not all drugs are good drugs: Kidney Flashcards
Drug induced kidney disease risk factors
- 65+
- CKD
- Conmitant nephrotoxins
- Renin-dependent state
- Low effective circulating volume
- HF
- Cirrhosis
- Low effective circulating volume
- Known drug allergy
- Duration of therapy
- DM
- HTN
Drug induced kidney disease general prevention
- Directly prevent the drugs MOA of kidney injury
- Avoid the drugs in high risk pts
- Maintain adequate kidney perfusiion
- Hydration
- IV isotonic crystalloids in pts at risk of AKI
- Lacated ringers
- Plasma-lyte A
- 0.9% NaCl
- TDM if relevant
Kidney function monitorinng
- SCr, BUN, eGFR, urinary output
- Novel biomarkers: are markers of damage;
- Traditional biomarkers: SCr and BUN are markers of function
Drugs that cause hemodynamic mediated renal injury via reduction in glomerular pressure dt alterations in arteriole tone
- ACE/ARB
- NSAID
- SGLT2
- CNI (cyclosporine, tacrolimus)
ACE/ARB mechanism of kidney injury
decrease angiotensin II → efferent arteriole dilation
NSAID mechanism of kidney injury
decrease PGE2 production → afferent arteriole constriction
Calcineurin inhibitor mechanism of kidney injury
afferent arteriole constriction
hemodynamic mediated renal injury via reduction in glomerular pressure dt alterations in arteriole tone risk factors
- dehydration/low volume state + the culprit drugs → highest risk for AKI
- NSAID + ACE/ARB = loss of autoregulation → increased risk of decreased intraglomerular hydrostatic pressure → decreased GFR
hemodynamic mediated renal injury via reduction in glomerular pressure dt alterations in arteriole tone prevention methods
- Adequate fluid intake
- Risk factor management
- Start with lowest dose in pts with highest risk
- monitor SCR, BUN, K, wt Q2W until stable
- hold diuretics during intiating/titrating - Avoid NSAID + ACE/ARB combo in pts with CKD, HF, liver disease
hemodynamic mediated renal injury via reduction in glomerular pressure dt alterations in arteriole tone treatment
- DC offending agent
- Provide sufficient fluids
- typically 0.9% NaCl - Monitor kidney function and electrolytes
Drugs that cause pre-renal kidney injury via reduced blood flow in the kidney
diuretics; decreases effective circulatory volume if over-diuresis occurs
Drugs that cause glomerulonephritis
- Gold
- Allopurinol
Drugs that cause acute tubular necrosis (ATN)
- aminoglycosides
- amphotericin B (conventional has higher risk than liposomal)
- IV contrast media (iohexol, iodixanol)
IV contrast media induced kidney injury risk factors
Agent specific
- Large volume
- High osmolal contrast
- Ionic contrast
- Short interval between contrast admin
Pt specific
- DM
- Age
- GFR < 60
- low ECV
- LVEF < 40%
Aminoglycoside risk factor for kidney injury
- related to trough [ ] → TDM and PK individualization much important
- no difference in extennded and regluar interval dosing → but most places use extended
Prevention method fo IV contrast media induced kidney injury
For contrast media: 0.9% NaCl give 1-1.5 ml/kg/hr 12 hours before and after
- can also add PO NAC 1200mg PO BID x 4 doses (limited evidence on efficacy but is well tolerated)
Drug induced acute tubular nerosis treatment
- SUPPORTIVE CARE
- DC offending agent
- Hydration
- Electrolyte management
- Dialysis if severe (anuria, uremia, edema, K>7)
THIS IS ATN TREATMENT
Drugs that cause acute interisitial nephritis
- Allopurinol
- Anti-epileptics
- Beta-lactams
- Diuretics
- *NSAIDs
Penicillins
PPIs
Sulfa drugs** - Vanco
Mechanism of injury for acute interstitial nephritis (AIN)
Immune activation / hypersensitivity → leukocyte infiltration → inflammation → AIN
Vanco AKI risk factors
- high trough >20 mg/L
- AUC >600
- TDD >4g
- LOT >7D
- wt >101.4kg
Prevention methods for vanco induced kidney injury
avoid concomitant use with aminoglycosides, amphotericin, and contrast
drug indcued acute interstitial nephritis treatment
- Stop offending drug
- Avoid cross-reacting drugs
- Supportive care
- Steroids: early aggressive steroid may improve long-term renal outcome
> give large bolus, then taper
MePn 250-500mg IV QD x 3-5 days
Then Pred 1 mg/kg/d tapered x 8-12 weeks
Drugs that cause vasculitis
- PTU
- Allopurinol
- Phenytoin
- Cocaine
Drugs that cause nephrolithiasis
- Acyclovir
- Allopurinol
- Furosemide
- Sulfonamides
- Topiramate
Prevention methods for drug indcued nephrolithaisis
- Adequate hydration
- goal urine output >2.5 L/day - TZD diuretic if high urinary Ca → decrease the amount of Ca that can precipitate into stones
Drug indudced nephrolithiasis treatment
- Hydration
- Pain management
- Lithotripsy: shockwave disintegration of stone
Drugs that cause rhabdomyolysis intra-tubular obstruction
- statins/statin-fibrate combos
Statin induced kidney injury MOA
Statins → rhabdomyolysis → muscle breakdown → precipitation of myoglobin in kidneys
drug induced rhabdomyolysis intra-tubular obstruction treatment
- DC offending agent
- Aggressive IV fluid -> treats the intra-tubular
myoglobin obstruction) - may require urinary alkanization if urine pH < 6.5
- alternate between IV NaCl and sodium bicarb to fix
- Target UOP ~ 3ml/hr
Lithium indcued CKD risk factors
cumulative lithium dose and other common sense things
lithium induced CKD prevention methods
- Lithium TDM
- Stay hydrated
- Renal monitoring
- Avoid DDI (e.g. HCTZ)
lithium induced CKD treatment
- damage is IRREVERSIBLE
- DC lithium
- Hydrate
- Amiloride 5-20mg QD if polydipsia/polyuria and especially if nephrogenic diabetes insipidus)
- Avoid other nephrotoxic drugs
- Monitor renal function
1 cause of CKD
diabetes
number 2 cause of CKD
HTN
A patient is considered high risk for drug induced kidney disease if:
Renin dependent disease states
- late stage CKD
- HF
- liver disease
- pronounced albuminuria @ baseline
On many nephrotoxic drugs
24 hour trough goal for EIAD
undetectable
EIAD = extended interval aminoglycoside dosing
CIN agent: Iohexol [Omnipaque 450]
nonionic
lower osmolality
CIN agent: Iodixanol [Visipaque 320]
- nonionic
- iso-osmolar
- preferred contrast media
Monitoring for CIN (contrast media)
Renal fx
- SCr, BUN Q12H x 2 days, then Q24H x 5-7 days inpatient
UOP
- strict in/out x 4 days
Med review
Electrolytes - only if renal injury develops
When monitoring for CIN, we regularly monitor for electrolytes: True/False?
False
Electrolytes only checked if kidney injury develops - does not tell you about RISK or the presence of injury
IBW
F: 45.5 + 2.3 (inches over 60)
M: 50 + 2.3 (inches over 60)
Cockcroft gault
[(140 - age ) x IBW] / (72xSCr)
- if female x 0.85
ATN presentation
- Acute progression - rapid recovery
- ↑SCr, BUN
- ↓GFR, UO (non-oligu/olig )
- Proteinuria
- Muddy brown casts, granular
- +/- acidosis, hyperkalemia
- FeNa >1% (pre-renal AKI would have FeNa<1%)
AIN presentation
- Type 4 hypersensitivity
- Fever, rash, eosinophilia
- WBC casts
