Drug induced renal disease Flashcards

1
Q

When should nephrotoxic drugs be avoid in patients

A

already existing renal insufficiency, already on nephrotoxic medications, intravascular volume depletion, elderly

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2
Q

What are the two types of drug induced renal disease

A

pseudo renal disease, drug induced renal disease

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3
Q

What are the three sub categories of drug induced renal disease

A

prerenal, intrinsic, obstructive

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4
Q

What is the main cause for pseudo drug induced renal disease

A

increased SCr due to competitive inhibition of creatinine secretion within the proximal tubule

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5
Q

What are two drugs that are known to cause pseudo drug induced renal disease

A

Trimethoprim and Dronaderone

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6
Q

What is the pathophysiology of pre renal AKI

A

Reduction in renal blood flow

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7
Q

What are drugs that can cause pre renal AKI

A

Loop diuretics, ACEIs and ARBs, NSAIDs, cyclosporine and tacrolimus

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8
Q

How can loop diuretics lead to pre renal AKI

A

Too high of dose can lead to dehydration leading to decreased intravascular volume

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9
Q

How can NSAIDs lead to pre renal AKI

A

NSAIDS block prostaglandin mediated vasodilation leading to afferent arteriolar vasoconstion lead to less blood for the glomerulas

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10
Q

What drug class can worsen how NSAIDs cause AKIs

A

ACEIs and ARBs

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11
Q

How do tacrolimus and cyclosporine use lead to pre renal AKI

A

Vasoconstiction of afferent arterioles can result in chronic ischemia leading to chronic tubulointerstitial nephritis

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12
Q

What are the four types of drug induced intrinsic renal diseases

A

glomerular disease, Acute Tubular Necrosis, Intratubular Obstruction, Acute Interstitial Nephritis

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13
Q

What is drug induced glomerular disease, what does it cause, what drugs can bring it about

A

drug-induced autoimmune disease, causes proteinuria, NSAIDs, lithium, quinolones, bisphosphonates

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14
Q

What drugs cause drug induced Acute Tubular Necrosis

A

Aminoglycosides, contrast media, cisplatin and carboplatin, Amphotericin

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15
Q

What drug class has the highest rates of drug-induced AKI,

A

Aminoglycosides, accumulates in lysosomes of proximal tubules causing autodigestion leading to high output

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16
Q

T/F: Contrast increases SCr within 24 to 48 hours and the AKI is usally non-oliguric, with falsely elevated proteinuria

A

True

17
Q

What patients should avoid contrast

A

Patients with CKD and CrCl less than 60, reduced renal perfusion

18
Q

What is the ranking for types of contrast that have the most risk for AKI

A

High osmolar to Low osmolar to Iso-osmolar

19
Q

T/F: If there is no risk factors the risk of AKI from contrast is over 5%

A

False: If no risk factors, risk of AKI is less than 1%

20
Q

What is a hallmark feature of AKI due to cisplatin, how should the be handled

A

hypomagnesemia, Use IV hydration to maintain urine output to 3-4 L/day

21
Q

What are the two mechanisms to which amphotericin causes AKI

A

cause necrosis of proximal tubule, afferent arteriolar vasoconstriction

22
Q

What are common features of amphotericin induced AKI

A

Non-oliguric, hypokalemia, hypomagnesemia,acidosis

23
Q

What ways to prevent amphotericin induced AKI

A

use lipid formations, long infusion time over 4-6 hours, pre infusion with 1 liter of normal saline

24
Q

T/F: Intratubular obstruction can be caused by precipitation of drug crystals in the distal tubule

A

True

25
Q

What drugs can lead to intratubular obstruction

A

Acyclovir, Foscarnet, methotrexate

26
Q

What drugs can aid in metabolizing methotrexate

A

glucarpidase

27
Q

What drug drug interaction causes rhabdomyolysis leading to intratubular obstruction

A

cyclosporine and atorvastatin (increase statin levels 800 to 1000%)

28
Q

What is the clinical presentation of rhabdomylosis

A

muscle pain, weakness, dark brown or red urine due to myoglobinuria, no RBCs

29
Q

What enzyme will be increased due to rhadomylosis, when the problem is fixed when should this marker reduce

A

creatinine kinase, 1.5 days

30
Q

How should rhabdomyolysis be managed

A

agressive fluid resuscitation with normal saline, alkalization of the urine with IV sodium bicarbonate