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CRRAB II Week 3 > SIM Renal Failure > Flashcards

SIM Renal Failure Flashcards

1
Q

How do you determine if someone has intrinsic vs. pre-renal vs. post-renal failure?

A

It is intrinsic if there is no evidence of the other two (pre or post)

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2
Q

What is pre-renal failure?

A

Reduced blood flow to kidneys

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3
Q

What is post-renal failure?

A

Obstruction of urine flow

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4
Q

What tells us the patient didn’t have chronic renal failure?

A

She had a normal Cr 1 month ago.

She has few risk factors for CKD (only age, HTN)

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5
Q

What tells us the patient likely has acute renal failure?

A

Normal HCT, absence of renal cortical thinning on CT, oliguria, timing

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6
Q

What is the DDX for intrinsic renal disease?

A
  • Glomerulonephritis
  • Interstitial nephritis
  • Tubular disease
  • Vascular disease
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7
Q

What findings are consistent with a tubulointersitial process?

A
  • Proteinuria
  • Pyuria
  • Casts
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8
Q

What do patients with glomerulonephritis usually have in their urine?

A
  • Red cells

- Red cell casts

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9
Q

What is interstitial nephritis characterized by?

A

Inflammation & scarring of tubules & interstitial spaces with sparing of glomeruli and vasculature

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10
Q

What are the three categories of interstitial nephritis?

A
  1. Immune-mediated
  2. Infection-mediated
  3. Idiopathic
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11
Q

What are examples of immune-mediated interstitial nephritis?

A
  • Drug hypersensitiivity
  • W/Glomerulonephritis
  • W/out Glomerulonephritis
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12
Q

What immune-mediated interstitial nephritis includes glomerulonephritis?

A

Lupus

IgA nephropathy

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13
Q

What immune-mediated interstitial nephritis doesn’t include glomerulonephritis?

A

Sarcoid, Sjogren’s, Transplant rejection

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14
Q

What are examples of Infection-mediated interstitial nephritis?

A
  • Pyelonephritis
  • Post-infectious
  • Granulomatous disease
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15
Q

What are examples of post-infection interstitial nephritis?

A

Streptococci, staphylococci, diphtheria, legionella, yersinia, leptospira, mycobacterium, mycoplasma, rickettsia, syphilis, toxoplasmosis, and numerous viruses (EBV, HIV, CMV)

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16
Q

What are examples of granulomatous disease interstitial nephritis?

A

TB, sarcoid

17
Q

What types of drugs are associated with interstitial nephritis?

A
  • Antibiotics
  • Diuretics
  • Nonsteriodal anti-inflammatory drugs (NSAIDS)
  • Others
18
Q

What antibiotics are associated with interstitial nephritis?

A
  • Penicillins
  • Cephalosporins
  • Sulfonamides
  • Fluoroquinolones
  • Rifampin
  • Trimethoprim
19
Q

What Diuretics are associated with interstitial nephritis?

A
  • Furosemide (lasix)

- Thiazide-type diuretics

20
Q

What “other” drugs are associated with interstitial nephritis?

A
  • Allopurinol (Zyloprim)
  • Cimetidine (Tagamet)
  • Phenytoin (Dilantin)
  • Proton pump inhibitors (PPIs)
  • 5-aminosalicylates
  • Protease inhibitors
  • Lithium
  • Carbamazepine
21
Q

What features of the SIM patient were consistent with interstitial nephritis associated with NSAID use?

A
  • Addition of ibuprofen (recent)
  • Pruritis (skin hypersensitivity)
  • UA results
22
Q

What makes NSAIDs a more likely cause than Thiazide?

A

Eosinophilia

-Can’t complete exclude thiazides though

23
Q

What percentage of NSAID induced interstitial nephritis requires dialysis?

A

1/3 of cases

24
Q

What are key features of NSAID induced interstitial nephritis?

A
  • Rash
  • Eosinophilia (40% of cases)
  • Hematuria (40% of cases)
  • Pyuria
  • Eosinophiluria
  • Proteinuria
  • Renal failure (may require dialysis)
  • Nephrotic syndrome (70% of cases - develops over time - protein spilling due to damage to kidneys)
25
Q

What causes NSAID induced hyponatremia?

A
  1. NSAIDs inhibit prostaglandins production
  2. Role for prostaglandins in water balance
  3. Antagonizes ADH
  4. Inhibits Cl- transport in thick ascending limb of LoH
  5. Regulates medullary blood flow
26
Q

What caused the hypokalemia in this case?

A
  • Likely caused by hydrochlorothiazide

- May be worse due to vomiting

27
Q

What is the mechanism behind drug induced interstitial nephritis?

A
  1. CD4+ T-cell mediated reactivity
    OR
    CD8+ cytotoxic T-cell mediated tubular damage
  2. Antigen is likely the drug or drug metabolite attached to autologous macromolecules
    [BC it stops when drug is stopped, it’s less likely to be an autoimmune condition]
28
Q

How was this case of NSAID induced interstitial nephritis treated?

A

Dialysis x3, corticosteroids

29
Q

How did the case resolve?

A

Renal fxn improved and returned to normal over 3 weeks. Prednisone was stopped and kidney fxn remained normal.

CRRAB II Week 3 (10 decks)

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