IE 3: DIKD

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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

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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

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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)

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4

How do ACEI cause kidney injury?

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

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5

How do NSAIDs cause kidney injury?

  • Constrict the AFFERENT ARTERIOLE → decrease GFR

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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

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7

How do calcineurin inhibitors cause kidney injury?

  • Afferent vasoconstriction with reduced GFR

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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

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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

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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

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11

How does Cisplatin cause nephrotoxicity?

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

    • Accumulation in proximal tubular epithelial cells

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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

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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

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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

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15

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

  • Lithium

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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

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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

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18

In tubulointersititial disease, what is papillary necrosis?

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

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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

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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

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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

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