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Nephrology > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What is the definition of acute kidney injury

A

Decrease in creatinine clearance, resulting in sudden rise in BUN and creatinine

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2
Q

There are three general causes of acute kidney injury (i.e. failure). What are the three causes

A
  1. ) Prerenal azotemia - decreased perfusion
  2. ) Postrenal azotemia - obstruction
  3. ) Instrinsic renal disease - ischemia and toxins
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3
Q

Prerenal azotemia, where this is inadequate perfusion of the kidney despite having normal kidneys, is considered a kidney injury with a rise in BUN and creatinine and the BUN rising more. What are the causes of this (8 causes)

A
  1. ) Hypotension
  2. ) Hypovolemia
  3. ) Renal artery stenosis
  4. ) Relative hypovolemia (heart not pumping properly)
  5. ) Hypoalbuminemia
  6. ) Cirrhosis
  7. ) NSAIDS (constrict afferent arteriole) and ACE inhibitors (dilate efferent arteriole)
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4
Q

What are two drugs that can cause prerenal (decreased perfusion) azotemia

A
  1. ) NSAIDs (constricts afferent arterioles)

2. ) ACE inhibitors (dilates efferent arterioles)

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5
Q

Postrenal azotemia is an obstruction that damages kidney by blocking filtration at glomerulus. What are the causes

A
  1. ) Prostate hypertrophy
  2. ) Stone in ureter
  3. ) Cervical cancer
  4. ) Urethral stricture
  5. ) Neurogenic bladdar
  6. ) Retroperitoneal fibrosis - bleomycin, radiation, methylsergide
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6
Q

What is the general management of prerenal and postrenal azotemia

A

80% of causes and totally reversible by treating underlying cause

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7
Q

What is intrinsic renal disease

A

Another form of acute kidney injury. The most common is acute tubular necrosis from toxins or ischemia of kidney.

Other causes are

  1. ) Acute interstitial nephritis - penicillin
  2. ) Rhabdomyolsis and hemoglobinuria
  3. ) Contrast agents (happens quickly)
  4. ) Toxins - aminoglycosides, cisplatin, amphotericin, cyclosporine and NSAIDs (these just cause ATN, not acute interstitial nephritis)
  5. ) Hyperuricemia crystals, hyper oxalate crystals (ethylene glycol ingestion) and hypercalcemia
  6. ) Bence Jones Proteins (multiple myeloma)
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8
Q

No matter what the cause of acute kidney injury is (prerenal, postrenal, ATN), the presentations are essentially the same. How would a patient present depending on severity

A

N/V, tired, edema/shortness of breath from fluid overload

Severe: Confusion, hyperkalemia, pericarditis, with hyperkalemia and metabolic acidosis

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9
Q

No matter how well your guess for what the cause of acute kidney injury is, you must do laboratory testing to determine what the cause is, whether prerenal, postrenal, or ATN. What is the best initial test, and what are some hints that clue you in certain directions

A

Best initial test: SERUM BUN to creatinine ratio with renal ultrasound since no contrast required (not urinalysis).

If BUN:Creatinine is greater than 20 to 1, then either prerenal and postrenal.

Prerenal will have history of hypotension, while postrenal will have massive diuresis after catheter or distended bladdar or hydrophephrosis on sonogram

If BUN:Creatnine is around 15:1 or less, then think ATN. Kidney biopsy is never the right answer

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10
Q

After serum BUN and creatinine ratio is determined and you still do not know the cause, then what are your next steps for diagnostic studies

A

Urinalysis - main thing to do

Other options are urine sodium, fractional excretion of sodium, and urine osmolality. All of these help to determine further whether it is prerenal, postrenal, or acute tubular necrosis

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11
Q

If you were unsure and you got FENA and urine osmolality, explain how these will help you distinguish prerenal azotemia from ATN

A

If intravascular volume is low, ADH will rise and will reabsorb water, causing the urine to concentrate (urine osmolality goes up > 500). If intravascular volume is low, aldosterone will increase which will reabsorb more sodium, so sodium will be low in the urine (FENA less than 1 percent)

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12
Q

In the end, the distinguish prerenal azotemia from acute tubular necrosis, you can check BUN:creatinine, urine sodium, FENA, and urine osmolality. What are the summaries of numbers

A

Prerenal: BUN to creatinine > 20:1, urine osmolality 1%, urine osmolality

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13
Q

What does urine specific gravity mean

A

Correlates to urine osmolality - high UOsm = high specific gravity

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14
Q

Would you expect to see proteinuria in acute tubular necrosis

A

NO - only consider proteinuria if glomeruli are damaged, not if tubules are damaged

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15
Q

What is the time duration of acute tubular necrosis from CT contrast vs. toxic drugs

A
  1. ) CT contrast - immediate damage - treat with saline hydration
  2. ) Drugs - 5 to 10 days and need to be the ones that are renally cleared
  3. ) Contrast has different lab values from any other cause of acute tubular necrosis in that it causes spasm of afferent arteriole, causing tremendous reabsorption of sodium and water (like prerenal lab values) - treat with saline hydration
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16
Q

What is tumor lysis syndrome and why does it cause acute kidney injury

A

When you treat a tumor with radiation/chemotherapy that produces hyperuricemia, destroying the kidney

To prevent: Give allopurinol, hydration, and rasburicase (urate oxidase) that converts uric acid to allantoin

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17
Q

How does ethylene glycol cause acute kidney injury

A

Oxalate crystals precipitates in kidney tubules causing ATN, also consumes calcium so expect serum calcium values to be low - ENVELOPE shaped crystals (pg 231).

Remember that methanol, opiates (glomerulonephritis), do not cause acute kidney injury, but NSAIDs do

Treatment: Ethanol or fomepizole with dialysis

18
Q

How do nephrotoxins cause acute tubular necrosis

A

Damage is dose dependant, happens 5 to 10 days later, and the effect is worse if kidney is already hypoperfused or they have another conditions such as diabetes or hypertension.

Low magnesium levels increase risk of aminoglycoside/cisplatin toxicity

19
Q

What is rhabdomyolysis and how does it cause acute tubuler necrosis

A

Caused by trauma, immobility, crush injuries and seizures.

Best initial test: Urinalysis - dipstick positive for blood but on microscopy no blood, will have myoglobin - do urine test for myoglobin specifically. Damages tubular cells by myoglobin serving as an oxidant stress.

Check CPK levels which are elevated in rhabdomyolsis, but only myoglobin in UA will tell if ATN is happening

20
Q

What are the side effects of rhabdomyolsis

A
  1. ) Hyperkalemia - gets released from injured muscle cells - determine indirectly by DOING EKG immediately since this is the most important concern for these patients
  2. ) Hyperuricemia - uric acid released from injured muscle cells made from nucleic acids
  3. ) Hypocalcemia - calcium binds damaged muscle cells
21
Q

What is the treatment of rhabdomyolsis

A

Mainstay of treatment is to ensure that myoglobin has the least amount of time to contact tubular cells, so you want to give saline and mannitol for this. You also want to treat the hyperkalemia by giving bicarbonate infusion which will put bicarb back into cells

  1. ) Saline hydration
  2. ) Mannitol
  3. ) Bicarbonate infusion
  4. ) Don’t treat hypocalcemia, will return to normal on own
22
Q

Which treatments should not be used for ATN

A

Diuretics, steroids, low dose dopamine - would just treat symptoms, not reverse kidney failure so not right answer.

Always correct underlying cause of ATN instead

23
Q

Dialysis is a last resort therapy used for acute tubular necrosis should a complication that is life threatening arise that cannot be treated another way (i.e. hypocalcemia can be treated with calcium and vitamin D). What are potential life threatening complications of ATN

A
  1. ) Fluid overload - pulmonary edema
  2. ) Encephalopathy
  3. ) Pericarditis
  4. ) Metabolic acidosis
  5. ) Hyperkalemia - can cause cardiac arrest
24
Q

Which two medications that are potentially used for kidney can also cause hearing loss

A

Aminoglycoside and furosemide

25
Q

What is renal failure from hepatorenal syndrome

A

Renal failure secondary to liver failure even though kidneys are totally normal. This mimics prerenal azotemia with low urine sodium, fena > 20:1

26
Q

What is the treatment for hepatorenal syndrome

A

Albumin, midodrine, octeotride.

Only cure is liver transplant

27
Q

What is renal failure (AKI) from atheroemboli

A

Cholesterol plaques in aorta or near coronary arteries that are large and fragile, break off during catheter procedures

Symptoms: Blue/purple skin lesions in fingers/toes, livedo reticularis, ocular symptoms

28
Q

What would you see on diagnostic testing for atheroemboli

A

Eosinophilia and eosinophiluria, with low complements and elevated ESR.

Most accurate: Biopsy of skin lesion showing cholesterol crystals.

No treatment

29
Q

What is acute interstitial nephritis

A

Acute renal failure where tubules are damaged from antibodies and eosinophils as a reaction to drugs, infection, or autoimmune disorder

30
Q

What are the more common medications to cause acute interstitial nephritis

A

Penicillins, sulfa drugs (including furesomide and thiazides), phenytoin, rifampin, quinolones, allopurinol, PPI’s

31
Q

One interesting fact is that the same drugs that cause acute interstitial nephritis are also the same drugs that cause drug allergy and rash, steven johnsons, TEN, and hemolysis. What are the main organs affected by allergies

A

Skin, kidney, and red blood cells

32
Q

Aside from drugs (70%), what are some other causes of acute interstitial nephritis

A

Infections and autoimmune diseases: SLE, sjogren, sarcoidosis

33
Q

How would someone with acute interstial nephritis present

A

This time, look for fever and rash, as well as eosinophilia and eosinophiluria

34
Q

What do the diagnostic lab studies show for acute interstitial nephritis

A
  1. ) Elevated BUN:Creatinine but less than 20 to 1

2. ) White and red cells in urine- Do hansel and wright stain to identify eosinophils

35
Q

What is the treatment for acute interstitial nephritis

A

Resolves spontaneously by removing drug.

If creatninine continues to rise after cessation of drug, give steroid

36
Q

What is analgesic (NSAID) nephropathy and what are all the things it can present with

A
  1. ) Acute tubular necrosis
  2. ) Acute interstitial nephritis
  3. ) Membranous glomerulonephritis
  4. ) Vascular insufficiency (afferent constriction via inhibitiation of PG’s)
  5. ) Papillary necrosis
37
Q

What is papillary necrosis

A

Soughing off of renal papillae from NSAID’s or sudden vascular insufficiency. Look for NSAID use with already unhealthy (healthy people dont get this) such as diabetes, sickle cell disease, urinary obstruction, chronic pyelonephritis

38
Q

What is a common presentation of papillary necrosis and what can it be confused with

A

Sudden onset of flank pain with fever and hematuria

39
Q

What is the diagnostic test for papillary necrosis

A

UA showing red and white blood cells and necrotic kidney tissue.

Best test: CT scan showing abnormal kidney structure

40
Q

What is the treatment for papillary necrosis

A

None - can’t fix this

41
Q

The summary of tubular disease

A
  1. ) Acute
  2. ) Toxins include drugs, myoglobin, hemoglobin, oxalate, urate, NSAIDs, contrast
  3. ) No nephrotic syndrome or proteinuria
  4. ) Biopsy not needed to establish diagnosis
  5. ) Do not treat with steroids
  6. ) Correct hypoperfusion and remove toxin if present
42
Q

Crystal induced renal failure is a broad topic caused by many drugs. What are these drugs

A

1,) Ethylene glycol (antifreeze) - oxalate crystals (envelope)
2.) Acyclovir - drug itself precipitates - prevent by giving fluid with the drug

Nephrology (4 decks)

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