AKI Flashcards

1
Q

Acute tubular necrosis or ATN

A

most common cause of acute renal failure in hospitalized pts

see abrupt renal ischemia from shock, sepsis, crush injuries and medications that decrease renal flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

treatment of ATN

A

IVF replacement and treatment of reasons for renal ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

allergic interstitial nephritis AIN

A

nephritis that affects interstitum of kidneys and surrounding renal tubules.

AIN causes are infections and reactions to medications such as nafcillin, methicillin, NSAIDS, rifampin, sulfa drugs, quinolones, diuretics, allopurinol, phenytoin.

also can be caused by Legionella or Streptococcus, systemic disease like SLE and sarcoidosis and Sjogren’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

treatment of AIN

A

supportive therapy, and stopping offending cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

labs seen on AIN

A

eosinophilia, rash, high WBC in urine
see AKI, can see pyuria, hematuria, WBC casts

can see urinary eosinophils
renal biopsy shows: inflammatory infiltrate and edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

clinical features of AIN

A

see allergic symptoms (urticaria) and new drug exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

most common cause of AIN

A

drugs.

PPI, NSADS and antibiotics and this happens about weeks or months after primary exposure. Rapidly develops on second exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

triad of AIN:

A

rash, fever, eosinophilia but also can no symptoms or not have all three

urinary eosinophils only seen 40% of the time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when do we see renal involvement of RA (with renal vasculitis or glomerulonephritis or membranous nephropathy)

A

see this is someone with advanced joint destructive dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Renal atheroembolic dx risk factors

A

aortic arteriography, angioplasty, or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

clinical features of renal atheroemoblic dx (cholesterol emboli to renal)

A

subacute onset AKI (1-2 weeks after procedure
active urinary sediment (hematuria, eosinophilia, WBCs, mild proteinuria)

Peripheral eosinophilia, and low complement levels

cyanosis or gangrene of toes with intact pulses

livedo reticularis rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment of cholesterol emboli

A

supportive and directed at 2nd prevention against CAD with statin, aspirin, BP control and smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

when does cholesterol emboli AKI and livedo reticularis rash occur after procedure?

A

it happens 1-2 weeks after.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

mottled lacy rash is

A

livedo reticularis rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of crystal induced AKI

A
acyclovir
sulfonamides (sulfadiazine)
methotrexate
ethylene glycol
protease inhibitors
uric acid (tumor lysis syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

clinical presentation of crystal induced AKI

A

usually asymptomatic
AKI<7 days after starting drug
UA: hematuria and pyuria and crystals
increased risk for volume depletion and CKD

17
Q

management of crystal induced AKI

A

discontinuation of drug
volume repletion
loop diuretic

18
Q

how does crystal induced AKI occur?

A

see poorly soluble drugs can precipitate into crystals in the renal tubules

seen with sulfadiazine

19
Q

sulfadiazine crystal induced AKI on UA

A

see acidic urinary pH (also seen with uric acid, sulfonamides and methotrexate)

see needle shaped, rosettes, or “clumped stacks of wheat” crystals

see hematuria and pyuria too.

see flank pain

20
Q

prevention and treatment of sulfadiazine induced AKI would be

A

adequate hydration 3l/day and alkalinization of urine to increase solubulity (ph>7.5)

21
Q

what predisposes the formation of crystals in the urine?

A

high doses of drugs, dydration (increased intratubular concentration) and acidic urinary pH

22
Q

is ultrasound helpful for diagnosing crystal induced AKI?

A

not really. can’t confirm diagnosis

Can show normal, or sludge or small calyceal stones (due to sulfonamide precpitation) or reveal hydronephrosis in rare cases)

but findings are likely nonspecific and unlikely to change management.

23
Q

how to prevent AKI in the treatment of HSV encephalitis

A

Acyclovir is a very poorly soluble medication and you can have AKI develop within 48 hrs of using this medication and so need to prevent this happening.

will see hematuria, pyruia, and birefringent needle shaped crystals on urinalysis.

Can give loop diuretics ot help flush crystals from renal tubules.

24
Q

FeNA is calculated by:

A

(urine sodium x serum creatinine) / (serum sodium x urine creatinine) to get a percentage

<1% pre renal etiologies of acute AKI need to be considered

1-2% intrarenal

> 2% consider post renal or obstructive causes

25
Q

intrarenal causes of AKI are

A

diabetic and hypertensive nephropathy

allergic interstitial nephritis

26
Q

post renal causes of AKI

A

BPH and nephrolithiasis and masses

27
Q

pre renal causes of AKI

A

meds and dehydration

28
Q

If there’s hematuria in the blood and dysmorphic cells then consider

A

renal biopsy

29
Q

if undifferentiated causes of AKI consider getting a

A

U/S of renal

not renal biopsy unless concerned about glomerulonephritis

30
Q

best way to prevent CIN in someone with AKI?

A

give NS at 3ml/kg hourly for one hour prior to proceure and 1 ml/kg hourly for 6 hours following.

do this over stopping ACEi

31
Q

fenofibrate nephrotoxicity occurs

A

> 6 months use

see a rise in serum cr after initiation and sediment is bland and no significant proteinuria.