This document discusses drug-induced acute kidney injury (AKI). It notes that AKI is characterized by an abrupt reduction in kidney function over 48 hours, shown by decreased urine output and increased creatinine levels. Between 5-20% of AKI cases are caused by medications, as kidneys excrete many water-soluble drugs and metabolites. Common culprits include contrast media, ACE inhibitors, NSAIDs, diuretics, and ARBs. Other "red flag" drugs mentioned are aminoglycosides, anticoagulants, anticonvulsants, antivirals, digoxin, immunosuppressants, and hypoglycemic medicines. Treatment focuses on supportive care like fluid management

1. Druginduced
kidneyinjury
Clinical Pharmacology

3. AKI
 It is characterized by an abrupt reduction
(usually within a 48-h period) in kidney
function, characterized by reduced urine
output and increased serum creatinine.
 Between 5 and 20 % of all AKI cases occur
as a direct result of medication
 Kidneys are responsible for the excretion of
many water soluble drugs and their
metabolites
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4. 3 TYPES
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5. COMMON
UK Renal Pharmacy Group – AKI Medicines
Optimisation Toolkit (March 2012)
Consider Acute Nephrotoxic Drug Action
• Contrast media
• ACE Inhibitors
• NSAID’S
• Diuretics
• ARB’s
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6. OTHERS
The toolkit also lists “red flag” drugs.
● Aminoglycosides
● Anticoagulants
● Anticonvulsants (e.g., phenytoin, gabapentin)
● Antivirals (e.g., acyclovir, ganciclovir)
● Digoxin
● Immunosuppressants (e.g., ciclosporin)
● hypoglycemic medicines
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10. Elevated Scr (normal range approximately 0.6-1.2
mg/dL [53 to 106 μmol/L])
Elevated BUN concentration (normal range
approximately 8 to 25 mg/dL [2.9-8.9 mmol/L])
Decreased CrCl (normal 90–120 mL/min)
BUN: creatinine ratio
greater than 20:1 in Prerenal AKI
Less than 20:1 in intrinsic or Postrenal AKI
Hyperkalemia
Metabolic acidosis
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12. Goal of treatment:
Minimize the degree of kidney insult
Reduce extrarenal complication
Restoration of renal function to pre AKI is the
ultimate goal
Currently, there is no definitive therapy for
AKI, supportive care is the mainstay of
management regardless of etiology.
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13. Non-pharmacological therapy
Maintenance of adequate cardiac output and blood
pressure to optimize tissue perfusion
Discontinue medication associated with diminished renal
blood flow
Initiate appropriate fluid and electrolyte
Renal replacement therapy RRT in sever AKI
Hemodialysis
Peritoneal dialysis
Absolute indications for dialysis usually include:
BUN greater than 100 mg/dL (35.7 mmol/L)
Potassium greater than 6 mEq/L (6 mmol/L)
Magnesium greater than 9.7 mg/dL (4.0 mmol/L)
Metabolic acidosis with a pH less than 7.15
Diuretic-resistant fluid overload.
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14. Preventing AKI and reducing risk involves:
● Early assessment
● Treating infections and other medical
conditions promptly
● Ensuring patients are hydrated
appropriately
● Avoiding hypotension (systolic BP
<110mmHg)
● Medicines optimisation
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 https://www.uspharmacist.com/article/drug-
induced-acute-renal-failure
 https://www.facebook.com/manualofmedicine/
 [Roger Walker] Clinical Pharmacy and
Therapeutics (5th Ed.).pdf
 Kidney Disease: Improving Global Outcomes
(KDIGO) Acute Kidney Injury Work Group.
 KDIGO clinical practice guideline for acute kidney
injury. Kidney Int Suppl 2012;2:1-138.
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4
594214/#

16. STOP
kidneyattack!
Thankyou…