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CRRAB II > PBL W3 > Flashcards

PBL W3 Flashcards

1
Q

What does a renal biopy show for acute drug induced interstitial nephritis?

A
  • edema w/interstitial lymphoplasmocytic infiltrate
  • no glomeruli involvement
  • eosinophils prominent.
  • edema w/mild tubulointerstitial fibrosis - lymphocytes and plasma cells present.
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2
Q

What are the side effects of furosemide?

A
  • Ototoxicity
  • HYPOkalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout
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3
Q

What is the issue with using BOTH furosemide and ibuprofen (NSAIDs)?

A
  • Furosemide normally stimulates PGE release for vasodilation. NSAIDs inhibit this and make them less effective.
  • NSAIDs then constrict the afferent tubule reducing the flow. Could cause renal ischemia.
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4
Q

What is the spectrum of causes for acute interstitial nephritis?

A
  • antibiotics
  • NSAIDs
  • diruetics
  • anticonvulsants
  • Bacteria
  • Viruses
  • Mycoplasma
  • Sjogren’s
  • Lupus
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5
Q

What is the mechanism for the peripheral edema with renal failure?

A
  • Serum albumin is decreased due to loss through the glomerulus.
  • Oncotic pressure of the vessel goes down.
    • Less reabsorptive forces.
  • P capillary increases - more filtration.
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6
Q

Why do we see eosinophils with acute interstitial nephritis?

A
  • IL-5 and IgG lead to increased mast cells and eosinophil recruitment.
  • NSAIDs creates more leuoktrienes, that leads to increased eosinohpil survival.
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7
Q

What are the symptoms of acute intersitital nephritis?

A
  • fever
  • Rash
  • Joint pain
  • Eosinophilia (increased serum IgE)
  • MILD proteinuria
  • hematuria
  • pyuria - pus in the urine

Coud lead to acute renal failure

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8
Q

What are changes in the labs you see w/acute interstitial nephritis?

A
  • increased creatinine
  • granular and epithelial casts
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9
Q

What is the pathogensis of nephritis syndrome?

A
  • T cells and cytokines cause podocytes to lose negative charge, in addition to damage.
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10
Q

What are the symptoms of nephritic syndrome?

A
  • Proteinuria - >3 grams of protein lost per day in urine
  • Hypoalbuminemia - serum albumin less than 3gm/dL
  • Generalized pitting edema
  • hyperlipidema & hypercholesterolemia
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11
Q

What causes hyperlipidemia with nephritic syndrome?

What do you see in the urine?

A
  • LOW serum protein –> reactive hepatitis protein synthesis in the liver –> makes lipoproteins and decreaes catabolism –> increases serum cholesterol and LDL
  • Can cause loss of HDL
  • urinanalysis - shows FATTY CASTS
    • ​maltese interference pattern under UV light
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12
Q

What are the drugs that can cause acute interstitial nephritis?

use pneumonic.

A
  • Please Note All Drugs That Can Possibly Scar Renals
  • penicillin derivatives - methicillin
  • NSAIDs
  • Allopurinal
  • Sulfa derived diuretics - thiazides, furosemides, acetazolamide
  • Cephalosporins
  • Proton pump inhibitors
  • Sulfonamide antibiotics
  • Rifampin
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13
Q

How should you treat drug-induced interstitial nephritis?

A
  • REMOVE DRUG that is offending agent
  • Treatment is supportive - hydration, symptom relief, removal of drugs
  • Corticosteroids if SEVERE
    • 1mg/kg for 2-3 wks followed by tapering of PREDNISONE.
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14
Q

What is the urine albumin/creatinine used for?

How do you calculate it?

A
  • used to determine if nephritic syndrome
  • compare urine protein to urine creatinine
    • patients was 100/50 = 2
    • If > 2 - significant proteinuria - estimated 24 hour urine is 2 grams
    • If <1 it isn’t significant
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15
Q

How do you determine if its nephritic syndrome?

A

Do a urine albumin/creatinine ratio

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16
Q

What is the FeNa used for?

A
  • Pre-renal vs. renal disease

urineNa x plasmaCr x 100/ UrineCr x plasmaNa

  • If FeNa < 1% = pre-renal
  • If FeNa >1% = ATN
17
Q

What is the Bun: Cr used for?

A
  • determining pre-renal vs. renal disease
  • Normal ratio is 15:1
    • if greater than 15:1 it’s pre-renal
  • Pre-renal has excessively increased BUN
18
Q

What are 2 tests you can do to determine if pre-renal or renal disease?

A
  • FeNa
  • Bun:Cr
19
Q

What are some of the renal toxicity of NSAIDs?

A
  • Inhibit prostaglandins - decrease renal blood flow –> ischemic necrosis
  • Increase Na reabsorption –> peripheral edema - really exacerbates the edema
  • divert AA passage to produce leukotrienes –> increases vascular permeability in capillaires and glomerulus –> proteinuria + interstitial nephritis
20
Q

What is a truncating variant? How does it relate to EMP2?

A
  • truncating variant shortens the coding sequence of a gene
  • should be 167 amino acids, however, it is Glu62 - stops at amino acid 62.
21
Q

What are missense mutations?

A
  • change in single nucleotide
  • Phe7leu
    • ​Phe at amino acid 7 was changed to leucine
22
Q

How do we know if the EMP2 protein sequences are conserved?

A
  • compare with mouse at blast sequence - if over a bunch of sequences, the Phe7leu at amino acid never changes, it’s conserved evolutionarily
23
Q

What is the potential protein that can be mutated with nephritis syndrome?

A
  • EMP2
    • epithelial membrane protein 2
24
Q

How does EMP2 affect the kidney?

A
  • acts on keviolin 1
  • decreases podocytes & epithelial cells
  • allows albumin to enter the urine through the glomerulus
    • MORE CHILDHOOD CAUSE
25
Q

What is the most genetically signficant renal disease?

A
  • Polycystic kidney disease
26
Q

When should you do a renal biopsy w/drug induced interstitial nephritis?

A
  • acute renal failure
  • exposure while off meds
  • RASH
  • fever
  • arthralgia

contraindications

  • solitary kidney
  • bleeding
27
Q

How can you diagnose drug-induced interstitial nephritis?

A
  • Urinanalysis - check sodium
  • Urine albumin - will be increased
  • renal ultrasound - could indicated renal disease w/increase echogenicity
  • renal biospy

CRRAB II (26 decks)

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