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Renal > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What characterizes renal failure?

A

Impairment of the GFR, elevation of serum BUN/creatinine, decreased GFR leads to accumulation of substances and drugs normally excreted by the kidney.

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2
Q

How is acute kidney injury characterized?

A

Rapid: hours to days but 0.5 mg/dL increase in serum creatinine or increase of 50% over baseline.

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3
Q

T or F. Urine output is always decreased with AKI.

A

F: sometimes, but not always.

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4
Q

What is oliguria? Anuria?

A

Oliguria is defined as < 400 mL urine output in 24 hours whereas anuria is defined as < 100 mL.

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5
Q

How does AKI manifest?

A

It doesn’t. Usually asymptomatic and discovered on routine labs.

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6
Q

T or F. AKI is usually reversible if underlying disease is treated.

A

T

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7
Q

What are the 3 classifications of AKI? Briefly describe each.

A
  1. Prerenal: kidney structurally intact but is not receiving enough blood flow; urine is normal.
  2. Intrinsic Renal: something is damaging structures within the kidney.
  3. Postrenal: urine flow obstruction.
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8
Q

What is seen in the urine with intrinsic renal AKI?

A

Granular casts.

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9
Q

RBC casts are indicative of what?

A

Glomerulonephritis.

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10
Q

Eosinophiluria is indicative of what?

A

Allergic reaction in the kidney.

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11
Q

Postrenal AKI can be caused by what diseases?

A

Prostate disease, pelvic or retroperitoneal malignancies, neurogenic bladder.

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12
Q

How does a patient present with postrenal AKI?

A

Voiding complaints. PE may reveal distended bladder but probs not. Urinalysis will be unremarkable.

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13
Q

What are the 2 ways to diagnose postrenal AKI?

A
  1. Ultrasound: reveals dilated calyxes

2. Catheter: insert catheter and if alot of urine drains then you know it is postrenal

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14
Q

What are the causes of prerenal AKI?

A

Volume depletion (GI bleed etc), CHF, shock from fluid losses, sepsis, heart failure.

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15
Q

What are the 3 types of prerenal AKI?

A
  1. Hepatorenal Syndrome
  2. Renal Artery Stenosis
  3. Drugs that impair auto-regulation i.e. NSAIDS
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16
Q

What are the diagnostic clues of prerenal AKI?

A
  1. Fractional Na excretion < 1%
  2. Urine Na concentration < 25
  3. Urine osmolarity > 500
    Note: prerenal will activate RAAS, so Na is conserved thus all of this makes sense.
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17
Q

Hepatorenal syndrome occurs in what condition?

A

Liver cirrhosis.

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18
Q

What are the characteristics of hepatorenal syndrome?

A
  1. Decreased BP despite an increased ECFV
  2. Kidneys are structurally intact and urinalysis is usually normal
  3. Worsening azotemia and progressive oliguria
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19
Q

What is the only true curative treatment for hepatorenal syndrome?

A

LIver transplant

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20
Q

Briefly describe the pathophysiology of hepatorenal syndrome.

A

Portal HTN. Splanchnic vasodilation. Decreased effective circulatory volume. RAAS activation. Renal Na conservation and renal vasoconstriction leads to ascites and hepatorenal syndrome.

21
Q

How do you diagnose hepatorenal syndrome?

A

It is a diagnosis of exclusion. Must rule out other causes like NSAIDS, nephrotoxic drugs, contrast, etc. Urine sodium will be very low (< 10)- perform trial of volume infusion.

22
Q

T or F. Renal artery stenosis is only seen clinically if arteries are affected bilaterally.

A

T: if unilateral, the other kidney can compensate.

23
Q

In respect to afferent and efferent arterioles, how does the kidney maintain GFR?

A

Afferent arteriole vasodilated. Efferent arteriole vasoconstricted.

24
Q

What causes vasodilation of afferent arteriole?

A

Prostaglandins

25
Q

What causes vasoconstriction of efferent arteriole?

A

Angiotensin II

26
Q

What classes of drugs can cause a form of prerenal AKI in patients with bilateral renal artery stenosis?

A

ACE inhibitors or Angiotensin II blockers: impairs autoregulation by effing up constriction of efferent arteriole.

27
Q

What class of drugs can lead to AKI in patients with true volume depletion, CHF, or cirrhosis?

A

NSAIDS: they block PG synthesis thus blocking afferent arteriole vasodilation. Note, COX-2 inhibitors have similar intra-renal effects in those patients.

28
Q

Intrarenal AKI can be caused by defects in which 3 parts of the nephron? List their respective diseases.

A
  1. Glomerulus: post-strep GN, lupus, rapidly progressive GN, hepatitis related, IgA nephropathy
  2. Tubular: acute tubular necrosis, acute interstitial nephritis
  3. Vascular: vasculitis
29
Q

What are the 2 major causes of acute tubular necrosis?

A
  1. Ischemic injury (major)

2. Toxic injury from radiocontrast or medications

30
Q

What is seen histologically with ATN?

A

Tubular necrosis with denuding of renal tubular epithelial cells. Most ischemic injury in proximal tubules and thick ascending limb. Occlusion of tubular lumens with cells and casts.

31
Q

Why is the proximal tubule and thick ascending limb most susceptible to ischemic injury?

A

These segments have alot of ATP dependent transport.

32
Q

What are the 3 clinical clues to diagnosing ATN?

A
  1. Granular casts (muddy brown color)
  2. Urine Na > 20
  3. Fractional Na excretion > 1%
33
Q

In regards to BUN:Cr ratio, urinalysis, urine Na concentration, fractional Na excretion, and urine osmolarity, how do you distinguish prerenal AKI vs. ATN?

A

(prerenal vs. ATN format)

  1. BUN:Cr ratio: >20:1 vs. 10-15:1
  2. Urinalysis: hyaline casts vs. granular casts with tubular epithelial cells
  3. Urine [Na]: < 20 vs. > 25
  4. Fractional Na Excretion: 1%
  5. Urine Osm: > 500 vs. 300-350
34
Q

What causes the increased concentration of urea, creatinine, etc. in the blood in ATN?

A

Tubular cells are dying and there is leaking of tubular fluid back into the peritubular capillaries.

35
Q

Since there is no specific treatment for ATN, how is it managed?

A
  1. Restore perfusion
  2. Avoid nephrotoxins
  3. Supportive care
36
Q

What 2 classes of drugs can cause prerenal AKI?

A
  1. NSAIDS: by blocking PG synthesis

2. ACE Inhibitors: by inhibiting formation of Angiotensin II

37
Q

What 2 classes of drugs can cause ATN, an intrarenal AKI?

A
  1. Aminoglycosides (the “mycins”)

2. Amphotericin B

38
Q

What 4 classes of drugs can cause acute interstitial nephritis, another intrarenal AKI?

A
  1. Penicillins
  2. Cephalosporins
  3. Sulfonamides
  4. NSAIDS
39
Q

Describe aminoglycoside toxicity.

A

10-20% of patients will have rise in serum creatinine. Drug accumulates in proximal tubule cells. Drug inhibits lysosomal function. Toxicity is associated with dose and duration of therapy.

40
Q

How do you prevent aminoglycoside toxicity?

A

Once daily dosing results in high urinary concentrations which exceed the reasbsorptive capacity of the proximal tubule. Careful monitoring of drug levels and minimizing duration of therapy.

41
Q

How do contrast agents/dyes used in tomography cause AKI?

A

They directly vasoconstrict arterioles and are toxic to tubular cells.

42
Q

What are the risk factors for developing AKI with use of contrast agents?

A

Pre-existing renal disease, heart failure, hypovolemia, high doses, multiple closely spaced studies.

43
Q

How do you prevent contrast nephropathy?

A

Give lower dose of contrast agent. Avoid closely spaced studies. Avoid volume depletion by giving IV fluids. Avoid other nephrotoxins i.e. NSAIDS, ACE inhibitors, etc.

44
Q

Define acute interstitial nephritis.

A

Allergic reaction in the kidney characterized by infiltration of the interstitium by granulocytes (often eosinophils).

45
Q

Which classes of drugs commonly cause acute interstitiall nephritis?

A

The beta-lactams (penicillins, cephalosporins, sulfa drugs) and NSAIDS.

46
Q

What are the symptoms of acute interstitial nephritis?

A

Fever, rash, joint pain, increased eosinophils on CBC.

47
Q

Urinalysis of acute interstitial nephritis will reveal what?

A

Pyuria (pus in the urine) and eosinophils are usually seen in the urine.

48
Q

What are the 2 ways to prevent AKI?

A
  1. Avoid nephrotoxins

2. Assure good renal perfusion prior to contrast studies and surgery

49
Q

What are the 4 ways to provide supportive care to AKI patients?

A
  1. Avoid further injury
  2. Watch volume status and electrolytes
  3. Dialysis (in some cases)
  4. Wait for kidneys to get better

Renal (33 decks)

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