Medstudy im core curriculum, 16e book 2 pulmonary medicine & nephrology unitedvrg

Page 129

ACUTE KIDNEY INJURY

4-34

Table 4-11: Category

FENa

Causes

Volume depletion

Prerenal

Acute K1dney Injury Labs and Clues

FEuricacid

<1%

<12%

FE urea

<35%

Decreased

Uosm >400

Urine

Urine

Na+

Sediment

Suspect

<20

in Patient with

...

Bleeding

mOsm/L

CHF

EABV *

Cirrhosis!hepatorenal

NSAIDs

Abdominal compartment

ACEI

syndrome (ACS) Nephrotic syndrome GI fluid loss (nausea! vomiting/diarrhea)

Intrinsic

Diseases of,

ATN*>2%

renal

or damage to,

GN*<l%

>20%

>50%

>20

300-350 mOsm/L

Red cell casts

Infections

and/or protein

SLE

the glomeruli,

(GN)

Vasculitis

tubules, or

Dirty brown

Drugs (aminoglycosides,

casts (ATN*)

amphotericin, cisplatin,

Eos (AIN*)

NSAIDs)

interstitium

Contrasts/IV dyes Atheroembolism Heroin Myeloma Diabetes H TN Hypotension, shock Postrenal

Varies

Varies

Varies

Obstruction

Normal

Elderly males Colicky pain

Level indicating prerenal

Fractional excretion**

Changed by diuretics

*EABV

AKJ

ATN

FEurea

<35

No

FEuricacid

<12

No

=

AIN

effective arterial blood volume

acute tubular necrosis

glomerulonephritis

=

acute interstitial nephritis

**Recent diuretics use can alter the FENa and, in this setting, FEurea and FEuric acid are more reliable.

dysfunction. ACS can occur with abdominal trauma, mas­

No evidence of parenchymal kidney disease (normal U/A, proteinuria<

GN

Yes

<1

=

=

500 mg/d, normal renal

sive ascites, intraperitoneal bleeding, acute pancreatitis,

ultrasound)

and any other condition that raises the intraabdominal

Absence of any other apparent cause of AKI,

pressures. AKI in ACS most likely occurs secondary to

including shock, nephrotoxins, and infection

renal vein compression, which increases venous resis­

(except peritonitis)

tance and impairs venous drainage.

Therapy with midodrine and octreotide is aimed at stabilizing patients until they receive a liver transplant. Abdominal compartment syndrome as a cause of prerenal

AKI:

Abdominal

compartment

syndrome

(ACS) refers to organ dysfunction caused by intraab­ dominal hypertension. Intraabdominal pressure (lAP) is

Similar

to

other

causes

of

prerenal

AKI

induced

by reduced perfusion, the renal indices usually are decreased (FENa < Treat

with

1% and FEurea< 35%).

either

surgical

decompression

(trauma

patients) or high-volume paracentesis (in patients with massive ascites).

the steady state pressure concealed within the abdomi­ nal cavity. Abdominal perfusion pressure (APP) is calculated as the mean arterial pressure (MAP) minus the lAP (APP

=

MAP- lAP).

Elevated intraabdominal pressure reduces blood flow to the abdominal viscera. ACS is defined as a sustained

Prerenal AKI: Labs BUN:Cr ratio is typically increased to>

20.

Urine is very concentrated with osmolality > often>

400, and

700.

intraabdominal pressure >

UrineNa+ is< 20, indicating normal tubular function (and

APP <

avid reabsorption ofNa+ to increase glomerular pressure).

20 mmHg (with or without 60 mrnHg) that is associated with new organ

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