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Renal Week 2 > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What are some signs of kidney damage?

A

increased BUN and creatinine are indicative of a decreased GFR

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2
Q

What is the definition of acute kidney function?

A

rapid deterioration of renal function (hours to days but less than 1 month)

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3
Q

How is ‘rapid’ deterioration defined?

A

Greater than .5 mg/dl increase in creatinine or increase of 50% over baseline value

Sometimes decreased urine output but not always

Inability of the kidney to regulate electrolytes/water

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4
Q

What is oliguria?

A

less than 400 ml urine output in 24 hours

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5
Q

What is anuria?

A

less than 100 ml urine output in 24 hours

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6
Q

What symptoms are associated with acute kidney injury?

A

typically none. Patients will be asymptomatic and it will be caught on routine labs and can be reversible if the underlying disease can be treated

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7
Q

What are the three major types of acute renal failure/injury?

A
  • prerenal (55%)
  • intrinsic renal ARF (40%)
  • postrenal ARF (5%)
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8
Q

What is happening in pre-renal ARF?

A

the kidney is not receiving adequate blood flow, therefore the GFR begins to drop

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9
Q

The lack of or low quantity of RBCS or WBCS with ARF in a urinalysis suggests what?

A
  • prerenal ARF
  • arterial thrombosis or embolism
  • preglomerular vasculitiis
  • hemolytic urea syndrome or TTP
  • scleroderma crisis
  • postrenal ARF
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10
Q

Granular casts with ARF in a urinalysis suggests what?

A
  • acute tubular necrosis
  • glomerulonephritis or vasculiitis
  • interstitial nephritis
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11
Q

RBC casts with ARF in a urinalysis suggests what?

A
  • glomerulonephritis or vasculiitis
  • acute interstitial nephritis or glomerulonephritis rarely
  • malignant HTN
  • rarely interstitial nephritis
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12
Q

WBC casts with ARF in a urinalysis suggests what?

A
  • severe pyelonephritis

- allograft rejection

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13
Q

Eosinophiluria suggests what?

A
  • allergic interstitial nephritis

- atheroembolic disease

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14
Q

What three things on urinalysis can help differentiate between the type of ARF?

A
  • Uosm
  • Una
  • Fractional excretion of Na+
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15
Q

What Uosm, Una, and Fractional excretion of Na+ suggest prerenal ARF?

A
  • Uosm above 500
  • Una less than 10-25
  • Fractional excretion less than 1
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16
Q

What Uosm, Una, and Fractional excretion of Na+ suggest intrinsic ARF?

A
  • Uosm less than 250
  • Una more than 20
  • Fractional excretion more than 2
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17
Q

What things cause postrenal ARF?

A

old men typically with:

  • Prostate disease
  • Pelvic or retroperitoneal malignancies (often younger- cervical cancer)
  • Neurogenic bladder

anything that blocks urine flow

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18
Q

How is diagnosis of postrenal ARF made

A

by ultrasound (U/A not really remarkable)

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19
Q

What things cause pre-renal ARF?

A
  • Volume depletion (GI, renal, 3rd space loss) or CHF

-Shock from fluid losses, sepsis,
heart failure

-systemic or renal vasodilation

  • Hepatorenal syndrome
  • Renal Artery stenosis
  • Drugs that impair auto-regulation (NSAIDS)
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20
Q

Pathophyisology of prerenal ARF.

A

volume depletion activates baroceptors to release ADH, RAAS, and sympathetic input causing decreased renal blood flow, GFR, and urine output

21
Q

T or F. Hyaline casts are very non-specific but can be seen in PRE-renal ARF

A

T.

22
Q

What is the equation for fractional filtration of Na?

A

UNa *PCr/ PNa *UCr

23
Q

What is hepatorenal syndrome?

A

type of pre-renal ARF seen in cirrhosis patients where there is decreased BP despite increased extracellular fluid volume leading to edema

renal failure occurs because of vasoconstriction of the renal circulation and intense systemic arteriolar vasodilatation resulting in reduced systemic vascular resistance and arterial hypotension.

24
Q

T or F. In hepatorenal syndrome, the kidneys are structurally intact and histologically normal and urinalysis is usually normal

A

T.

25
Q

How does hepatorenal syndrome progress?

A

worsening azotemia and progressive oliguria that has a poor prognosis without liver transplant

26
Q

What happens in HRS?

A

Portal HTN leads to splanchnic vasodilation that decreases effective circulatory volume, activating the RAAS

27
Q

How is HRS diagnosed?

A

You must rule of other causes (NSAIDS, nephrotoxic drugs, contrast) and confirm that Una is below 10

And even then, there is usually a trial of simple volume infusion with albumin rule out a simple pre-renal syndrome

28
Q

How does the kidney respond to low GFR?

A

Autoregulation:
-It will dilate the afferent arterioles via prostaglandins (NSAIDS block this) and

-efferents will constrict via angio II action (blocked by ACEIs/ARBs)

29
Q

So what do ACEIs/ARBs do to GFR at low BPs?

A

The kidney can usually maintain GFR at low MAPs (80), but it will drop below to conserve volume BUT

On an ACEI you can no longer auto-regulate as well as GFR begins to drop at much high MAPs

Thus, ACEIs/ARBs can cause a form of pre-renal AKI in patients with BILATERAL renal artery stenosis

30
Q

Why would you check K+ levels once you start an ACEI or ARB?

A

decreased aldosterone leads to increased K+ via DCT effects

31
Q

T or F. NSAIDS can cause ARF in patients with normal health

A

T. BUT the use of NSAIDS would have to be incredibly high. Typically you’ll see this more often in patients with volume depletion, CHF, cirrhosis

Cox-2 inhibitors have similar intra-renal effects

32
Q

Intrinsic ARF can occur in any part of the nephron structure including the glomerular, tubular, and vascular. What are some causes of tubular intrinsic ARF?

A
  • Acute tubular necrosis (ATN)

- Acute Interstitial Nephritis

33
Q

What is acute tubular necrosis caused by?

A

caused by ischemic injury or toxic injury from radio contrast or meds

34
Q

What happens in acute tubular necrosis?

A

tubular epithelial cells die and fall off the BM

35
Q

Where does most ischemic acute tubular necrosis occur?

A

PT (S3 segment) and thick ALH

36
Q

Clinical clues of intrinsic acute tubular necrosis?

A

Muddy brown granular casts on urinalysis

SG of 1.010 and Uosm of 300

Una>20

Fractional excretion of Na >1%

37
Q

What BUN:Cr ratio favors pre-renal? ATN?

A

pre-renal: 20:1

ATN: 10-15:1

38
Q

How is ischemic ATN managed?

A
  • Restore perfusion (hard)
  • Avoid nephrotoxins
  • Provide supportive care
39
Q

What drugs can cause ATN?

A
  • aminoglycosides,

- amphotericin B

40
Q

What drugs can cause Acute interstitial nephritis?

A
  • penicillins,
  • cephalosporins,
  • sulfonamides,
  • NSAIDS
41
Q

Aminoglycoside Toxicity

A

10-20% receiving the drug will have rise in creatinine

Toxicity associated with dose and duration of therapy

42
Q

Why does aminoglycosides cause rise in creatinine?

A

It accumulates in proximal tubule cells and inhibits normal lysosomal function

43
Q

How can aminoglycosides toxicity be avoided?

A

1x daily (results in high urinary concentrations which exceed the reabsorptive capacity of the proximal tubule)

Careful monitoring of drug levels and minimizing duration of therapy

44
Q

How do contrast agents cause AKI?

A

Direct vasoconstrictive effects on arterioles and tubular toxicity

45
Q

What are the risk factors of AKI induced by contrast agents?

A

pre-existing renal disease,

heart failure,

hypovolemia,

high dose of contrast,

multiple closely spaced studies.

46
Q

How can you avoid AKI induced by contrast agents?

A
  • Lower dose of contrast and Avoidance of closely spaced studies
  • Avoid volume depletion by giving IV fluids before imaging
  • Avoid other nephrotoxins (NSAIDS, ACEIs)
47
Q

What is acute interstitial nephritis?

A

Intrinsic ARF - “Allergic” reaction in kidney-infiltration of interstitium with granulocytes (often eosinophils)

48
Q

What causes acute interstitial nephritis?

A

Most commonly caused by antibiotics (e.g. penicillins, cephalosporins, sulfa), NSAIDS.

49
Q

How does acute interstitial nephritis present?

A

Fever, rash, joint pain, increased eosinophils on CBC; possibly only renal dysfunction

UA with pyuria, +/- urine eosinophils

Renal Week 2 (13 decks)

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