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Clin Med GI > Acute Kidney Injury (INC) > Flashcards

Acute Kidney Injury (INC) Flashcards

1
Q

What are the three types of acute kidney injuries?

A

Prerenal: something that goes into the kidney is the issue. Caused by renal hypoperfusion
Intrarenal: the kidney itself is the issue. Direct injury to 1+ renal structures
Postrenal: (rarest), there is something DOWNSTREAM of the kidney causing a problem. Caused by obstruction of urinary flow

There is some overlap though

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2
Q

What is wrong with Prerenal Azotemia? What are 3 examples of these.

A

Inadequate renal perfusion

  1. Hypovolemia
  2. Decreased Cardiac Output (have enough blood, but the kidney is not getting enough blood)
  3. Change in vascular resistance
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3
Q

What are some examples of changed vascular resistance that can lead to prerenal azotemia?

A

￬ - sepsis, anaphylaxis, anesthesia
￪ - epinephrine, high-dose dopamine, renal artery stenosis
Meds that interfere with renal vascular autoregulation
NSAIDs, iodinated contrast, ACEIs/ARBs

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4
Q

If there is decreased perfusion pressure, leading to less blood in kidneys, what is the body’s response?

A

Increased angiotensin 2 (constricts efferent) and increased vasodilatory prostaglandins (dilates afferent)

Both maintain GFR but work on other parts - meds can interfere with this!

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5
Q

What is the MOA of NSAIDs and ACE inhibitors/ ARBs on the kidney? What is the resulting GFR?

A

NSAIDs block vasodilatory prostoglandins in the afferent arteriole, leading to an increase in the release of angiotensin II (constricting efferent), but still overall reduction in GFR

ACE inhibitors and ARBs decrease angiotensin II, leading to a slight increase in vasodilatory prostoglandin release, but still overall reduction in GFR

Both lead to reduced GFR by
1. NSAIDs leading to less vasodilation of AFFERENT and
2. ACE-I and ARBs leading to less vasoconstriction of EFFERENT

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6
Q

What happens to the GFR and BUN in prerenal azotemia? What happens to sodium if oliguric?

A

￬ GFR ￪ BUN/Cr with BUN:Cr ratio > 20:1 usually

If oliguric, there should be a low fractional excretion of sodium (FENa+) in the urine - <1%

Reabsorbing urea and sodium to retain fluid (water). Remember, the kidneys are still functional, so sodium retention is possible. This leads to a Urine osmality that is normal (>500).

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7
Q

What is urinary sediment in prenrenal azotemia, what can sometimes happen? What protein does this come from?

A

usually normal, may see hyaline casts (means that there is not movement of fluid, leading to highlight of tubules, normally benign)
Formed from Tamm-Horsfall mucoprotein secreted by tubule

Horsfall = hyaline

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8
Q

What are the S/S of prerenal azotemia depending on the stage?

A

Uremia is possible (depending on stage)
Signs of cause - vary, may include:
Dehydration (decreased skin turgor) and/or hypovolemia
Arrhythmias, cardiomegaly (to try to pump blood)
Sepsis
Nonspecific diffuse abdominal pain and ileus (no bowel movement)
May see decreased urine output (d/t hypovolemia)

symptoms are NOT that helpful, but labs are

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9
Q

What is the treatment for prerenal azotemia reliant on?

A

Resolve the underlying cause:
1. Maintain euvolemia
2. Correct abnormal electrolytes
3. Avoid nephrotoxic drugs

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10
Q

Should kidney function in prerenal azotemia normalize if we restore the blood flow to the kidneys?

A

YES, because it does not directly involve dmg to the kidneys

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11
Q

What do you see in postrenal obstruction? What are some common complications that can cause this?

A

Obstruction leads to elevated intraluminal pressure leading to damaged renal parenchyma

This obstruction of urethra, bladder, ureters, or renal pelvises is often d/t:

  1. BPH in men (MC cause)
  2. Devices Obstructed Foley catheter
  3. anticholinergic medications (slows down bladder and decreases peristalsis d/t blocking parasympathetic response)

Rare things such as blood clots, stones, cancer, etc.

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12
Q

What are the s/s of postrenal obstruction and what can be used to look for this?

A

S/S: Anuria or polyuria possible
May have lower abdominal pain
May see large prostate, distended bladder, pelvic/abdominal mass
Bladder catheterization and/or abdominopelvic
US can be helpful to look for hydroureter and obstruction

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13
Q

What does a normal renal US look like compared to diseased?

A

The diseased kidney looks dark in areas where there is backup

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14
Q

What are the lab findings for postrenal obstruction? How about urine sediment?

A

￬ GFR and ￪ BUN/Cr with BUN:Cr > 20:1 usually

Sodium varies
Urine osmolality - 400 mosm/kg or less (d/t obstruction impairing the kidney’s ability to concentrate the urine)
Urine sediment - often normal; may see RBCs, WBCs, crystals

depends on underlying condition!

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15
Q

What are some areas that can lead to intrinsic kidney injury? What often leads to this?

A

Direct damage to the tubules, glomeruli, interstitium, vasculature

prerenal azotemia often leads to tubular injury because there is not enough O2 for them to survive.

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16
Q

What are the 3 major forms of intrinsic kidney injury? What is the MC one of these?

A

Acute Tubular Necrosis (MC)
Acute Glomerulonephritis
Acute Interstitial Nephritis

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17
Q

What are the three causes of acute tubular necrosis?

A
  1. Ischemia (death d/t reduced blood flow)
  2. Nephrotoxins (exogenous and endogenous, with exogenous is the worse)
  3. Sepsis - causes both hypoperfusion and direct injury
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18
Q

What are the exogenous nephrotoxic antimicrobials? Which is the least nephrotoxic?

A

Aminoglycosides (1/3 times patients will be nephrotoxic, typically w/in 5-7 days and damage can continue up to 30 days), streptomycin is the least though
Amphotericin B (ampho terrible)

try to use others

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19
Q

What are some other exogenous nephrotoxins?

A
  1. Radiographic contrast media (can increase fluid to reduce the concentration of this)
  2. Chemotherapy (methotrexate, cyclosporine, cisplatin)
  3. Environmental toxins in workplace hazards (heavy metals, insecticides/herbicides)
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20
Q

What are some endogenous nephortoxins? What can cause this?

A

Myoglobinuria - due to rhabdomyolysis, muscle necrosis

Often crush injuries

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21
Q

How do you tell the difference between mygoglobinurea and hemoglobinurea?

A

Same: Both lead to a positive urine dipstick for hemogloblin (which is a false positive in the case of myoglobinurea), both lead to dark brown urine.

Different: Myglobinurea has no RBCs on microscopy. Often seen with creatine kinase > 20,000-50,000 IU/L d/t crush injury

22
Q

How do you treat myglobinurea?

A

REHYDRATION

treatment of Hypocalcemia if symptomatic (trousseaus, twitching, etc). Typically self-corrects after hydration

possibly Hyperkalemia, hyperphosphatemia, hyperuricemia

23
Q

What are the three other endogenous nephrotoxins other than myglobinurea? How to treat

A
  1. Hemoglobinuria: Tx - Reversal of underlying disorder, hydration
  2. Hyperuricemia: in rapid cell turnover and lysis. Usual cause - chemo for germ cell neoplasms, leukemia, lymphoma
    Intratubular deposition of uric acid crystals
    Serum uric acid often > 15-20 mg/dL
    Medications to lower uric acid level can help
  3. Bence Jones Protein, in multiple myeloma, which is directly toxic by obstructing tubule. Correct the cancer
24
Q

What are the S/S of Acute tubular necrosis (ATN)?

A

Not helpful

Signs of underlying cause
May see arrhythmias, abdominal pain, uremia
Oliguric or nonoliguric

25
Q

What are the labs of ATN? What is the urinary sediment - and how do you know that there is tubular necrosis?

A

Hyperkalemia (d/t less exchange with sodium in tubules) and hyperphosphatemia (d/t less excretion of phosphate) are common
￬ GFR and ￪ BUN/Cr with BUN:Cr < 20:1 usually
Urine sodium is often elevated (d/t not being able to reabsorb)
Urinary sediment - pigmented granular casts or “muddy brown” casts (think muddy drainage tube), renal tubular cells, epithelial cell casts

26
Q

What do you see for BUN:Cr ratio and urine sodium in ATN? What does this mean?

A

Decreased BUN:Cr ratio (meaning there is less urea in the blood) and high urine sodium d/t inability to reabsorb sodium and urea

27
Q

What is worse, oliguric or non-oliguric ATN? Why?

A

Oliguric, because there is concern of build up of toxins

28
Q

How do you treat ATN? What are some dietary changes?

A

Avoid volume overload (because the kidneys will have trouble processing too much fluid)
Use loop diuretics if volume overloaded
Dietary changes include protein restriction, ￪or ￬ dietary phosphate, calcium, magnesium depending on status

29
Q

What is the prognosis of ATN?

A

May never go back to full kidney function
20-50% mortality and up to 70% require dialysis
non-oliguric have better long-term outcomes though

30
Q

What allows us to know that there are in a maintanence ATN?

A

The BUN/Cr levels off and does not get worse

31
Q

Why will they not go back to basic renal function in ATN?

A

Lost too many nephrons

32
Q

What are the five lab findings you may see in ATN

A
  1. myglobinuria (endogenous nephrotoxin)
  2. Uric acid crystals (endogenous nephrotoxin)
  3. Bence-Jones proteins (endogenous nephrotoxin)
  4. Muddy brown/ granular cells (indicative of tubular injury)
  5. Renal epithelial cell casts (indicative of tubular injury)
33
Q

What often leads to Acute Glomerulonephritis?

A

It is an Intrinsic glomerular AKI

Most are nephritic (involving inflammation)
A few are nephrotic (minimal inflammation, proteinuria) - usually seen more in chronic cases

Involve inflammatory glomerular lesions
Crescent lesions - severe breaks in glomerular walls (think about the shape)

34
Q

What is the classic presentation of Acute Glomerulonephritis

A

HTN, edema (periorbital or scrotal d/t low tissue tension), and urine containing protein, RBCs, WBCs, and RBC casts (because breaks in capillary walls allow protein to cross)

35
Q

What are the 5 types of Acute Glomerulonephritis? How do you distinguish each?

A
  1. Immune Complex Deposition - when antigen excess over antibody production occurs

Antigen-antibody complexes lodge in glomerular basement membrane (GBM)
Complement activation to resolve complexes → destruction of GBM

Often lupus, endocarditis, and streptococcus

  1. Anti-GBM-associated acute glomerulonephritis Autoantibodies against glomerular basement membrane (GBM)
    May be confined to kidney or involve lungs as well. Goodpasture’s Syndrome - renal + pulmonary involvement
  2. C3 Glomerulopathy: leads to deposits. Caused by abnormalities in the alternative complement pathway (little role of Ig unlike others) happens in acute flare, so you may see normal C3 levels, but you can see low serum C3 in acute problems
  3. Monoclonal Ig-Mediated Glomerulonephritis: there are so many antibodies that float around for no good reason and cause destruction of basement membrane, can use Serum Protein Electrophoresis (SPEP) can help identify, as well as other tests like immunofixation and free light chain analysis
  4. Pauci-Immune Glomerulonephritis, CELLS cause the problems. Cell-mediated immune response.

Other causes: hypertensive emergencies, thrombotic microangiopathies (HUS, TTP)

36
Q

What acute glomerulonephritis type involves Antigen-antibody complexes being lodge in glomerular basement membrane (GBM)? How does this result in injury? What can cause this?

A

Immune Complex Deposition - when antigen excess over antibody production occurs

when these antigen-antibody complexes get lodge into the GBM, the complement system is activated to resolve this, leading to destruction of GBM
Often caused by streptococcus, endocarditis, and lupus

37
Q

What acute glomerulonephritis type involves autoantibodies that directly attack the GBM? What can this lead to?

A

Anti-GBM-associated acute glomerulonephritis

Can also lead to pulmonary hemorrage, known as Goodpasture’s Syndrome - having renal + pulmonary involvement (think of the autoantibodies not knowing what to target)

38
Q

What acute glomerulonephritis type involves abnormalities in the alternative complement pathway? When do you notice issues?

A

C3 glomerulopathy
There is minimal role of Ig, but involves C3 deposition into the glomerulus, and overall less C3 in the blood as a result. Often seen in acute flares.

39
Q

What acute glomerulonephritis type does not involve excess antigens, but involves Ig? How do you identify this?

A

Monoclonal Ig-Mediated Glomerulonephritis - where Monoclonal Ig deposited in GBM and/or tubular basement membrane, but no excess amounts of antigen as seen in immune complex GN

Serum Protein Electrophoresis (SPEP) can help identify, as well as other tests like immunofixation and free light chain analysis d/t monoclonal gammopathies

40
Q

What acute glomerulonephritis type does not involve immune complexes or Ig binding, but instead involves cell-mediated immune response? What additional manifestations can you see in this case?

A

Pauci-Immune Glomerulonephritis - small-vessel vasculitis associated with ANCAs

Can see manifestations in other areas of the body (lungs, skin, upper airway)

41
Q

Other than the 5 main types of acute glomerulonephritis, what are some other causes?

A

Hypertensive emergencies, thrombotic microangiopathies (HUS, TTP)

42
Q

Why are 2 reasons that you see swelling in Acute Glomerulonephritis?

A

Retaining sodium, peeing out protein (water moves out of blood vessels into the tissues)

43
Q

What lab findings clue us into Acute Glomerulonephritis?

A

Protein in urine
More RBCs
Complement level differences
Anti-strep titers
anti-GBM antibodies
SPEP
P-ANCA and C-ANCA levels
Other general autoimmune labs - CRP, ESR, ANA

Order all of these if you suspect

44
Q

What is the treatment of Acute Glomerulonephritis?

A

Underlying issues!

Steroids to calm down immune system
Sometimes cytotoxic agents
Plasma exchange to get rid of bad things floating around

45
Q

What is Acute Interstitial Nephritis and what is the MC cause of this?

A

10-15% of intrinsic AKI

MC is meds

It is an Interstitial inflammatory response

46
Q

What are the MC medications that cause Acute Interstitial Nephritis?

A

Antimicrobials (MC)

diuretics, NSAIDs, rifampin, anticonvulsants, allopurinol, PPIs, H2 blockers

47
Q

Besides meds, what can cause Acute Interstitial Nephritis?

A

Infections (bacterial, viral, and fungal)
Immunologic: SLE, Sjogren’s, sarcoidosis, etc.
Rare others: allergic reaction, collagen vascular disease

48
Q

What is the classic triad of acute interstitial nephritis, and what percent show all three?

A

fever, rash, arthralgia
All 3 only present in 10% of pts

49
Q

What does a CBC and urinary sediment show for acute interstitial nephritis? What does biopsy show?

A

CBC = eosinophilia
Urine sediment: minimal protein, WBCs (95%), WBC casts
Biopsy: inflammatory cells within renal interstitium

50
Q

Treatment of acute interstitial nephritis and prognosis

A

removal of cause, supportive care
May use course of IV or oral corticosteroids if renal injury persists after agent is removed
Urgent dialysis may be necessary in up to ⅓ of all pts

Prognosis:
Recovery over weeks to months
May have slightly better outcomes than other AKI causes

51
Q

What imaging do you typically use for AKI? What do you typically see? What are some other imaging modalities you can use?

A

Abdominal/Pelvic US
typically normal sized kidneys

Can also do -
Urethral Cath - r/o urethral obstruction
Bladder Scan - r/o urethral obstruction

52
Q

When do you do a kidney biopsy How do you do this? What does a biopsy show?

A

Some weird glomerulonephritis, vasculitis, interstitial nephritis, etc.
Numb the outside of the skin.
The patterns of biopsy allow you to see what type of AKI it is.

Clin Med GI (10 decks)

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