DIKD Flashcards by Garima Khanal

What are the 3 most common manifestations of drug induced kidney disease? (DIKD)

Decline in GFR
Rise in serum creatinine (S_cr)
Rise in BUN (blood urea nitrogen)

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BUN is a marker of reanl health. If GFR and blood volume are decreased, will BUN be elevated or decreased?

Increased

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How is nephrotoxicity reversible?

Offending agent discontinued

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6 things to look out for in DIKD

“HE A PUP”

Hematuria
Electrolyte imalances
Acid-base abnormalities
Proteinuria
Urine sediment abnormalities
Pyuria-neutrophils (pus) in urine

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Blood flows through the ___ arteriole, to the glomerulus, and exits through the __ arteriole.

afferent (arrives)
efferent (exits)

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A decrease in blood flow and renal perfusion can lead to _____.

a pre-renal reduction in renal function

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Under conditions in which renal blood flow is diminished, the kidney maintains glomerular ultrafiltration by _____ the _____ arterioles and _____ the _____ arterioles.

vasodilating the afferent
vasoconstricting the efferent

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Damage to the glomerular or tubular regions can lead to…

intrinsic AKI

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Obstruction of urine flow in the collecting tubule, ureter, bladder, or urethra is termed _____

post-renal impairment

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3 parameters to assess for possible drug-induced AKI

Abrupt (48 hrs) reduction in kidney function defined as absolute increase in S_cr of greater than or equal to 0.3mg/dL
Percentage increase in S_cr of greater than or equal to 50% (1.5 fold from baseline) within 7 days
Reduction in urine output (documented oliguria of less than 0.5 mL/kg/h for more than 6 hrs), when correlated temporally w/ the initiation od drug

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3 causes of pre-renal AKI

Transient renal hypoperfusion:
- Hypotension
- Decreased CO
- Decreased effective arterial blood volume

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1 cause of Post-renal AKI

Obstruction of urinary tract

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3 causes of Intrinsic AKI

Acute glomerulonephritis (inflammation/damage to glomerular membrane)
Acute interstitial nephritis (allergic rxn may be caused by drugs)
Acute tubular necrosis (accounts for more than 50% of cases of AKI)
- nephrotoxic agents
- prolonged renal hypoperfusion

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Causes of what?

drug-induced osmotic diuresis
Diabetes Insipidus
burns
3rd space losses (hypoalbuminemia)

Volume Depletion leading to Pre-renal AKI

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3 drugs which cause Pre-Renal AKI

NSAIDS
ACE-I
ARBs

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Cause of what?

Exogenous Toxins (nephrotoxic drugs, contrast dyes)

Acute Tubular Necrosis

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Causes of what?

NSAIDS and certain abx

Acute Interstitial Nephritis

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Causes of what?

BPH
Malignancy
Anticholinergic drugs
Displaced bladder catheter

Bladder outlet obstruction –> Post-renal AKI

____ is the most common presentation of DIKD in hospitalized patients

Acute Tubular Necrosis (ATN)

What are the 6 primary agents causing ATN –> DIKD in hospitalized pts?

RAACO

Radiocontrast media**
Aminoglycoside abx**
Amphotericin B**
Cisplatin
Osmotically active agents

Pathogenesis is a decrease in glomerular capillary hydrostatic pressure

ACI-I
NSAIDS

Hemodynamically mediated kidney injury

27% of kidney biopsies performed for hospitalized pts w/ unexplained AKI
Clinical manifestations present approximately 14 days after initiation of therapy:
- fever, maculopapular rash, eosinophilia
- arthralgia, pyuria, hematuria
- proteinuria, oliguria

Acute Allergic Interstitial Nephritis (AAIN)

Which 2 drugs cause the majority of allergic rxns?

PCN
Sulfa

Pharmacokinetic Alterations

What can significantly increase the volume of distribution of many drugs
What is often an accompanying problem resulting in: -reduction in CO -reduction in liver function

Edema
Multisystem organ failure

What 3 medications are affected by Pharmacokinetic Alterations?

* Vancomycin (tx MRSA and gram +) * Aminoglycosides * Low-molecular-weight heparins

**Electrolyte Disorders** * Most common electrolyte disorder * \>\_\_% of ___ is renally eliminated * Life-threatening cardiac arrhythmias * Frequent monitoring needed

Hyperkalemia

Which 2 elements are both eliminated by the kidneys and are not removed efficiently by dialysis?

Phosphorus & Magnesium

What 3 drugs can cause hyperkalemia? We don't "recycle" potassium. But we can prevent the excretion. It is NOT well regulated by the kidneys.

* ACE * ARB * K-sparing (spirinolactone)

Amphotericin is a terrible drug which kills what?

Fungi

**Types of what?** * Acute Tubular Necrosis * Osmotic nephrosis

Tubular Epithelial Cell Damage

**Types of what?** * Intratubular obstruction * Nephrolithiasis * Nephrocalcinosis

Obstructive nephropathy

**Types of what?** * Acute allergic interstitial nephritis * Chronic interstitial nephritis * Papillary necrosis

Tubulointerstitial disease

3 agents causing osmotic nephrosis (Tubular Epithelial Damage)

* Dextran * IV immunoglobulin * Mannitol

**Pathogenesis of what?** * Accumulation of high drug concentrations within proximal tubular epithelial cells * Produces reactive oxygen species causing mitochondrial injury * LEADS TO KIDNEY NECROSIS\*\* * Toxicity is related to the # of cationic groups on the molecule * Neomycin\>Gentamicin\>Tobramycin\>Amkacin

Aminoglycoside (AG) Nephrotoxicity

_Clinical presentation of what?_ * Nonoliguria * Evidence of injury **seen within 5-10 days after initiation of therapy\*\*\*** (not abrupt) * **Gradual progressive rise in S_cr and BUN and decrease in CrCl** * **Full recovery of renal function is common if therapy is immediately discontinuted**

Aminoglycoside Nephrotoxicity

If an aminoglycoside must be used, which one should be used?

Amikacin

3 risk factors of Aminoglycoside Nephrotoxicity

* **Aggressiveness of AG dosing** * large cumulative dose * prolonged therapy * **Synergistic toxicity w/ other nephrotoxins** * **Preexisting clinical conditions** * CKD * DM * Older age * Dehydration

How do you prevent Aminoglycoside Nephrotoxicity?

* **Avoid volume depletion\*\*** * Use alternative abx when possible * Limit total dose administered * Avoid concomitant nephrotoxic drugs

4 ways to manage Aminoglycosde Nephrotoxicity

* Discontinue AG or revise dosing regimen * Stop other nephrotoxic drugs * Adequate hydration * Renal Replacement Therapy (RRT) DARS

_Pathogenesis of what?_ * **Renal ischemia from systemic hypotension and acute vasoconstriction\*\*** * Disruption of normal renal blood flow may last for several hours * Increased contrast in renal tubules, exacerbating direct toxicity * extent of cellular toxicity directly related to contrast exposure

Contrast-Induced Nephrotoxicity (CIN)

_Presentation of what?_ * Nonoliguria (\>500ml urine/ day) * **Injury present within first 24-48 hrs after administration\*** * **S_cr usually peaks between 3 and 5 days after exposure\*** * **Recovery after 7 - 10 days\***

Contrast Induced Nephrotoxicity (CIN)

What are the 3 main risk factors of Contrast-Induced Nephrotoxicity (CIN)?

* **Pre-existing kidney disease\*** (GFR\<60) * **Decreased renal blood flow\*** (CHF, dehydration/volume depletion, hypotension, diabetes) * **Concurrent use of nephrotoxins\*** (NSAIDs, ACEIs) (as # of risk factors increase, mortality increases)

4 ways to prevent Contrast Induced Nephrotoxicity (CIN)

* **Use alternative imaging procedures\*** * Hydration * Antioxidants (ascorbic acid, N-acetylcysteine) * Hemofiltration

Management of Contrast Induced Nephrotoxicity (CIN)

* Supportive Care * Monitoring (renal function, electrolytes, volume status) * RRT when indicated (renal replacement therapy)