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PDAT3 > 21 - Drug Induced Renal Disease > Flashcards

21 - Drug Induced Renal Disease Flashcards

1
Q

How to ID
Drug-Induced AKI

A

Generally detected by routine daily labs, but:
SCr can LAG behind renal dmg by 1-2 days

Due to delay / not taking labs (outpatient setting) we check symptoms:
Decreased Urination
HYPERvolemia = EDEMA
Nausea / loss of appetite / Malaise
Confusion

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2
Q

Prevention of Drug-Induced AKI

A

_AVOID using nephrotoxic drug_s
in patients with these risk factors for AKI:

Already Existing:
Renal Insufficiency / Nephrotoxic Meds

IVF depletion
Dehydrated / HF / Cirrhosis / Loop Diurtics

ELDERLY

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3
Q

What causes:
PSEUDO-DRUG-induced Renal Disease?

A

Most commonly:

  • *TRIMETHOPRIM** (from bactrim)
  • also* Dronaderone (new drug)

↑SCr due to competitive inhibition of Creatinine secretion
within the proximal tubule
↑SCr by as much as 0.5 mg/dL
without changing GFR

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4
Q
  • *Causes of** PRE-RENAL
  • *Drug-Induced Renal Disease**

Drugs and Mechanism

A
  • *Pre-Renal AKI** is due to a
  • reduction in renal blood flow*

Loop Diuretics

ACE-I + ARBs

NSAIDs

Cyclosporine & Tacrolimus

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5
Q
  • *Types of** INTRINSIC
  • *Drug-Induced Renal Disease**
A

Glomerular Disease
Drug-Induced AutoImmune -
NSAID / Lithium / Quinolones / BisPhos

ATN = Acute Tubular Necrosis
AminoGlycosides / Contrast / CisPlatin-CarboPlatin / Amphotericin B

Intratubular Obstruction
Precipitation of Drug Crystals @ distal tubule
Acyclovir / Foscarnet / Methotrexate
Statin Induced Rhabdo (CSA + Statin)

AIN = Acute Interstitial Nephritis
Methicillin (most common) PPIs, ultimately ANY DRUG
not dose dependent, drug-induced ALLERGIC rxn

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6
Q

Loop Diuretic Induced AKI

What Type of AKI?

A

PRE-RENAL

  • *Too HIGH DOSE**
  • -> decreased IVF –> decreased Renal Blood Flow / filtration
  • *Increased SCr & AKI**

In HF or Cirrhosis, often have to choose between:
Relieving Edema/Ascites
OR
causing AKI / Hypotension

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7
Q

Inadvertant cause of

PRE-RENAL AKI

A

PRE-RENAL AKI

HCTZ
is used for HT in a patient that then gets EDEMA
VVV
Add LOOP DIURETIC, w/o holding HCTZ
VVV
PROFOUND DIURESIS

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8
Q

ACE + ARB Induced AKI

What Type of AKI?

A

PRE-RENAL AKI

ACE/ARB –BLOCK-> RAAS
VVV
E-fferent renal VasoDILATION
usually effects in NO or small increase in Scr

  • *Effect is GREATER if patient has** RENAL ARTERY STENOSIS
  • *RAAS used to COMPENSATE**

typically OKAY due to second kidney
BUT, Contraindicated in BILATERAL Stenosis

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9
Q
  • *Renal Artery Stenosis + ACE/ARBS**
  • *AKI**
A

Stenosis of A-ferrent Arterioles
VVV
Reduction in Blood flow TO KIDNEYS
less Arteriolar pressure
VVV
INCREASED RAAS system to COMPENSATE
(E-ferrent VasoCONSTRICTION, normally)

  • BUT:*
  • *ACE/ARBs are BLOCKING the COMPENSATION SYSTEM**

Normally would be able to compensate with SECOND KIDNEY, but in Bilateral Renal Artery Stenosis –> ACE/ARB are Contraindicated

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10
Q

NSAID Induced AKI

What Type of AKI?

A
  • *PRE-RENAL AKI**
  • can occur within days*

NSAIDs -block-> prostaglandin VasoDILATION
VVV
A-ferrent Arteriolar VasoConstriction
-> decreased IntraGLOMERULAR PRESSURE + FIltration
VVV
Increased SCr –> AKI

  • *Even be WORSE with ACEI or ARB**
  • *A-ferrent + E-ferrent Constriction**
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11
Q

What drugs cause

E-fferent VasoDILATION?

A
  • *ACE-Inhibitors**
  • prils
  • *ARBs**
  • sartans
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12
Q

What drugs cause

A-fferent VasoCONSTRICTION

A

NSAIDS
Pre-Renal, Induced AKI

CycloSporine A** + **TACrolimus
Pre-Renal, induced AKI –> chronic ischemia –> delayed chronic tubulointererstitial Nephritis

Amphotericin

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13
Q
  • *Cyclosporine_ & _Tacrolmus**
  • *Induced AKI**
A

PRE-RENAL AKI

irony for renal transplant patients

Cause Vasoconstriction of A-fferent Arterioles
Can result in Chronic Ischemia –> Delayed Chronic Tubulointerstitial Nephritis

  • *DOSE RELATED**
  • can reduce dose rather than DC*
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14
Q
  • *Drug Induced Glomerular Disease**
  • *INTRINSIC AKI**
A
  • *Drug-Induced AUTOIMMUNE DISEASE**
  • not a DIRECT cellular toxicity*

Causes: PROTEINURIA

NSAIDs / Lithium / Quonolones / Bisphosphonates

Management:

  • *D/C Drug**
  • *steroids** if renal fxn does not improve
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15
Q

What DRUGS cause

ATN
Drug-Induced Acute Tubular Necrosis
(INTRINSIC AKI)

A

Aminoglycosides
most common, insidiuous presentation, autodigestion of proximal tubules

  • *Cisplatin + Carboplatin**
  • hypomag*

Amphotericin B
A-fferent arterial vasoconstriction, hypomag

Radiographic Contrast Media

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16
Q

AminoGlycosides = AGs

Cause what type of AKI?

A

Drug-Induced ATN = Intrinsic AKI

Highest rates of drug-induced AKI

Risk factors:
High Trough Levels, want to keep < 1.0
Use with other nephrotoxic drugs
Kidney-Liver Disease / Age / HypoVolemia / Critically Ill

17
Q

How do AGs cause AKI?

A

AGs are freely filtered through glomerulus
VV
Accumulates in LYSOSOMES of the PROXIMAL tubule
–> Lysosomes BURST
= Autodigestion of Proximal Tubules
VV
unable to CONCENTRATE URINE –> High Output AKI

Keep Trough Levels < 1
INSIDIOUS NEPHROTOXICITY
keep repeateing trough –> can SPIKE

18
Q

AminoGlycoside Induced ATN
INTRINSIC AKI

TREATMENT / MANAGEMENT

A
  • Discontinue AG*
  • -> start ALTERNATIVE

START NS
to make sure the
associated HIGH URINE OUTPUT
does NOT exacerbate the AKI
by causing a PRE-RENAL AKI as well

19
Q

IV Radiographic Contrast Media

Causes what type of AKI?

A

ATN** = **Intrinsic AKI

Unknown Mechanism:

  • *renal vasoconstriction** –> medullary hypoxia
  • *cytotoxic effects** –> directly on tubular cells

Clinical Features:

  • ↑*SCrwithin24-48 hours after contrast
  • NON-oliguric AKI* + FALSELY elevated PROTEINURIA
20
Q

IV Radiographic Contrast Media
induced ATN - Intrinsic AKI

Risk Factors & Prevention

A

Prevention: Volume Expansion with NS
sodium bicarb / N-acetylceysteine is NO longer recommended

Risk Factors:
CKD w/ CrCl <60, especially if DM Nephropathy
HF / Hypovolemia / Hemodynamic instability
HIGH OSM / DOSE Contrast
Intra-arterial > intra venous
concurrant use of nephrotoxins

21
Q

Cisplatin & Carboplatin

Causes what type of AKI?

A

Drug-Induced ATN = INTRINSIC AKI

Carboplatin = low risk of AKI

CISplatin = DOSE RELATED

HypoMAGNESEMIA = HALLMARK FINDING

Treated with:
IV Hydration –> maintain urine output 3-4 L/day

22
Q

Amphotericin

Causes what type of AKI?

A

Drug-Induced ATN = INTRINSIC AKI

Ampho-terrible –> for fungal infections
Mechanism:
binds to ergo sterol in cell membranes of tubular cells –> necrosis of proximal tubile –> non-oliguric AKI

A-ferrent Ateriolar Vasoconstriction

Presentation:
HypoMagnesemia / HypoKalemia
Acidosis / Non-oliguric AKI

23
Q

Amphotericin-Induced ATN
INTRINSIC AKI

PREVENTION & Risk Factors

A

Prevention:
Use LIPID FORMULATION
liposomal amphotericin B, reduces renal concentrations
Long infusion Time (4-6 hours) + PRE-INFUSION of 1L NS

Risk Factors:
HypoVolemia / HypoKalemia
Large doses / other nephrotoxins

24
Q

Acyclovir / Foscarnet / Methotrexate / Statins

cause WHAT TYPE of AKI?

A

Intratubular Obstruction = INTRINSIC AKI

Precipitation of DRUG CRYSTALS –> DIstal Tubule
VV
can lead to obstruction of the tubule
as well as:
Interstitial nephritis due to autoimmune response or ATN

Risk Factors:
low Urine volume / low urinary pH (acidic)

25
Q

How to treat

Methotrexate-induced
INTRATUBULAR OBSTRUCTION?
Intrinsic AKI

A

Methotrexate:
low urinary pH + HIGH doses

Premedicate w/ FLUIDS + BICARB –> Urine pH > 7

AKI can be
treated with GLUCARPIDASE
which metabolizes the methotrexate

26
Q

Statin Induced Rhabdomyolysis

occurs more often with what other drug?

Clinical Presentation?

A

IntraTubular Obstruction = Intrinsic AKI

CYCLOSPORINE
with Atorvastatin –> 800-1000% increase in levels

Presentation:
MUSCLE PAIN + Weakness
RED-BROWN URINEdue tomyoglobunuria
Heme pigment –> obstruction of tubules -> AKI
Elevated Creatinine Kinase > 5x ULN (200)

27
Q

Statin Induced Rhabdomyolysis
IntraTubular Obstruction = Intrinsic AKI

MANAGEMENT

A

Red-Brown Urine due to Myoglobinuria + 5xULN of CK

FLUID RESUSCITATION w/ NS
to improve renal perfusion
dilution of heme pigment / wash out obstruction casts

IV SODIUM BICARB
for alkalization –> prevents HEME-PROTEIN precipitation
maintain urine pH >6.5
lacks evidence for efficacy

28
Q

Methicillin / PPIs

causes what type of AKI?

A

AIN = Acute Interstitial Nephritis
INTRINSIC AKI

  • *AIN can be caused by ANY DRUG**
  • just more commonly METHICILLIN + PPIs*

Drug-Induced ALLERGIC REACTION = not dose dependednt
can also be caused by:
Autoimmune disorders / Infections, but 75% drug-induced

29
Q

Acute Interstitial Nephritis = AIN
Intrinsic AKI

Clinical Manifestations + Management

A

Management:

  • *D/C THE DRUG,** if no improvement in SCr in 3-7 days
  • -> CORTICOSTEROIDS​ = Prednisone 40-60mg QD
  • until creatinine returns to baseline*, can be on therapy for 2-3 mo

Manifestation:
URINE WBC CASTS
Onset can be several weeks-months after stating drug
if previously exposed –> onset can be 1-3 days

Usually does NOT have significant PROTEINURIA
except with NSAID-induced AIN

allergic s/sx are typicaly NOT present

30
Q

What drugs cause

DRUG-INDUCED KIDNEY STONES?

Obstructive Post-Renal AKI

A

TRIAMTERENE
Drug precipitation - 0.4%

SULFADIAZINE
poorly soluble –> crystaluria
30% incidense

PDAT3 (23 decks)

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