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Copy of AKI

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by

Callie Davies

on 1 August 2013

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Transcript of Copy of AKI

The Wonderful World of Nephrology
ARF(AKI) Differential
Pre-renal (Prerenal azotemia)
Hypoperfusion, which if sustained may lead to intrinsic disease


Renal
Parenchymal damage


Post Renal
Must be bilateral to cause AKI


One Liner
14yF with history of rapidly progressive MPGN and ESRD s/p orthotopic kidney transplant in 2009 presents with acute on chronic kidney failure.
How do we Know
FeNa
BUN/Cr
Only helpful in adolescents and older children because of lower Cr levels in younger children
(More urea reabsorbed with H2O)
KFI
Imaging-
KUB, RUS,

CT
, VCUG, IVP, Mag 3, DMSA-pyelo
Case Continued
Physical Exam
Calories

FTT
Not enough in
Poor absorption
Too much
Case
Case Continued
Abrupt, life-threatening reduciton of urinary output to <300mL/m2/day
((Sodium urinary × Flow rate urinary) ÷/ (Sodium plasma) )/ ((Creatinine urinary × Flow rate urinary) ÷ /(Creatinine plasma) )× 100

((Sodium urinary × Flow rate urinary)x (Creatinine plasma) x 100 ))/
(Sodium plasma) (Creatinine urinary × Flow rate urinary)
Standard to "characterize the pattern of acute kidney injury in critically ill children"


Dehydration
Hemorrhage
Sepsis Hypoalbuminemia
Cardiac failure

Glomerulonephritis
HUS
ATN
Cortical necrosis
Renal vein thrombosis
Rhabdomyolysis
Acute interstitial nephritis
Tumor infiltration
Tumor lysis syndrome
Posterior urethral valves
Ureteropelvic junction obstruction
Ureterovesicular junction obstruction
Ureterocele
Tumor
Urolithiasis
Hemorrhagic cystitis
Neurogenic bladder
Pre-renal

U Na
FeNa
U Osm
Bun/Cr
ATN
<20
<1%
>500
>20:1
>30
>2%
<350
<20:1
History
Management
Difficult
Not as easy as bolus or restrict fluid
Lytes-K, Ca, Na

Acidosis-Does not usually require bicarb

Nutrition-most cases, sodium, potassium, and phosphorus should be restricted. Protein intake should be restricted

Anemia-mild/hemodilutional

Seizures/encephalopathy-Diazepam effective, treat underlying cause

Hypertension

Dialysis-
AEIOU
Prognosis-depends on underlying disease
RIFLE focuses on GFR, can also categorize severity by rise in serum creatinine: stage 1 >150%, stage II >200%, stage III >300%
Labs
Why AKI?
How Bad?
14yF with history of membranoproliferative glomerulonephritis and renal transplant in 2009, presentes with elevated creatinine. Baseline Cr is 1.1, patient had scheduled lab draw today and her Cr was 2.5. The level had been trending up since last visit with Dr. Garro in May 2013. No Fever, diarrhea, vomiting, or abdominal pain. Endorses compliance with medications, with no recent changes.
PMH: Steroid induced DM, HTN, Cardiomyopathy, hyperlipidemia, anemia, Guillan-Barre, recurrent UTIs.

SH: Renal transplant 2009, multiple Bx

FH: No history of renal disease

Social: Finished 9th grade, denies alcohol, tobacco, drugs.


Meds: Furosemide, tacrolimus, prednisone, magnesium oxide, TMP/SMX, ASA, Amlodipine, lisinopril, Iron, Mycophenolate, acyclovir, docusate, fluxonazole, Glargine, Nitrofurantoin, sodium Bicarb, Icosapent, Reno Caps.
ROS: Positive for swelling of LE, Steroid induced DM, immunosuppression
T 37.4 P
110
RR 20 Sat 100% BP 117/78 Wt 44kg 10-25%
Gen: Awake, alert, NAD. Skin: Warm, well perfused
Heent: NCAT, MMM, OP clear, clear conjuctivae
CV: normal s1, s2,
soft SEM LLSB
, CR <2 seconds, 2+ pulses
Resp: Good air entry B, no crackles or wheezes, Nml WOB
GI: +BS, soft, ND/NT,
kidney palpated in RLQ
GU: SMR 3, normal external genitalia
MSK:
1+ pitting edema LE
Psych: mom at bedside
Neuro: CN II-XII grossly intact, fluent speech, normal gait
Neck: FROM, no LAD Hem: no bleeding/bruising
Full transcript