Pharmaotherapeutis of Drug induced kidney disease

1. Drug induced kidney disease
Dr. V. S. Swathi
Assistant Professor
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2. Definition
It is defined as abrupt or gradual loss of renal function due to
drugs and is characterised by increased serum creatinine
value and blood urea nitrogen which is having temporal
relationship between renal toxicity and drug
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3. Epidemiology
• Acute tubular necrosis is most common cause of drug
induced kidney disease in hospitalised patients
• Mostly this problem is reversible with discontinuation of
offending agent but sometimes it is irreversible even after
withdrawl of drug
• In adults, it is approximately 14-26% in prospective studies of
acute kidney injury
• In paediatric population, it is responsible for 16% of drug
induced Acute kidney injury which leads to hospitalisation
• In India, it leads to 20% of total acute kidney injury cases
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4. Risk factors
• Increased age
• Alcohol abuse
• Pre existing kidney disease
• Critically ill patients
• Large total cumulative dose of drugs
• Prolonged therapy of nephrotoxic drugs
• Concomitant therapy of 2 or more nephrotoxic drugs
• Diabetes
• Poor nutrition
• Shock
• Liver diseases
• Dehydration
• Hypotension
• Cardiovascular diseases
• Administration of contrast media
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5. Causes
Tubular epithelial cell damage
• Acute tubular necrosis
• Aminoglycosides
• Amphotericin B
• Antiviral drugs
• Anticancer drugs
• Radiographic contrast media
Osmotic nephrosis
• Mannitol
• Sucrose
• IV immunoglobulin 5

6. Causes continued….
Hemodynamically mediated kidney injury
• Angiotensin converting enzyme inhibitors
• Angiotensin receptor blockers
• Non steroidal anti inflammatory drugs
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7. Causes continued….
Obstructive nephropathy
Crystal nephropathy
• Anti viral drugs
• Sulphonamides
• Methotrexate
Nephrolithiasis
• Sulphonamides
Nephrocalcinosis
• Oral sodium phosphate solution 7

8. Causes continued….
Glomerular disease
Minimal change disease
• Non steroidal anti inflammatory drugs
• Lithium
Focal segmental Glomerulosclerosis
• Interferon alpha and beta
• Anabolic steroids
Membranous disease
• Non steroidal anti inflammatory drugs
• Captopril
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9. Causes continued….
Tubulointerstitial disease
Acute allergic interstitial nephritis
• Pencillins
• Ciprofloxacin
• Non steroidal anti inflammatory drugs
• Proton pump inhibitors
• Loop diuretics
Chronic interstitial nephritis
• Lithium
• Cyclosporine
Papillary necrosis
• Non steroidal anti inflammatory drugs
• Aspirin
• Caffeine 9

10. Causes continued….
Renal Vasculitis, thrombosis and cholesterol emboli
Vasculitis and Thrombosis
• Allopurinol
• Propylthiouracil
Cholesterol emboli
• Warfarin
• Thrombolytic agents
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11. Pathogenesis
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12. Pathogenesis continued….
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13. Pathogenesis continued….
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14. Pathogenesis continued….
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15. Pathogenesis continued….
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16. Pathogenesis continued….
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19. Clinical presentation
• Decrease in glomerular filtration rate
• Increase in serum creatinine and blood urea nitrogen
• Malaise
• Anorexia
• Vomiting
• Oedema
• Shortness of breath
• Decreased urine output
• Metabolic acidosis with bicarbonaturia
• Glycosuria
• Polyuria
• Hyperkaelemia 19

20. Complications
• Tubulopathies
• Nephrotic syndrome
• Acute kidney disease
• Chronic kidney disease
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21. Diagnosis
• Medical and medication history
• Clinical presentation
• Renal function tests
• Electrolyte levels
• Urine microscopy
• Creatinine clearance
• CT scan of kidney and urinary tract
• MRI of kidney and urinary tract
• Kidney biopsy
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22. Prevention and Treatment
• Know about potentially nephrotoxic drugs
• Identify high risk groups of patients
• Avoid use of nephrotoxic drugs in high risk groups
• Avoid use of combination of 2 or more nephrotoxic drugs
• Adjust dose and duration of nephrotoxic drugs
• Maintain adequate hydration while using nephrotoxic drugs
• In severe cases of DIKD cases, go for renal replacement
therapy
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23. Tools to calculate eGFR
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24. Resources
• https://bmcnephrol.biomedcentral.com/track/pdf/10.1186/
s12882-017-0536-3
• https://cjasn.asnjournals.org/content/clinjasn/13/12/1897.f
ull.pdf
• file:///E:/TEST%20BOOK/DIKD%20ARTICLE.pdf
• https://sci-hub.tw/10.2174/1389200218666171108154419
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3794522/p
df/ooomb4-20-268.pdf
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