IE 3: DIKD

studied byStudied by 0 people
0.0(0)
learn
LearnA personalized and smart learning plan
exam
Practice TestTake a test on your terms and definitions
spaced repetition
Spaced RepetitionScientifically backed study method
heart puzzle
Matching GameHow quick can you match all your cards?
flashcards
FlashcardsStudy terms and definitions

1 / 20

encourage image

There's no tags or description

Looks like no one added any tags here yet for you.

21 Terms

1

What is the most common manifestation in Drug induced kidney injury?

  • Decline in glomerular filtration rate (GFR) which results in rise of Scr and BUN

New cards
2

Initial diagnosis of DIKD is delayed because what?

  • Bc it is based on detection of elevated Scr and BUN for which there is a temporal relationship between kidney injury and exposure to nephrotoxic drug

New cards
3

What causes hemodynamically mediated kidney injury? How do we prevent this?

  • ACEI and ARBs

  • NSAIDs and Selective COX2 inhibitors

  • Calcineurin inhibitors (Tacro and Cyclosporine)

New cards
4

How do ACEI cause kidney injury?

  • ACEI inhibit synthesis of angiotensin II which dilate the efferent arteriole → reduce outflow resistance and decrease GFR

New cards
5

How do NSAIDs cause kidney injury?

  • Constrict the AFFERENT ARTERIOLE → decrease GFR

New cards
6

Instead of NSAIDs and COX-2 inhibitors, what can you use?

  • AVOID indomethacin (potent)

  • Use APAP, nonacetylates salicylates, aspirin, and even nabumetone when anti inflammation needed

  • Tramadol (nonnarcotic analgesic) can be useful but do not provide anti-inflammatory activity

New cards
7

How do calcineurin inhibitors cause kidney injury?

  • Afferent vasoconstriction with reduced GFR

New cards
8

Aminoglycoside associated ATN is due to accumulation of high drug concentrations within what?

  • Within proximal tubular epithelial cells and subsequent generation of reactive oxygen species that produce mitochondrial injury → cellular apoptosis

New cards
9

What causes acute tubular necrosis in aminoglycosides?

  • Number of cationic groups (-NH2)

    • Neomycin, gentamycin, tobramycin, amikacin

    • The number of cationic groups on the drug appears to correlate to nephrotoxicity → Neomycin is most toxic because it has the most NH2 groups

New cards
10

How does radiographic contrast media cause nephrotoxicity? What are risk factors?

  • Renal ischemia results from systemic hypotension and nephrptoxiity and simultaneous acute vasoconstriction caused by disruption of normal prostaglandin synthesis

  • Cellular toxicity is also related to duration of tubular cell exposure to contrast

    • Risk factors: GFR <60, concurrent use of NSAIDs, ACEI, aminoglycosides

New cards
11

How does Cisplatin cause nephrotoxicity?

  • Tubular cell injury and death via necrosis and/or apoptosis

    • Accumulation in proximal tubular epithelial cells

New cards
12

If you have cisplatin nephrotoxicity, what can you do for prevention?

  • Dose reduction and decreased frequency of administration

  • Use of hypertonic saline (3% saline) to reduce tubular cisplatin uptake

  • Amifostine, an organic thiophosphate that is converted to active metabolite can reduce the Cisplatin nephrotoxicity

New cards
13

What is the pathogenesis of amphotericin B neprhotoxicity?

  • Direct tubular epithelial cell toxicity → interaction of amphotericin B with ergosterol in cell membrane → necrosis of proximal tubular cells

  • Exacerbated by ischemic injury which is result of reduction in renal blood flow and GFR bc vasoconstriction

New cards
14

What is characteristic of glomerular disease?

  • Proteinuria, particularly nephritic range PROTEINURIA (urine protein greater than 3.5 g/day per 1.73 m²) with or without a decline in the GFR is hallmark

New cards
15

In tubulointerstitial disease, what drug can cause chronic interstitial nephritis?

  • Lithium

New cards
16

What is the pathogenesis of lithium?

  • Lithium induced nephrogenic diabetes insipidus: lithium reduces the kidney’s ability to concentrate urine → lithium down regulates aquaprin 2 water channel expression

New cards
17

For tubulointersititial disease, what is the pathogenesis of aristolochic acid?

  • Aristolochic acid is metabolized to mutagenic compounds called aristolactam 1 and II → from aristolochic acid DNA adducts in humans → DNA damage and apotosis

New cards
18

In tubulointersititial disease, what is papillary necrosis?

  • Necrosis of renal papillae → collecting ducts enter renal pelvis which leads to progressive kidney disease

New cards
19

In Obstructive nephropathy, what is intratubular obstruction? (Direct)

  • Direct means precipitation of the drug itself

    • Acyclovir, Foscarnet complexation with CALCIUM ION

    • Indinavir, Sulfadiazine, methotrexate may precipitate in acidic urine

New cards
20

In Obstructive nephropathy, what is intratubular obstruction? (Indirect)

  • Antineoplastic drugs: intratubular precipitation of uric acid crystals

  • HMG-CoA reductase inhibitors or statins: intratubular precipitation of myoglobin (drug induced rhabdo)

  • Warfarin: RBCs

New cards
21

What is the pathogenesis in nephrocalcinosis for obstructive neprhopathy?

  • extensive tubulointerstitial precipitation and deposition of calcium phosphate crystals leading to marked tubular calcification. associated with hypercalcemia and hypercalciuria

New cards
robot