialysis)
Study N Low-
dose
modalit
y
High-
dose
modalit
y
Endpoi
nt
Resul
ts for
low-
dose
Resu
lt for
high-
dose
P
Schiffl 146 Thrice-
weekly
IHD
Daily
IHD
1-
mortali
ty
2-time
to renal
recover
46%

16
days
28%

9
days
Si
g
Ronco 425 CVVH
dose of
20ml/kg
/h
CVVHDF
dose of
35 or
45ml/kg
/h
90-day
survival
34% 59% Si
g
Palves
ky
110
0
High
dose:
CRRT
35m/kg/
h or
SLED x
6/wk or
IHD x
6/wk
Low
dose:
CRRT 20
ml/kg/h
or
SLED x
3/wk or
IHD x
3/wk
60-day
mortali
ty
51.8% 53.6
%
N
S
RENAL
clinical
trial
150
0
CVVHDF
25ml/kg
/h
CVVHDF
40
ml/kg/h
90-day
survival
N
S
Over-all conclusion on RRT modality benefit AKI
CRRT does not confer a survival advantage as compared
to IHD
SLED may replace CRRT although there is no outcome
benefit study up to this date
There is limited data regarding the ideal timing of RRT
initiation and the preferred mode of solute clearance
No evidence to support a more intensive strategy of
RRT in the setting of AKI

Case 1
26yo F is involve in MVA, with multiple fractures, blunt chest and
abdominal trauma. She was briefly hypotensive on arrival to ED,
received 6L NS and normalized BP. Non contract Ct showed small
retroperitoneal hematoma. On day 2 her Scr is 0.9 mg/dl, lipase is
elevated and tense abdominal distension is noted. US showed massive
ascites. UOP drops to <20 cc/hr despite of 10L total IVintake. On day 3
Scr is 2.1mg/dl CVP is 17 U-Na is 10meq/L with a bland sediment. What
is the cause of her AKI? What bedside diagnostic test and therapeutic
intervention is indicated?
Bladder pressure was 19mmHg
UOP and Scr improved with emergent paracenthesis
Dx: Abdominal Compartment Syndrome causing decreased renal
perfusion from increased renal vein pressure.
Always overlooked. Abdominal distention causes decrease in urine
output.
*Scr-serum creatinine

Case 2
58yo M s/p liver transplant in 2001 and acute chronic rejection , now
decompensated ESLD , is admitted with worsening ascites, hepatic
encephalopathy and GI bleed (which is now controlled). The only
medications he has been receiving are Lactulose and Prilosec. He has
been hemodynamically stable with average BP 100/70 mmHg. He had a
3.5L paracenthesis on day 2. His Scr has been slowly rising from 1.2 to
4.7mg/dl within the second to fourth day of admission and his UOP has
dropped to 150 cc/day. His daily Fe Na is <1% despite of 2L fluid
challenge. His urine sediment is bland. His renal US is normal. What is
the cause of AKI?
Patient required HD.
He had a second liver transplant and came off HD after the
surgery with stable Scr of 1.4mg/dl
Dx: hepatorenal syndrome (HRS)
Casue of AKI? That time px developed hepatorenal syndrome
Major criteria of HRS: crea >1.5, absent proteinuria, no obstruction, no
ATN, no improvement with atleast 1.5L fluid challenge
Hepatorenal Syndrome
Major diagnostic criteria:
No improvement with at least 1.5L fluid challenge
Scr>1.5mg/dl or GFR<40cc/min
Absence of proteinuria (<500mg/d)
Other causes are ruled out (obstruction, ATN, etc)
Minor diagnostic criteria:
Urine volume <400cc/day
UNa <10meq/L
SNa <130meq/L
Urine RBC <50/hpf

Case 3
52 y/o F underwent matched allo-hematopoietic stem cell transplant
(HSTC) for AML. Between days 3-7 she gradually gained 8 kg and edema
developed. Since day 7 her bili rose daily and peaked at 8 with jaundice,
RUQ tenderness and ascites. Liver US showed reversal of flow in the
portal vein. Since day 8 Scr rose slowly from baseline of 1.0 to 3.5mg/dl,
with 400cc/day UOP on day 10. Her FeNa was 0.05% despite of 1.5L
fluid challenge. Her urine sediment was blend.
What is the most likely cause of her AKI?
She required HD for volume control, and remained HD
dependent
DX: portal/hepatic veno-occlusive disease (VOD)
VOD is responsible for 90% of hepatorenal syndromes in HSCT
Basis: Reversal of flow in the portal vein

Case 4
45 y/o M with CHF and bipolar disorder on lithium for 10 years,
admitted for abdominal pain after a heavy meal, which turned out to be
due to acute cholecystitis. He was kept NPO on D5 1/2NS 50cc/hr. Next
morning he felt well but thirsty and hungry, BP=120/80,
I/O=1200/4500. His Scr rose from 1.2 to 1.9mg/dl. SNa 149 meq/L. UNa
10 meq/L. Uosm 190 mOsm/Kg. What is the cause of his AKI?
Patiens IVF was changed to NS replacing 80% of UOP per
hour. Scr and SNa improved to baseline in 2 days.
Dx: Prerenal Azotemia secondary to renal free water loss in DI.
Cause? Massive water loss because of DI caused by lithium

Case 5
68 yo F with CAD, DM, HTN, PVD, CKD with baseline Scr of 1.4mg/dl
underwent elective cardiac angio and stent placement. No new meds.
She has been hemodynamically stable throughout the procedure and
afterfward. Since day 2 post procedure, her Scr has been gradually
rising to 2.5mg/dl with 500-600 cc/day UOP. UA showed SG 1.025, 1+
protein. Urine eosinophils +, serology tests showed low complements.
She was discharged in her f/u visit in 3 weeks she had Scr of 2.7. What
could be the cause of her AKI?
She never required RRT but her Scr continued to rise slowly to
3. Mg/dl. She died 7 months later.
Dx: Cholesterol emboli
Bcoz of invasive procedures done on a px who is diabetic

Case 6
18yo F with no PMH admitted with projectile vomiting, fatigue and low
PO intake. Her BP=200/110, normal UOP with dry mucosa, trace
edema, and otherwise normal exam. BUN=120mg/dl, creat=10mg/dl
which continued to rise on the following days, Hct=25% without
schistocytes on PBS, UA: 3+ protein, 3+ blood, >50 RBC, many RBC
casts. FeNa1% US showed normal sized kidneys. What other tests do
you order? What may be the cause of her AKI?
ANA (-), normal complements, cryo (-), serology for Hepatitis
B, and C (-),P-ANCA (+), C-ANCA (-), anti-GBM (-), ASO (-),
UPEP and SPEP without M spike ESR 80.
Her renal bx showed crescenteric glomerulonephritis, minimal
non-specific immune complex deposits, without chronic
changes.
She remained dialysis dependent despite of steroid Cytoxan,
and 10 plasmapheresis treatments.
Dx: Pauci-immune Crescenteric Glomerulonephritis due to Wegeners
Granulomatosis
She developed actually RPGN
Plasma protein very very active urine sediment if positive think
always of GN!

Case 7
54yoF with CAD, on statin, started a new exercise program with intense
weight training. She was brought to ED with neck pain and LE weakness.
VS stable, normal UOP with dry mucosa. LE muscle strength 2/5
bilaterally. BUN 40mg/dl, creatinine =8mg/dl. FeNa 1.5%. Renal US
normal. UA: 1.010, 3+ blood, few RBCs, few granular casts. What would
be the next test to order? What may be the cause of her AKI?
Her CPK=57,700
She was treated with IV NaHCO3 gtt to alkalinize urine to
PH>6.5.
Her UOP remained normal but she required HD for uremia.
Dx: ATN due to Rhabdomyolysis
Statins can cause myopathy also; phabdomylosis bcoz of prolonged
statin therapy; alkalize the urine

Case 8
47yo M with CAD,and CHF, admitted with LE cellulitis, started on Zosyn.
On day 4 of admission BP 90/60, HR 68, normal UOP. LE edema (+), few
pruritic purpuric rash on the shins. Scr rose from 1.1 to 3.5 mg/dl.
BUN+96mg/dl. UA: trace protein, small blood, few RBCs, moderate
WBC, with few WBC casts. FeNa>1% urine eosinophil (+). Renal US
showed 13cm kidneys. What may be the cause of his AKI? What would
be your next step?
Zosyn was stopped
Patient required two HD treatment for uremia
Renal biopsy showed acute interstitial nephritis
Subsequently he was started on prednisone for one month
and remained HD independent with stable Scr of 1.8-2mg/dl
Dx: AIN secondary to Zosyn
Enlarged kidney basi nagreact sa Zosyn

Case 9
72 yo M with DM and prostate cancer metastatic to the bone, s/p XRT,
on hormonal therapy. He is admitted with weakness, progressive
weight loss, and persistent nausea. His med list also includes Diclofenac
sodium daily for hip pain. BP=150/90, 350cc of urine collection
immediately after foley placement, and normal exam. BUN=107mg/dl,
creatinine9.8mg/dl (2.0 almost 6 months PTA), which remained
unchanged with hydration. Uric acid = 8.2mg/dl. UA: 1.010, 1+protein,
1+blood, few RBCs, no cast, no WBC. US showed 10-11cm kidneys, no
hydronephrosis. What seems to be the cause for his AKI?
Patient was initiated on HD for uremia and remained HD
dependent for his symptomatic uremia
Patient and his family were concerned about his renal
recovery (outcome), so a renal bx was done showing severe
chronic interstitial nephritis, with fibrosis and
glomerulosclerosis
Dx: ESRD due to chronic tubule-interstitial disease secondary to NSAIDs
Fibrosis and sclerosis chronicity index!
Inflammatory, proliferative acute findings!

Case 10
32yo M s/p cadaveric renal transplant (CRT) in 2006 for adul pckd, on
prograf, prednisone, and cellcept (immunosuppressive drugs), and
history of BK viruria is admitted for increased creatinine 1.9 mg/dl,
hct=27%, WBC 2,500, plt 90,000. He seems well hydrated, with stable
VS, and normal exam. UA: 1.015, no protein, no blood, few granular
casts. FeNa 1%. (-)BK virus PCR in the blood. What would be your next
step? What seems to be the cause for his allograft failure?
Renal bx showed acute cellular rejection BANFF IIb. No BK
viral inclusions were identified.
He received IV solumedrol and thmoglobulin and his
creatinine dropped to a stable level of 1.3-1.4mg/dl
Dx: Acute cellular rejection
In a post KT px, sometimes make sure that this is not due to drugs or
cellular rejection.

Case 11
59yo F with prolonged HTN, s/p OLT in 2000, on Norvasc, prograf and
prednisone was brought in for AMS. T=39, BP=95/60, HR=104,
UOP=20cc/hr, intubated for airway protection, otherwise normal exam.
BUN=80 mg/dl, creatinine=6mg/dl (normal baseline), K=6.5meq/L,
Hct=20%, plt=20000, FeNa1%, urine eosinophil (-), UA: 2+ blood, no
protein, RBC >50/hpf, no WBC, no cast. What would be your next step?
What could be the reason for her AKI?
Her PBS showed many schistocytes and fragmented RBCs
Her prograf was replaced with sirolimus
She underwent plasmapharesis, and required HD for anuria,
and persistent hyperkalemia, she came off HD after
2.5months with stable creatinine=1.2mg/dl.
Dx: TTP secondary to prograf

Case 12
72yo F with depression and hypothyroidism,was found by neighbors on
the floor unconscious, in respiratory distress. Intubated for airway
protection. VS stable, anuric, lungs CTA. BUN 50mg/dl,
creatinine=4mg/dl, with high anion gap metabolic acidosis, and an
osmolar gap of >10. Lactic acid=1.8, FeNa 1%, urine eosinophil (-), UA:
1.0202, 1+ blood, no protein, few RBCs, many oxalate crystals, few
granular casts. US showed normal sized kidneys with no
hydronephrosis. What is your next step? What seems to be the cause
for her AKI?
Her ethylene glycol level came back after 2 days to be
40mg/dl
Pt was give fomepizole and initiated on HD for persistent
academia. She remained HD dependent,eventually extubated,
started therap for depression and discharged to NH.
Dx: Ethylene Glycol Toxicity
Common toxicity oxalic acid, in suicidal or accidental cases lactic
acidosis

Case 13
38yo M with post ERCP pancreatitis, is admitted to ICU, intubated for
hypoxic respiratory distress, is anuric, febrile, and hypotensive,
requiring massive volume resuscitation, on two vasopressors. He has
received 11L ofNS and other IV meds within the last 8 hours and
currently his CVP ~12, has coarse crackles, and 2+edema. His creatinine
rose from 1.2 to 3.5 the morning after the above event, FeNa>1%,
UNa45meq/L, UA: 1.010, no protein, no blood, moderate epithelial
cells, many muddy brown granular cell casts, moderate epithelial cell
casts. US showed normal-sized kidneys with no hydronephrosis. What is
the cause of his AKI?
He was started on CVVH for volume control. Has had a long
hospital stay complicated with polymicrobial bacteremia and
VAP.
Dx: ATN secondary to renal ischemia and sepsis.

Natural Clinical Course of ATN
Initiation phase (hours to days)
o Continuous ischemic or toxic insult
o Evolving renal injury
o ATN is potentially preventable at this time
o The time the insult is given to the kidneys
o Potentially reversible
o Problem is hindi mabal-an nga gahatag na ta gali
insult sa kidneys
Maintenance phase (typically 1-2 weeks)
o Maybe prolonged to 1-12 months
o Established renal injury
o GFR < 10cc/min, the lowest UOP
o May proceed to dialysis
Recovery Phase
o Gradual increase in UOP toward post-ATN diuresis
o Gradual fall in Scr (may lag behind the onset of
diuresis by several days)
o GN-recovery is longer

When to do renal biopsy in AKI?
Any evidence of glomerular disease
o Nephrotic range proteinuria
o Sub-nephrotic range proteinuria with hematuria
o RBC casts
AKI in renal allograft
Determine the prognosis and chance recovery of renal
function in dialysis dependent AKI
Whenever potential Bx result can change the management or
prognosis
In pxs with post renal transplant with AKI a must to do
biopsy; in order to know if the case is from the drug-
discontinue the drug; if not-administer more

When to initiate RRT in a patient with AKI?
Renal Replacement Therapy:
o Electrolyes imbalances esp. hyperkalemia coz pwede
magcardiac arrest
o Acid-base disturbances
o Uremic complications
Encephalopathy
Pericarditis
Persistent nausea, and food intolerance
Renal/Multi-organ Support Therapy
o Protects other organs by improving over-all body
milieu (balance of inflammatory mediators); dont
forget proper nutrition!
o Allowing therapies for other organs that pt could
not otherwise tolerate
Volume resuscitation
Aggressive nutrition
Removal of toxic agents in overdose
o Ethylene glycol
o Methanol
o Salicylates
o Lithium
o Theophylline
o Isopropanol